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Depressed and cognitively impaired
CASE Depressed and anxious
Five years ago, Ms. X, age 60, was diagnosed with treatment-resistant major depressive disorder (MDD) with anxiety. This diagnosis was established by a previous psychiatrist. She presents to a clinic for a second opinion.
Since her diagnosis, Ms. X has experienced sad mood, anhedonia, difficulty falling asleep, increased appetite and weight, and decreased concentration and attention. Her anxiety stems from her inability to work, which causes her to worry about her children. In the clinic, the treatment team conducts the Patient Health Questionnaire-9 (PHQ-9) and Generalized Anxiety Disorder-7 item scale (GAD-7) with Ms. X. She scores 16 on the PHQ-9, indicating moderately severe depression, and scores 12 on the GAD-7, indicating moderate anxiety.
Ms. X’s current medication regimen consists of venlafaxine extended-release (XR) 225 mg/d, trazodone 100 mg/d at bedtime, and clonazepam 1 mg twice daily. She reports no significant improvement of her symptoms from these medications. Additionally, Ms. X reports that in the past she had been prescribed fluoxetine, citalopram, and duloxetine, but she cannot recall the dosages.
Ms. X appears appropriately groomed, maintains appropriate eye contact, has clear speech, and does not show evidence of internal stimulation; however, she has difficulty following instructions. She makes negative comments about herself such as “I’m worthless” and “Nobody cares about me.” The treatment team decides to taper Ms. X off venlafaxine XR and initiates sertraline 50 mg/d, while continuing trazodone 50 mg/d at bedtime and clonazepam 1 mg twice daily. The team refers her for cognitive-behavioral therapy (CBT) to address her cognitive distortions, sad mood, and anxiety. Ms. X is asked to follow up with Psychiatry in 1 week.
EVALUATION Unusual behavior
At her CBT intake, Ms. X endorses depression and anxiety. Her PHQ-9 score at this visit is 19 (moderately severe depression) and GAD-7 score is 16 (severe anxiety). The psychologist notes that Ms. X is able to complete activities of daily living and instrumental activities of daily living without assistance. Ms. X denies any use of illicit substances or alcohol. No gross memory impairment is noted during this appointment, though Ms. X exhibits unusual behavior, including exiting and re-entering the clinic multiple times to repeatedly ask about follow-up appointments. The psychologist concludes that Ms. X’s presentation and behavior can be explained by MDD and pseudodementia.
[polldaddy:12189562]
The authors’ observations
Pseudodementia gained recognition in clinical research >100 years ago.1 Officially coined by Kiloh in 1961, the term was used broadly to categorize psychiatric cases that present like dementia but are the result of reversible causes. More recently, it has been used to describe older adults who present with cognitive deficits in the context of depressive symptoms.2 The goal of evaluation is to determine if the primary issue is a cognitive disorder or a depressive episode. DSM-5-TR does not classify pseudodementia as a distinct diagnosis, but instead categorizes its symptoms as components under other major diagnostic categories. Patients can present with MDD and associated cognitive symptoms, or with a cognitive disorder with depressive symptoms, which would be diagnosed as a cognitive disorder with a major depressive-like episode.3
Pseudodementia is rare. Brodaty et al4 found the prevalence of pseudodementia in primary care settings was 0.6%. Older adults (age >65) who live alone are at increased risk of developing pseudodementia, which can be worsened by poor social support and acute psychosocial and environmental changes.5 A key characteristic of this disorder is that as the patient’s depressed mood improves, their memory and cognition also improve.6Table 13,6 outlines overlapping features of MDD and pseudodementia.
Continue to: EVALUATION Worsening depression
EVALUATION Worsening depression
At her Psychiatry follow-up appointment, Ms. X reports that her mood is worse since she ended the relationship with her partner and she feels anxious because the partner was financially supporting her. Her PHQ-9 score is 24 (severe depression) and her GAD-7 score is 12 (moderate anxiety). Ms. X reports tolerating her transition from venlafaxine XR 225 mg/d to sertraline 50 mg/d well.
Additionally, Ms. X reports her children have called her “useless” since she continues to have difficulties following through on household tasks, even though she has no physical impairments that prevent her from completing them. The Psychiatry team observes that Ms. X has no problems walking or moving her arms or legs.
The Psychiatry team administers the Montreal Cognitive Assessment (MoCA). Ms. X scores 22, indicating mild impairment.
The team recommends a neuropsychological assessment to determine if this MoCA score is due to a cognitive disorder or is rooted in her mood symptoms. The team also recommends an MRI of the brain, complete blood count (CBC), comprehensive metabolic panel (CMP), and urinalysis (UA).
[polldaddy:12189567]
Continue to: The authors' observations
The authors’ observations
Neuropsychological assessments are important tools for exploring the behavioral manifestations of brain dysfunction (Table 2).7 These assessments factor in elements of neurology, psychiatry, and psychology to provide information about the diagnosis, prognosis, and functional status of patients with medical conditions, especially those with neurocognitive and psychiatric disorders. They combine information from the patient and collateral interviews, behavioral observations, a review of patient records, and objective tests of motor, emotional, and cognitive function.
Among other uses, neuropsychological assessments can help identify depression in patients with neurologic impairment, determine the diagnosis and plan of care for patients with concussions, determine the risk of a motor vehicle crash in patients with cognitive impairment, and distinguish Alzheimer disease from vascular dementia.8 Components of such assessments include the Beck Anxiety Inventory (BAI) to assess anxiety, the Dementia Rating Scale-2 and Neuropsychological Assessment Battery-Screening Module to assess dementia, and the Beck Depression Inventory (BDI) to assess depression.9
EVALUATION Continued cognitive decline
A different psychologist performs the neuropsychological assessment, who conducts the Repeatable Battery for the Assessment of Neuropsychological Status Update to determine if Ms. X is experiencing cognitive impairment. Her immediate memory, visuospatial/constructions, language, attention, and delayed memory are significantly impaired for someone her age. The psychologist also administers the Wechsler Adult Intelligence Scale IV and finds Ms. X’s general cognitive ability is within the low average range of intellectual functioning as measured by Full-Scale IQ. Ms. X scores 29 on the BDI-II, indicating significant depressive symptoms, and 13 on the BAI, indicating mild anxiety symptoms.
Ms. X is diagnosed with MDD and an unspecified neurocognitive disorder. The psychologist recommends she start CBT to address her mood and anxiety symptoms.
Upon reviewing the results with Ms. X, the treatment team again recommends a brain MRI, CBC, CMP, and UA to rule out organic causes of her cognitive decline. Ms. X decides against the MRI and laboratory workup and elects to continue her present medication regimen and CBT.
Several weeks later, Ms. X’s family brings her to the emergency department (ED) for evaluation of worsening mood, decreased personal hygiene, increased irritability, and further cognitive decline. They report she is having an increasingly difficult time remembering things such as where she parked her car. The ED team decides to discontinue clonazepam but continues sertraline and trazodone.
Continue to: CBC, CMP, and UA...
CBC, CMP, and UA are unremarkable. Ms. X undergoes a brain CT scan without contrast, which reveals hyperdense lesions in the inferior left tentorium, posterior fossa. A subsequent brain MRI with contrast reveals a dural-based enhancing mass, inferior to the left tentorium, in the left posterior fossa measuring 2.2 cm x 2.1 cm, suggestive of a meningioma. The team orders a Neurosurgery consult.
[polldaddy:12189571]
The authors’ observations
While most brain tumors are secondary to metastasis, meningiomas are the most common primary CNS tumor. Typically, they are asymptomatic; their diagnosis is often delayed until the patient presents with psychiatric symptoms without any focal neurologic findings. The frontal lobe is the most common location of meningioma. Data from 48 case reports of patients with meningiomas and psychiatric symptoms suggest symptoms do not always correlate with specific brain regions.10,11
Indications for neuroimaging in cases such as Ms. X include an abrupt change in behavior or personality, lack of response to psychiatric treatment, presence of focal neurologic signs, and an unusual psychiatric presentation and development of symptoms.11
TREATMENT Neurosurgery
Neurosurgery recommends and performs a suboccipital craniotomy for biopsy and resection. Ms. X tolerates the procedure well. A meningioma is found in the posterior fossa, near the cerebellar convexity. A biopsy finds no evidence of malignancies.
At her postoperative follow-up appointment several days after the procedure, Ms. X reports new-onset hearing loss and tinnitus.
[polldaddy:12189747]
Continue to: The authors' observations
The authors’ observations
Patients who require neurosurgery typically already carry a heavy psychiatric burden, which makes it challenging to determine the exact psychiatric consequences of neurosurgery.12-14 For example, research shows that temporal lobe resection and temporal lobectomy for treatment-resistant epilepsy can lead to an exacerbation of baseline psychiatric symptoms and the development of new symptoms (31% to 34%).15,16 However, Bommakanti et al13 found no new psychiatric symptoms after resection of meningiomas, and surgery seemed to play a role in ameliorating psychiatric symptoms in patients with intracranial tumors. Research attempting to document the psychiatric sequelae of neurosurgery has had mixed results, and it is difficult to determine what effects brain surgery has on mental health.
OUTCOME Minimal improvement
Several weeks after neurosurgery, Ms. X and her family report her mood is improved. Her PHQ-9 score improves to 15, but her GAD-7 score increases to 13, 1 point above her previous score.
The treatment team recommends Ms. X continue taking sertraline 50 mg/d and trazodone 50 mg/d at bedtime. Ms. X’s family reports her cognition and memory have not improved; her MoCA score increases by 1 point to 23. The treatment team discusses with Ms. X and her family the possibility that her cognitive problems maybe better explained as a neurocognitive disorder rather than as a result of the meningioma, since her MoCA score has not significantly improved. Ms. X and her family decide to seek a second opinion from a neurologist.
Bottom Line
Pseudodementia is a term used to describe older adults who present with cognitive issues in the context of depressive symptoms. Even in the absence of focal findings, neuroimaging should be considered as part of the workup in patients who continue to experience a progressive decline in mood and cognitive function.
Related Resources
- Moller MD, Parmenter BA, Lane DW. Neuropsychological testing: a useful but underutilized resource. Current Psychiatry. 2019;18(11):40-46,51.
- Pollak J. Psychological/neuropsychological testing: when to refer for reexamination. Current Psychiatry. 2021;20(9):18- 19,30-31,37. doi:10.12788/cp.0157
Drug Brand Names
Citalopram • Celexa
Clonazepam • Klonopin
Duloxetine • Cymbalta
Fluoxetine • Prozac
Sertraline • Zoloft
Trazodone • Oleptro
Venlafaxine extended- release • Effexor XR
1. Nussbaum PD. (1994). Pseudodementia: a slow death. Neuropsychol Rev. 1994;4(2):71-90. doi:10.1007/BF01874829
2. Kang H, Zhao F, You L, et al. (2014). Pseudo-dementia: a neuropsychological review. Ann Indian Acad Neurol. 17(2):147-154. doi:10.4103/0972-2327.132613
3. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed, text revision. American Psychiatric Association; 2022.
4. Brodaty H, Connors MH. Pseudodementia, pseudo-pseudodementia, and pseudodepression. Alzheimers Dement (Amst). 2020;12(1):e12027. doi:10.1002/dad2.12027
5. Sekhon S, Marwaha R. Depressive Cognitive Disorders. StatPearls Publishing; 2022. https://www.ncbi.nlm.nih.gov/books/NBK559256/
6. Brown WA. Pseudodementia: issues in diagnosis. Psychiatric Times. April 9, 2005. Accessed February 3, 2023. www.psychiatrictimes.com/view/pseudodementia-issues-diagnosis
7. Kulas JF, Naugle RI. (2003). Indications for neuropsychological assessment. Cleve Clin J Med. 2003;70(9):785-792.
8. Braun M, Tupper D, Kaufmann P, et al. Neuropsychological assessment: a valuable tool in the diagnosis and management of neurological, neurodevelopmental, medical, and psychiatric disorders. Cogn Behav Neurol. 2011;24(3):107-114.
9. Michels TC, Tiu AY, Graver CJ. Neuropsychological evaluation in primary care. Am Fam Physician. 2010;82(5):495-502.
10. Wiemels J, Wrensch M, Claus EB. Epidemiology and etiology of meningioma. J Neurooncol. 2010;99(3):307-314. doi:10.1007/s11060-010-0386-3
11. Gyawali S, Sharma P, Mahapatra A. Meningioma and psychiatric symptoms: an individual patient data analysis. Asian J Psychiatr. 2019;42:94-103. doi:10.1016/j.ajp.2019.03.029
12. McAllister TW. Neurobehavioral sequelae of traumatic brain injury: evaluation and management. World Psychiatry. 2008;7(1):3-10. doi:10.1002/j.2051-5545.2008.tb00139.x
13. Bommakanti K, Gaddamanugu P, Alladi S, et al. Pre-operative and post-operative psychiatric manifestations in patients with supratentorial meningiomas. Clin Neurol Neurosurg. 2016;147:24-29. doi:10.1016/j.clineuro.2016.05.018
14. Devinsky O, Barr WB, Vickrey BG, et al. Changes in depression and anxiety after resective surgery for epilepsy. Neurology. 2005;65(11):1744-1749. doi:10.1212/01.wnl.0000187114.71524.c3
15. Blumer D, Wakhlu S, Davies K, et al. Psychiatric outcome of temporal lobectomy for epilepsy: incidence and treatment of psychiatric complications. Epilepsia. 1998;39(5):478-486. doi:10.1111/j.1528-1157.1998.tb01409.x
16. Glosser G, Zwil AS, Glosser DS, et al. Psychiatric aspects of temporal lobe epilepsy before and after anterior temporal lobectomy. J Neurol Neurosurg Psychiatry. 2000;68(1):53-58. doi:10.1136/jnnp.68.1.53
CASE Depressed and anxious
Five years ago, Ms. X, age 60, was diagnosed with treatment-resistant major depressive disorder (MDD) with anxiety. This diagnosis was established by a previous psychiatrist. She presents to a clinic for a second opinion.
Since her diagnosis, Ms. X has experienced sad mood, anhedonia, difficulty falling asleep, increased appetite and weight, and decreased concentration and attention. Her anxiety stems from her inability to work, which causes her to worry about her children. In the clinic, the treatment team conducts the Patient Health Questionnaire-9 (PHQ-9) and Generalized Anxiety Disorder-7 item scale (GAD-7) with Ms. X. She scores 16 on the PHQ-9, indicating moderately severe depression, and scores 12 on the GAD-7, indicating moderate anxiety.
Ms. X’s current medication regimen consists of venlafaxine extended-release (XR) 225 mg/d, trazodone 100 mg/d at bedtime, and clonazepam 1 mg twice daily. She reports no significant improvement of her symptoms from these medications. Additionally, Ms. X reports that in the past she had been prescribed fluoxetine, citalopram, and duloxetine, but she cannot recall the dosages.
Ms. X appears appropriately groomed, maintains appropriate eye contact, has clear speech, and does not show evidence of internal stimulation; however, she has difficulty following instructions. She makes negative comments about herself such as “I’m worthless” and “Nobody cares about me.” The treatment team decides to taper Ms. X off venlafaxine XR and initiates sertraline 50 mg/d, while continuing trazodone 50 mg/d at bedtime and clonazepam 1 mg twice daily. The team refers her for cognitive-behavioral therapy (CBT) to address her cognitive distortions, sad mood, and anxiety. Ms. X is asked to follow up with Psychiatry in 1 week.
EVALUATION Unusual behavior
At her CBT intake, Ms. X endorses depression and anxiety. Her PHQ-9 score at this visit is 19 (moderately severe depression) and GAD-7 score is 16 (severe anxiety). The psychologist notes that Ms. X is able to complete activities of daily living and instrumental activities of daily living without assistance. Ms. X denies any use of illicit substances or alcohol. No gross memory impairment is noted during this appointment, though Ms. X exhibits unusual behavior, including exiting and re-entering the clinic multiple times to repeatedly ask about follow-up appointments. The psychologist concludes that Ms. X’s presentation and behavior can be explained by MDD and pseudodementia.
[polldaddy:12189562]
The authors’ observations
Pseudodementia gained recognition in clinical research >100 years ago.1 Officially coined by Kiloh in 1961, the term was used broadly to categorize psychiatric cases that present like dementia but are the result of reversible causes. More recently, it has been used to describe older adults who present with cognitive deficits in the context of depressive symptoms.2 The goal of evaluation is to determine if the primary issue is a cognitive disorder or a depressive episode. DSM-5-TR does not classify pseudodementia as a distinct diagnosis, but instead categorizes its symptoms as components under other major diagnostic categories. Patients can present with MDD and associated cognitive symptoms, or with a cognitive disorder with depressive symptoms, which would be diagnosed as a cognitive disorder with a major depressive-like episode.3
Pseudodementia is rare. Brodaty et al4 found the prevalence of pseudodementia in primary care settings was 0.6%. Older adults (age >65) who live alone are at increased risk of developing pseudodementia, which can be worsened by poor social support and acute psychosocial and environmental changes.5 A key characteristic of this disorder is that as the patient’s depressed mood improves, their memory and cognition also improve.6Table 13,6 outlines overlapping features of MDD and pseudodementia.
Continue to: EVALUATION Worsening depression
EVALUATION Worsening depression
At her Psychiatry follow-up appointment, Ms. X reports that her mood is worse since she ended the relationship with her partner and she feels anxious because the partner was financially supporting her. Her PHQ-9 score is 24 (severe depression) and her GAD-7 score is 12 (moderate anxiety). Ms. X reports tolerating her transition from venlafaxine XR 225 mg/d to sertraline 50 mg/d well.
Additionally, Ms. X reports her children have called her “useless” since she continues to have difficulties following through on household tasks, even though she has no physical impairments that prevent her from completing them. The Psychiatry team observes that Ms. X has no problems walking or moving her arms or legs.
The Psychiatry team administers the Montreal Cognitive Assessment (MoCA). Ms. X scores 22, indicating mild impairment.
The team recommends a neuropsychological assessment to determine if this MoCA score is due to a cognitive disorder or is rooted in her mood symptoms. The team also recommends an MRI of the brain, complete blood count (CBC), comprehensive metabolic panel (CMP), and urinalysis (UA).
[polldaddy:12189567]
Continue to: The authors' observations
The authors’ observations
Neuropsychological assessments are important tools for exploring the behavioral manifestations of brain dysfunction (Table 2).7 These assessments factor in elements of neurology, psychiatry, and psychology to provide information about the diagnosis, prognosis, and functional status of patients with medical conditions, especially those with neurocognitive and psychiatric disorders. They combine information from the patient and collateral interviews, behavioral observations, a review of patient records, and objective tests of motor, emotional, and cognitive function.
Among other uses, neuropsychological assessments can help identify depression in patients with neurologic impairment, determine the diagnosis and plan of care for patients with concussions, determine the risk of a motor vehicle crash in patients with cognitive impairment, and distinguish Alzheimer disease from vascular dementia.8 Components of such assessments include the Beck Anxiety Inventory (BAI) to assess anxiety, the Dementia Rating Scale-2 and Neuropsychological Assessment Battery-Screening Module to assess dementia, and the Beck Depression Inventory (BDI) to assess depression.9
EVALUATION Continued cognitive decline
A different psychologist performs the neuropsychological assessment, who conducts the Repeatable Battery for the Assessment of Neuropsychological Status Update to determine if Ms. X is experiencing cognitive impairment. Her immediate memory, visuospatial/constructions, language, attention, and delayed memory are significantly impaired for someone her age. The psychologist also administers the Wechsler Adult Intelligence Scale IV and finds Ms. X’s general cognitive ability is within the low average range of intellectual functioning as measured by Full-Scale IQ. Ms. X scores 29 on the BDI-II, indicating significant depressive symptoms, and 13 on the BAI, indicating mild anxiety symptoms.
Ms. X is diagnosed with MDD and an unspecified neurocognitive disorder. The psychologist recommends she start CBT to address her mood and anxiety symptoms.
Upon reviewing the results with Ms. X, the treatment team again recommends a brain MRI, CBC, CMP, and UA to rule out organic causes of her cognitive decline. Ms. X decides against the MRI and laboratory workup and elects to continue her present medication regimen and CBT.
Several weeks later, Ms. X’s family brings her to the emergency department (ED) for evaluation of worsening mood, decreased personal hygiene, increased irritability, and further cognitive decline. They report she is having an increasingly difficult time remembering things such as where she parked her car. The ED team decides to discontinue clonazepam but continues sertraline and trazodone.
Continue to: CBC, CMP, and UA...
CBC, CMP, and UA are unremarkable. Ms. X undergoes a brain CT scan without contrast, which reveals hyperdense lesions in the inferior left tentorium, posterior fossa. A subsequent brain MRI with contrast reveals a dural-based enhancing mass, inferior to the left tentorium, in the left posterior fossa measuring 2.2 cm x 2.1 cm, suggestive of a meningioma. The team orders a Neurosurgery consult.
[polldaddy:12189571]
The authors’ observations
While most brain tumors are secondary to metastasis, meningiomas are the most common primary CNS tumor. Typically, they are asymptomatic; their diagnosis is often delayed until the patient presents with psychiatric symptoms without any focal neurologic findings. The frontal lobe is the most common location of meningioma. Data from 48 case reports of patients with meningiomas and psychiatric symptoms suggest symptoms do not always correlate with specific brain regions.10,11
Indications for neuroimaging in cases such as Ms. X include an abrupt change in behavior or personality, lack of response to psychiatric treatment, presence of focal neurologic signs, and an unusual psychiatric presentation and development of symptoms.11
TREATMENT Neurosurgery
Neurosurgery recommends and performs a suboccipital craniotomy for biopsy and resection. Ms. X tolerates the procedure well. A meningioma is found in the posterior fossa, near the cerebellar convexity. A biopsy finds no evidence of malignancies.
At her postoperative follow-up appointment several days after the procedure, Ms. X reports new-onset hearing loss and tinnitus.
[polldaddy:12189747]
Continue to: The authors' observations
The authors’ observations
Patients who require neurosurgery typically already carry a heavy psychiatric burden, which makes it challenging to determine the exact psychiatric consequences of neurosurgery.12-14 For example, research shows that temporal lobe resection and temporal lobectomy for treatment-resistant epilepsy can lead to an exacerbation of baseline psychiatric symptoms and the development of new symptoms (31% to 34%).15,16 However, Bommakanti et al13 found no new psychiatric symptoms after resection of meningiomas, and surgery seemed to play a role in ameliorating psychiatric symptoms in patients with intracranial tumors. Research attempting to document the psychiatric sequelae of neurosurgery has had mixed results, and it is difficult to determine what effects brain surgery has on mental health.
OUTCOME Minimal improvement
Several weeks after neurosurgery, Ms. X and her family report her mood is improved. Her PHQ-9 score improves to 15, but her GAD-7 score increases to 13, 1 point above her previous score.
The treatment team recommends Ms. X continue taking sertraline 50 mg/d and trazodone 50 mg/d at bedtime. Ms. X’s family reports her cognition and memory have not improved; her MoCA score increases by 1 point to 23. The treatment team discusses with Ms. X and her family the possibility that her cognitive problems maybe better explained as a neurocognitive disorder rather than as a result of the meningioma, since her MoCA score has not significantly improved. Ms. X and her family decide to seek a second opinion from a neurologist.
Bottom Line
Pseudodementia is a term used to describe older adults who present with cognitive issues in the context of depressive symptoms. Even in the absence of focal findings, neuroimaging should be considered as part of the workup in patients who continue to experience a progressive decline in mood and cognitive function.
Related Resources
- Moller MD, Parmenter BA, Lane DW. Neuropsychological testing: a useful but underutilized resource. Current Psychiatry. 2019;18(11):40-46,51.
- Pollak J. Psychological/neuropsychological testing: when to refer for reexamination. Current Psychiatry. 2021;20(9):18- 19,30-31,37. doi:10.12788/cp.0157
Drug Brand Names
Citalopram • Celexa
Clonazepam • Klonopin
Duloxetine • Cymbalta
Fluoxetine • Prozac
Sertraline • Zoloft
Trazodone • Oleptro
Venlafaxine extended- release • Effexor XR
CASE Depressed and anxious
Five years ago, Ms. X, age 60, was diagnosed with treatment-resistant major depressive disorder (MDD) with anxiety. This diagnosis was established by a previous psychiatrist. She presents to a clinic for a second opinion.
Since her diagnosis, Ms. X has experienced sad mood, anhedonia, difficulty falling asleep, increased appetite and weight, and decreased concentration and attention. Her anxiety stems from her inability to work, which causes her to worry about her children. In the clinic, the treatment team conducts the Patient Health Questionnaire-9 (PHQ-9) and Generalized Anxiety Disorder-7 item scale (GAD-7) with Ms. X. She scores 16 on the PHQ-9, indicating moderately severe depression, and scores 12 on the GAD-7, indicating moderate anxiety.
Ms. X’s current medication regimen consists of venlafaxine extended-release (XR) 225 mg/d, trazodone 100 mg/d at bedtime, and clonazepam 1 mg twice daily. She reports no significant improvement of her symptoms from these medications. Additionally, Ms. X reports that in the past she had been prescribed fluoxetine, citalopram, and duloxetine, but she cannot recall the dosages.
Ms. X appears appropriately groomed, maintains appropriate eye contact, has clear speech, and does not show evidence of internal stimulation; however, she has difficulty following instructions. She makes negative comments about herself such as “I’m worthless” and “Nobody cares about me.” The treatment team decides to taper Ms. X off venlafaxine XR and initiates sertraline 50 mg/d, while continuing trazodone 50 mg/d at bedtime and clonazepam 1 mg twice daily. The team refers her for cognitive-behavioral therapy (CBT) to address her cognitive distortions, sad mood, and anxiety. Ms. X is asked to follow up with Psychiatry in 1 week.
EVALUATION Unusual behavior
At her CBT intake, Ms. X endorses depression and anxiety. Her PHQ-9 score at this visit is 19 (moderately severe depression) and GAD-7 score is 16 (severe anxiety). The psychologist notes that Ms. X is able to complete activities of daily living and instrumental activities of daily living without assistance. Ms. X denies any use of illicit substances or alcohol. No gross memory impairment is noted during this appointment, though Ms. X exhibits unusual behavior, including exiting and re-entering the clinic multiple times to repeatedly ask about follow-up appointments. The psychologist concludes that Ms. X’s presentation and behavior can be explained by MDD and pseudodementia.
[polldaddy:12189562]
The authors’ observations
Pseudodementia gained recognition in clinical research >100 years ago.1 Officially coined by Kiloh in 1961, the term was used broadly to categorize psychiatric cases that present like dementia but are the result of reversible causes. More recently, it has been used to describe older adults who present with cognitive deficits in the context of depressive symptoms.2 The goal of evaluation is to determine if the primary issue is a cognitive disorder or a depressive episode. DSM-5-TR does not classify pseudodementia as a distinct diagnosis, but instead categorizes its symptoms as components under other major diagnostic categories. Patients can present with MDD and associated cognitive symptoms, or with a cognitive disorder with depressive symptoms, which would be diagnosed as a cognitive disorder with a major depressive-like episode.3
Pseudodementia is rare. Brodaty et al4 found the prevalence of pseudodementia in primary care settings was 0.6%. Older adults (age >65) who live alone are at increased risk of developing pseudodementia, which can be worsened by poor social support and acute psychosocial and environmental changes.5 A key characteristic of this disorder is that as the patient’s depressed mood improves, their memory and cognition also improve.6Table 13,6 outlines overlapping features of MDD and pseudodementia.
Continue to: EVALUATION Worsening depression
EVALUATION Worsening depression
At her Psychiatry follow-up appointment, Ms. X reports that her mood is worse since she ended the relationship with her partner and she feels anxious because the partner was financially supporting her. Her PHQ-9 score is 24 (severe depression) and her GAD-7 score is 12 (moderate anxiety). Ms. X reports tolerating her transition from venlafaxine XR 225 mg/d to sertraline 50 mg/d well.
Additionally, Ms. X reports her children have called her “useless” since she continues to have difficulties following through on household tasks, even though she has no physical impairments that prevent her from completing them. The Psychiatry team observes that Ms. X has no problems walking or moving her arms or legs.
The Psychiatry team administers the Montreal Cognitive Assessment (MoCA). Ms. X scores 22, indicating mild impairment.
The team recommends a neuropsychological assessment to determine if this MoCA score is due to a cognitive disorder or is rooted in her mood symptoms. The team also recommends an MRI of the brain, complete blood count (CBC), comprehensive metabolic panel (CMP), and urinalysis (UA).
[polldaddy:12189567]
Continue to: The authors' observations
The authors’ observations
Neuropsychological assessments are important tools for exploring the behavioral manifestations of brain dysfunction (Table 2).7 These assessments factor in elements of neurology, psychiatry, and psychology to provide information about the diagnosis, prognosis, and functional status of patients with medical conditions, especially those with neurocognitive and psychiatric disorders. They combine information from the patient and collateral interviews, behavioral observations, a review of patient records, and objective tests of motor, emotional, and cognitive function.
Among other uses, neuropsychological assessments can help identify depression in patients with neurologic impairment, determine the diagnosis and plan of care for patients with concussions, determine the risk of a motor vehicle crash in patients with cognitive impairment, and distinguish Alzheimer disease from vascular dementia.8 Components of such assessments include the Beck Anxiety Inventory (BAI) to assess anxiety, the Dementia Rating Scale-2 and Neuropsychological Assessment Battery-Screening Module to assess dementia, and the Beck Depression Inventory (BDI) to assess depression.9
EVALUATION Continued cognitive decline
A different psychologist performs the neuropsychological assessment, who conducts the Repeatable Battery for the Assessment of Neuropsychological Status Update to determine if Ms. X is experiencing cognitive impairment. Her immediate memory, visuospatial/constructions, language, attention, and delayed memory are significantly impaired for someone her age. The psychologist also administers the Wechsler Adult Intelligence Scale IV and finds Ms. X’s general cognitive ability is within the low average range of intellectual functioning as measured by Full-Scale IQ. Ms. X scores 29 on the BDI-II, indicating significant depressive symptoms, and 13 on the BAI, indicating mild anxiety symptoms.
Ms. X is diagnosed with MDD and an unspecified neurocognitive disorder. The psychologist recommends she start CBT to address her mood and anxiety symptoms.
Upon reviewing the results with Ms. X, the treatment team again recommends a brain MRI, CBC, CMP, and UA to rule out organic causes of her cognitive decline. Ms. X decides against the MRI and laboratory workup and elects to continue her present medication regimen and CBT.
Several weeks later, Ms. X’s family brings her to the emergency department (ED) for evaluation of worsening mood, decreased personal hygiene, increased irritability, and further cognitive decline. They report she is having an increasingly difficult time remembering things such as where she parked her car. The ED team decides to discontinue clonazepam but continues sertraline and trazodone.
Continue to: CBC, CMP, and UA...
CBC, CMP, and UA are unremarkable. Ms. X undergoes a brain CT scan without contrast, which reveals hyperdense lesions in the inferior left tentorium, posterior fossa. A subsequent brain MRI with contrast reveals a dural-based enhancing mass, inferior to the left tentorium, in the left posterior fossa measuring 2.2 cm x 2.1 cm, suggestive of a meningioma. The team orders a Neurosurgery consult.
[polldaddy:12189571]
The authors’ observations
While most brain tumors are secondary to metastasis, meningiomas are the most common primary CNS tumor. Typically, they are asymptomatic; their diagnosis is often delayed until the patient presents with psychiatric symptoms without any focal neurologic findings. The frontal lobe is the most common location of meningioma. Data from 48 case reports of patients with meningiomas and psychiatric symptoms suggest symptoms do not always correlate with specific brain regions.10,11
Indications for neuroimaging in cases such as Ms. X include an abrupt change in behavior or personality, lack of response to psychiatric treatment, presence of focal neurologic signs, and an unusual psychiatric presentation and development of symptoms.11
TREATMENT Neurosurgery
Neurosurgery recommends and performs a suboccipital craniotomy for biopsy and resection. Ms. X tolerates the procedure well. A meningioma is found in the posterior fossa, near the cerebellar convexity. A biopsy finds no evidence of malignancies.
At her postoperative follow-up appointment several days after the procedure, Ms. X reports new-onset hearing loss and tinnitus.
[polldaddy:12189747]
Continue to: The authors' observations
The authors’ observations
Patients who require neurosurgery typically already carry a heavy psychiatric burden, which makes it challenging to determine the exact psychiatric consequences of neurosurgery.12-14 For example, research shows that temporal lobe resection and temporal lobectomy for treatment-resistant epilepsy can lead to an exacerbation of baseline psychiatric symptoms and the development of new symptoms (31% to 34%).15,16 However, Bommakanti et al13 found no new psychiatric symptoms after resection of meningiomas, and surgery seemed to play a role in ameliorating psychiatric symptoms in patients with intracranial tumors. Research attempting to document the psychiatric sequelae of neurosurgery has had mixed results, and it is difficult to determine what effects brain surgery has on mental health.
OUTCOME Minimal improvement
Several weeks after neurosurgery, Ms. X and her family report her mood is improved. Her PHQ-9 score improves to 15, but her GAD-7 score increases to 13, 1 point above her previous score.
The treatment team recommends Ms. X continue taking sertraline 50 mg/d and trazodone 50 mg/d at bedtime. Ms. X’s family reports her cognition and memory have not improved; her MoCA score increases by 1 point to 23. The treatment team discusses with Ms. X and her family the possibility that her cognitive problems maybe better explained as a neurocognitive disorder rather than as a result of the meningioma, since her MoCA score has not significantly improved. Ms. X and her family decide to seek a second opinion from a neurologist.
Bottom Line
Pseudodementia is a term used to describe older adults who present with cognitive issues in the context of depressive symptoms. Even in the absence of focal findings, neuroimaging should be considered as part of the workup in patients who continue to experience a progressive decline in mood and cognitive function.
Related Resources
- Moller MD, Parmenter BA, Lane DW. Neuropsychological testing: a useful but underutilized resource. Current Psychiatry. 2019;18(11):40-46,51.
- Pollak J. Psychological/neuropsychological testing: when to refer for reexamination. Current Psychiatry. 2021;20(9):18- 19,30-31,37. doi:10.12788/cp.0157
Drug Brand Names
Citalopram • Celexa
Clonazepam • Klonopin
Duloxetine • Cymbalta
Fluoxetine • Prozac
Sertraline • Zoloft
Trazodone • Oleptro
Venlafaxine extended- release • Effexor XR
1. Nussbaum PD. (1994). Pseudodementia: a slow death. Neuropsychol Rev. 1994;4(2):71-90. doi:10.1007/BF01874829
2. Kang H, Zhao F, You L, et al. (2014). Pseudo-dementia: a neuropsychological review. Ann Indian Acad Neurol. 17(2):147-154. doi:10.4103/0972-2327.132613
3. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed, text revision. American Psychiatric Association; 2022.
4. Brodaty H, Connors MH. Pseudodementia, pseudo-pseudodementia, and pseudodepression. Alzheimers Dement (Amst). 2020;12(1):e12027. doi:10.1002/dad2.12027
5. Sekhon S, Marwaha R. Depressive Cognitive Disorders. StatPearls Publishing; 2022. https://www.ncbi.nlm.nih.gov/books/NBK559256/
6. Brown WA. Pseudodementia: issues in diagnosis. Psychiatric Times. April 9, 2005. Accessed February 3, 2023. www.psychiatrictimes.com/view/pseudodementia-issues-diagnosis
7. Kulas JF, Naugle RI. (2003). Indications for neuropsychological assessment. Cleve Clin J Med. 2003;70(9):785-792.
8. Braun M, Tupper D, Kaufmann P, et al. Neuropsychological assessment: a valuable tool in the diagnosis and management of neurological, neurodevelopmental, medical, and psychiatric disorders. Cogn Behav Neurol. 2011;24(3):107-114.
9. Michels TC, Tiu AY, Graver CJ. Neuropsychological evaluation in primary care. Am Fam Physician. 2010;82(5):495-502.
10. Wiemels J, Wrensch M, Claus EB. Epidemiology and etiology of meningioma. J Neurooncol. 2010;99(3):307-314. doi:10.1007/s11060-010-0386-3
11. Gyawali S, Sharma P, Mahapatra A. Meningioma and psychiatric symptoms: an individual patient data analysis. Asian J Psychiatr. 2019;42:94-103. doi:10.1016/j.ajp.2019.03.029
12. McAllister TW. Neurobehavioral sequelae of traumatic brain injury: evaluation and management. World Psychiatry. 2008;7(1):3-10. doi:10.1002/j.2051-5545.2008.tb00139.x
13. Bommakanti K, Gaddamanugu P, Alladi S, et al. Pre-operative and post-operative psychiatric manifestations in patients with supratentorial meningiomas. Clin Neurol Neurosurg. 2016;147:24-29. doi:10.1016/j.clineuro.2016.05.018
14. Devinsky O, Barr WB, Vickrey BG, et al. Changes in depression and anxiety after resective surgery for epilepsy. Neurology. 2005;65(11):1744-1749. doi:10.1212/01.wnl.0000187114.71524.c3
15. Blumer D, Wakhlu S, Davies K, et al. Psychiatric outcome of temporal lobectomy for epilepsy: incidence and treatment of psychiatric complications. Epilepsia. 1998;39(5):478-486. doi:10.1111/j.1528-1157.1998.tb01409.x
16. Glosser G, Zwil AS, Glosser DS, et al. Psychiatric aspects of temporal lobe epilepsy before and after anterior temporal lobectomy. J Neurol Neurosurg Psychiatry. 2000;68(1):53-58. doi:10.1136/jnnp.68.1.53
1. Nussbaum PD. (1994). Pseudodementia: a slow death. Neuropsychol Rev. 1994;4(2):71-90. doi:10.1007/BF01874829
2. Kang H, Zhao F, You L, et al. (2014). Pseudo-dementia: a neuropsychological review. Ann Indian Acad Neurol. 17(2):147-154. doi:10.4103/0972-2327.132613
3. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed, text revision. American Psychiatric Association; 2022.
4. Brodaty H, Connors MH. Pseudodementia, pseudo-pseudodementia, and pseudodepression. Alzheimers Dement (Amst). 2020;12(1):e12027. doi:10.1002/dad2.12027
5. Sekhon S, Marwaha R. Depressive Cognitive Disorders. StatPearls Publishing; 2022. https://www.ncbi.nlm.nih.gov/books/NBK559256/
6. Brown WA. Pseudodementia: issues in diagnosis. Psychiatric Times. April 9, 2005. Accessed February 3, 2023. www.psychiatrictimes.com/view/pseudodementia-issues-diagnosis
7. Kulas JF, Naugle RI. (2003). Indications for neuropsychological assessment. Cleve Clin J Med. 2003;70(9):785-792.
8. Braun M, Tupper D, Kaufmann P, et al. Neuropsychological assessment: a valuable tool in the diagnosis and management of neurological, neurodevelopmental, medical, and psychiatric disorders. Cogn Behav Neurol. 2011;24(3):107-114.
9. Michels TC, Tiu AY, Graver CJ. Neuropsychological evaluation in primary care. Am Fam Physician. 2010;82(5):495-502.
10. Wiemels J, Wrensch M, Claus EB. Epidemiology and etiology of meningioma. J Neurooncol. 2010;99(3):307-314. doi:10.1007/s11060-010-0386-3
11. Gyawali S, Sharma P, Mahapatra A. Meningioma and psychiatric symptoms: an individual patient data analysis. Asian J Psychiatr. 2019;42:94-103. doi:10.1016/j.ajp.2019.03.029
12. McAllister TW. Neurobehavioral sequelae of traumatic brain injury: evaluation and management. World Psychiatry. 2008;7(1):3-10. doi:10.1002/j.2051-5545.2008.tb00139.x
13. Bommakanti K, Gaddamanugu P, Alladi S, et al. Pre-operative and post-operative psychiatric manifestations in patients with supratentorial meningiomas. Clin Neurol Neurosurg. 2016;147:24-29. doi:10.1016/j.clineuro.2016.05.018
14. Devinsky O, Barr WB, Vickrey BG, et al. Changes in depression and anxiety after resective surgery for epilepsy. Neurology. 2005;65(11):1744-1749. doi:10.1212/01.wnl.0000187114.71524.c3
15. Blumer D, Wakhlu S, Davies K, et al. Psychiatric outcome of temporal lobectomy for epilepsy: incidence and treatment of psychiatric complications. Epilepsia. 1998;39(5):478-486. doi:10.1111/j.1528-1157.1998.tb01409.x
16. Glosser G, Zwil AS, Glosser DS, et al. Psychiatric aspects of temporal lobe epilepsy before and after anterior temporal lobectomy. J Neurol Neurosurg Psychiatry. 2000;68(1):53-58. doi:10.1136/jnnp.68.1.53
Unawareness of memory slips could indicate risk for Alzheimer’s
Everyone’s memory fades to some extent as we age, but not everyone will develop Alzheimer’s disease. Screening the most likely people to develop Alzheimer’s remains an ongoing challenge, as some people present only unambiguous symptoms once their disease is advanced.
A new study in JAMA Network Open suggests that one early clue is found in people’s own self-perception of their memory skills. People who are more aware of their own declining memory capacity are less likely to develop Alzheimer’s, the study suggests.
“Some people are very aware of changes in their memory, but many people are unaware,” said study author Patrizia Vannini, PhD, a neurologist at Brigham and Women’s Hospital in Boston. There are gradations of unawareness of memory loss, Dr. Vannini said, from complete unawareness that anything is wrong, to a partial unawareness that memory is declining.
The study compared the records of 436 participants in the Alzheimer’s Disease Neuroimaging Initiative, an Alzheimer’s research institute housed at the University of Southern California. More than 90% of the participants were White, and generally had a college education. Their average age was 75 years, and 53% of participants were women.
Dr. Vannini and colleagues tracked people whose cognitive function was normal at the beginning of the study, based on the Clinical Dementia Rating. Throughout the course of the study, which included data from 2010 to 2021, 91 of the 436 participants experienced a sustained decline in their Clinical Dementia Rating scores, indicating a risk for eventual Alzheimer’s, whereas the other participants held steady.
The people who declined in cognitive function were less aware of slips in their memory, as assessed by discrepancies between people’s self-reports of their own memory skills and the perceptions of someone in their lives. For this part of the study, Dr. Vannini and colleagues used the Everyday Cognition Questionnaire, which evaluates memory tasks such as shopping without a grocery list or recalling conversations from a few days ago. Both the participant and the study partner rated their performance on such tasks compared to 10 years earlier. Those who were less aware of their memory slips were more likely to experience declines in the Clinical Dementia Rating, compared with people with a heightened concern about memory loss (as measured by being more concerned about memory decline than their study partners).
“Partial or complete unawareness is often related to delayed diagnosis of Alzheimer’s, because the patient is unaware they are having problems,” Dr. Vannini said, adding that this is associated with a poorer prognosis as well.
Implications for clinicians
Soo Borson, MD, professor of clinical family medicine at the University of Southern California and coleader of a CDC-funded early dementia detection center at New York University, pointed out that sometimes people are genuinely unaware that their memory is declining, while at other times they know it all too well but say everything is fine when a doctor asks about their current memory status. That may be because people fear the label of “Alzheimer’s,” Dr. Borson suggested, or simply because they don’t want to start a protracted diagnostic pathway that could involve lots of tests and time.
Dr. Borson, who was not involved in the study, noted that the population was predominantly White and well-educated, and by definition included people who were concerned enough about potential memory loss to become part of an Alzheimer’s research network. This limits the generalizability of this study’s results to other populations, Dr. Borson said.
Despite that limitation, in Dr. Borson’s view the study points to the continued importance of clinicians (ideally a primary care doctor who knows the patient well) engaging with patients about their brain health once they reach midlife. A doctor could ask if patients have noticed a decline in their thinking or memory over the last year, for example, or a more open-ended question about any memory concerns.
Although some patients may choose to withhold concerns about their memory, Dr. Borson acknowledged, the overall thrust of these questions is to provide a safe space for patients to air their concerns if they so choose. In some cases it would be appropriate to do a simple memory test on the spot, and then proceed accordingly – either for further tests if something of concern emerges, or to reassure the patient if the test doesn’t yield anything of note. In the latter case some patients will still want further tests for additional reassurance, and Dr. Borson thinks doctors should facilitate that request even if in their own judgment nothing is wrong.
“This is not like testing for impaired kidney function by doing a serum creatinine test,” Dr. Borson said. While the orientation of the health care system is toward quick and easy answers for everything, detecting possible dementia eludes such an approach.
Dr. Vannini reports funding from the National Institutes of Health National Institute on Aging. Dr. Borson reported no disclosures.
Everyone’s memory fades to some extent as we age, but not everyone will develop Alzheimer’s disease. Screening the most likely people to develop Alzheimer’s remains an ongoing challenge, as some people present only unambiguous symptoms once their disease is advanced.
A new study in JAMA Network Open suggests that one early clue is found in people’s own self-perception of their memory skills. People who are more aware of their own declining memory capacity are less likely to develop Alzheimer’s, the study suggests.
“Some people are very aware of changes in their memory, but many people are unaware,” said study author Patrizia Vannini, PhD, a neurologist at Brigham and Women’s Hospital in Boston. There are gradations of unawareness of memory loss, Dr. Vannini said, from complete unawareness that anything is wrong, to a partial unawareness that memory is declining.
The study compared the records of 436 participants in the Alzheimer’s Disease Neuroimaging Initiative, an Alzheimer’s research institute housed at the University of Southern California. More than 90% of the participants were White, and generally had a college education. Their average age was 75 years, and 53% of participants were women.
Dr. Vannini and colleagues tracked people whose cognitive function was normal at the beginning of the study, based on the Clinical Dementia Rating. Throughout the course of the study, which included data from 2010 to 2021, 91 of the 436 participants experienced a sustained decline in their Clinical Dementia Rating scores, indicating a risk for eventual Alzheimer’s, whereas the other participants held steady.
The people who declined in cognitive function were less aware of slips in their memory, as assessed by discrepancies between people’s self-reports of their own memory skills and the perceptions of someone in their lives. For this part of the study, Dr. Vannini and colleagues used the Everyday Cognition Questionnaire, which evaluates memory tasks such as shopping without a grocery list or recalling conversations from a few days ago. Both the participant and the study partner rated their performance on such tasks compared to 10 years earlier. Those who were less aware of their memory slips were more likely to experience declines in the Clinical Dementia Rating, compared with people with a heightened concern about memory loss (as measured by being more concerned about memory decline than their study partners).
“Partial or complete unawareness is often related to delayed diagnosis of Alzheimer’s, because the patient is unaware they are having problems,” Dr. Vannini said, adding that this is associated with a poorer prognosis as well.
Implications for clinicians
Soo Borson, MD, professor of clinical family medicine at the University of Southern California and coleader of a CDC-funded early dementia detection center at New York University, pointed out that sometimes people are genuinely unaware that their memory is declining, while at other times they know it all too well but say everything is fine when a doctor asks about their current memory status. That may be because people fear the label of “Alzheimer’s,” Dr. Borson suggested, or simply because they don’t want to start a protracted diagnostic pathway that could involve lots of tests and time.
Dr. Borson, who was not involved in the study, noted that the population was predominantly White and well-educated, and by definition included people who were concerned enough about potential memory loss to become part of an Alzheimer’s research network. This limits the generalizability of this study’s results to other populations, Dr. Borson said.
Despite that limitation, in Dr. Borson’s view the study points to the continued importance of clinicians (ideally a primary care doctor who knows the patient well) engaging with patients about their brain health once they reach midlife. A doctor could ask if patients have noticed a decline in their thinking or memory over the last year, for example, or a more open-ended question about any memory concerns.
Although some patients may choose to withhold concerns about their memory, Dr. Borson acknowledged, the overall thrust of these questions is to provide a safe space for patients to air their concerns if they so choose. In some cases it would be appropriate to do a simple memory test on the spot, and then proceed accordingly – either for further tests if something of concern emerges, or to reassure the patient if the test doesn’t yield anything of note. In the latter case some patients will still want further tests for additional reassurance, and Dr. Borson thinks doctors should facilitate that request even if in their own judgment nothing is wrong.
“This is not like testing for impaired kidney function by doing a serum creatinine test,” Dr. Borson said. While the orientation of the health care system is toward quick and easy answers for everything, detecting possible dementia eludes such an approach.
Dr. Vannini reports funding from the National Institutes of Health National Institute on Aging. Dr. Borson reported no disclosures.
Everyone’s memory fades to some extent as we age, but not everyone will develop Alzheimer’s disease. Screening the most likely people to develop Alzheimer’s remains an ongoing challenge, as some people present only unambiguous symptoms once their disease is advanced.
A new study in JAMA Network Open suggests that one early clue is found in people’s own self-perception of their memory skills. People who are more aware of their own declining memory capacity are less likely to develop Alzheimer’s, the study suggests.
“Some people are very aware of changes in their memory, but many people are unaware,” said study author Patrizia Vannini, PhD, a neurologist at Brigham and Women’s Hospital in Boston. There are gradations of unawareness of memory loss, Dr. Vannini said, from complete unawareness that anything is wrong, to a partial unawareness that memory is declining.
The study compared the records of 436 participants in the Alzheimer’s Disease Neuroimaging Initiative, an Alzheimer’s research institute housed at the University of Southern California. More than 90% of the participants were White, and generally had a college education. Their average age was 75 years, and 53% of participants were women.
Dr. Vannini and colleagues tracked people whose cognitive function was normal at the beginning of the study, based on the Clinical Dementia Rating. Throughout the course of the study, which included data from 2010 to 2021, 91 of the 436 participants experienced a sustained decline in their Clinical Dementia Rating scores, indicating a risk for eventual Alzheimer’s, whereas the other participants held steady.
The people who declined in cognitive function were less aware of slips in their memory, as assessed by discrepancies between people’s self-reports of their own memory skills and the perceptions of someone in their lives. For this part of the study, Dr. Vannini and colleagues used the Everyday Cognition Questionnaire, which evaluates memory tasks such as shopping without a grocery list or recalling conversations from a few days ago. Both the participant and the study partner rated their performance on such tasks compared to 10 years earlier. Those who were less aware of their memory slips were more likely to experience declines in the Clinical Dementia Rating, compared with people with a heightened concern about memory loss (as measured by being more concerned about memory decline than their study partners).
“Partial or complete unawareness is often related to delayed diagnosis of Alzheimer’s, because the patient is unaware they are having problems,” Dr. Vannini said, adding that this is associated with a poorer prognosis as well.
Implications for clinicians
Soo Borson, MD, professor of clinical family medicine at the University of Southern California and coleader of a CDC-funded early dementia detection center at New York University, pointed out that sometimes people are genuinely unaware that their memory is declining, while at other times they know it all too well but say everything is fine when a doctor asks about their current memory status. That may be because people fear the label of “Alzheimer’s,” Dr. Borson suggested, or simply because they don’t want to start a protracted diagnostic pathway that could involve lots of tests and time.
Dr. Borson, who was not involved in the study, noted that the population was predominantly White and well-educated, and by definition included people who were concerned enough about potential memory loss to become part of an Alzheimer’s research network. This limits the generalizability of this study’s results to other populations, Dr. Borson said.
Despite that limitation, in Dr. Borson’s view the study points to the continued importance of clinicians (ideally a primary care doctor who knows the patient well) engaging with patients about their brain health once they reach midlife. A doctor could ask if patients have noticed a decline in their thinking or memory over the last year, for example, or a more open-ended question about any memory concerns.
Although some patients may choose to withhold concerns about their memory, Dr. Borson acknowledged, the overall thrust of these questions is to provide a safe space for patients to air their concerns if they so choose. In some cases it would be appropriate to do a simple memory test on the spot, and then proceed accordingly – either for further tests if something of concern emerges, or to reassure the patient if the test doesn’t yield anything of note. In the latter case some patients will still want further tests for additional reassurance, and Dr. Borson thinks doctors should facilitate that request even if in their own judgment nothing is wrong.
“This is not like testing for impaired kidney function by doing a serum creatinine test,” Dr. Borson said. While the orientation of the health care system is toward quick and easy answers for everything, detecting possible dementia eludes such an approach.
Dr. Vannini reports funding from the National Institutes of Health National Institute on Aging. Dr. Borson reported no disclosures.
FROM JAMA NETWORK OPEN
Walnuts linked to improved attention, psychological maturity in teens
, new research shows. Adolescents who consumed walnuts for at least 100 days showed improved sustained attention and fluid intelligence as well as a reduction in symptoms of attension deficit hyperactivity disorder, compared with matched controls who did not consume the nuts. However, there were no statistically significant changes between the groups in other parameters, such as working memory and executive function.
Clinicians should advise adolescents “to eat a handful of walnuts three times a week for the rest of their lives. They may have a healthier brain with better cognitive function,” said senior investigator Jordi Julvez, PhD, group leader at the Institute of Health Research Pere Virgili, Barcelona, and associated researcher at the Barcelona Institute for Global Health.
The study was published online in eClinicalMedicine.
Rich source of omega-3s
Adolescence is “a period of refinement of brain connectivity and complex behaviors,” the investigators noted.
Previous research suggests polyunsaturated fatty acids are key in central nervous system architecture and function during times of neural development, with three specific PUFAs playing an “essential developmental role.”
Two omega-3 fatty acids – docosahexaenoic acid and eicosapentaenoic acid – are PUFAs that must be obtained through diet, mainly from seafood. Walnuts are “among the richest sources” of plant-derived omega-3 fatty acids, particularly alpha-linolenic acid (ALA), a precursor for longer-chain EPA and DHA.
ALA independently “has positive effects on brain function and plasticity,” the authors wrote. In addition, walnut constituents – particularly polyphenols and other bioactive compounds – “may act synergistically with ALA to foster brain health.”
Earlier small studies have found positive associations between walnut consumption and cognitive function in children, adolescents, and young adults, but to date, no randomized controlled trial has focused on the effect of walnut consumption on adolescent neuropsychological function.
The researchers studied 771 healthy adolescents (aged 11-16 years, mean age 14) drawn from 12 Spanish high schools. Participants were instructed to follow healthy eating recommendations and were randomly assigned 1:1 to the intervention (n = 386) or the control group (n = 385).
At baseline and after 6 months, they completed neuropsychological tests and behavioral rating scales. The Attention Network Test assessed attention, and the N-back test was used to assess working memory. The Tests of Primary Mental Abilities assessed fluid intelligence. Risky decision-making was tested using the Roulettes Task.
Fruit and nuts
Participants also completed the Strengths and Difficulties Questionnaire, which provided a total score of problem behavior. Teachers filled out the ADHD DSM-IV form list to provide additional information about ADHD behaviors.
The intervention group received 30 grams/day of raw California walnut kernels to incorporate into their daily diet. It is estimated that this walnut contains about 9 g of ALA per 100 g.
All participants received a seasonal fruit calendar and were asked to eat at least one piece of seasonal fruit daily.
Parents reported their child’s daily walnut consumption, with adherence defined as 100 or more days of eating walnuts during the 6-month period.
All main analyses were based on an intention-to-treat method (participants were analyzed according to their original group assignment, regardless of their adherence to the intervention).
The researchers also conducted a secondary per-protocol analysis, comparing the intervention and control groups to estimate the effect if all participants had adhered to their assigned intervention. They censored data for participants who reported eating walnuts for less than 100 days during the 6-month trial period.
Secondary outcomes included changes in height, weight, waist circumference, and BMI, as well as red blood cell proportions of omega-3 fatty acids (DHA, EPA, and ALA) at baseline and after 6 months.
Adherence counts
Most participants had “medium” or “high” levels of adherence to the Mediterranean diet, with “no meaningful differences” at baseline between the intervention and control groups in lifestyle characteristics or mean scores in all primary endpoints.
In the ITT analysis, there were no statistically significant differences in primary outcomes between the groups following the intervention. As for secondary outcomes, the RBC ALA significantly increased in the walnuts group but not the control group (coefficient, 0.04%; 95% confidence interval, 0.03%-0.06%; P < .0001).
However, there were differences in primary outcomes between the groups in the per-protocol analysis: The adherence-adjusted effect on improvement in attention score was −11.26 ms; 95% CI, −19.92 to −2.60; P = .011) for the intervention versus the control group.
The per-protocol analysis showed other differences: an improvement in fluid intelligence score (1.78; 95% CI, 0.90 - 2.67; P < .0001) and a reduction in ADHD symptom score (−2.18; 95% CI, −3.70 to −0.67; P = .0050).
“Overall, no significant differences were found in the intervention group in relation to the control group,” Dr. Julvez said in a news release. “But if the adherence factor is considered, then positive results are observed, since participants who most closely followed the guidelines – in terms of the recommended dose of walnuts and the number of days of consumption – did show improvements in the neuropsychological functions evaluated.”
Adolescence “is a time of great biological changes. Hormonal transformation occurs, which in turn is responsible for stimulating the synaptic growth of the frontal lobe,” he continued, adding that this brain region “enables neuropsychological maturation of more complex emotional and cognitive functions.”
“Neurons that are well nourished with these types of fatty acids will be able to grow and form new, stronger synapses,” he said.
Food as medicine
Uma Naidoo, MD, director of nutritional and lifestyle psychiatry at Massachusetts General Hospital, Boston, “commends” the researchers for conducting an RCT with a “robust” sample size and said she is “excited to see research like this furthering functional nutrition for mental health,” as she believes that “food is medicine.”
Dr. Naidoo, a professional chef, nutritional biologist, and author of the book “This Is Your Brain on Food,” said the findings “align” with her own approach to nutritional psychiatry and are also “in line” with her clinical practice.
However, although these results are “promising,” more research is needed across more diverse populations to “make sure these results are truly generalizable,” said Dr. Naidoo, a faculty member at Harvard Medical School, Boston, who was not involved with the study.
She “envisions a future where the research is so advanced that we can ‘dose’ these healthy whole foods for specific psychiatric symptoms and conditions.”
This study was supported by Instituto de Salud Carlos III (co-funded by European Union Regional Development Fund “A way to make Europe”). The California Walnut Commission has given support by supplying the walnuts for free for the Walnuts Smart Snack Dietary Intervention Trial. Dr. Julvez holds a Miguel Servet-II contract awarded by the Instituto de Salud Carlos III (co-funded by European Union Social Fund). The other authors’ disclosures are listed in the original article. Dr. Naidoo reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, new research shows. Adolescents who consumed walnuts for at least 100 days showed improved sustained attention and fluid intelligence as well as a reduction in symptoms of attension deficit hyperactivity disorder, compared with matched controls who did not consume the nuts. However, there were no statistically significant changes between the groups in other parameters, such as working memory and executive function.
Clinicians should advise adolescents “to eat a handful of walnuts three times a week for the rest of their lives. They may have a healthier brain with better cognitive function,” said senior investigator Jordi Julvez, PhD, group leader at the Institute of Health Research Pere Virgili, Barcelona, and associated researcher at the Barcelona Institute for Global Health.
The study was published online in eClinicalMedicine.
Rich source of omega-3s
Adolescence is “a period of refinement of brain connectivity and complex behaviors,” the investigators noted.
Previous research suggests polyunsaturated fatty acids are key in central nervous system architecture and function during times of neural development, with three specific PUFAs playing an “essential developmental role.”
Two omega-3 fatty acids – docosahexaenoic acid and eicosapentaenoic acid – are PUFAs that must be obtained through diet, mainly from seafood. Walnuts are “among the richest sources” of plant-derived omega-3 fatty acids, particularly alpha-linolenic acid (ALA), a precursor for longer-chain EPA and DHA.
ALA independently “has positive effects on brain function and plasticity,” the authors wrote. In addition, walnut constituents – particularly polyphenols and other bioactive compounds – “may act synergistically with ALA to foster brain health.”
Earlier small studies have found positive associations between walnut consumption and cognitive function in children, adolescents, and young adults, but to date, no randomized controlled trial has focused on the effect of walnut consumption on adolescent neuropsychological function.
The researchers studied 771 healthy adolescents (aged 11-16 years, mean age 14) drawn from 12 Spanish high schools. Participants were instructed to follow healthy eating recommendations and were randomly assigned 1:1 to the intervention (n = 386) or the control group (n = 385).
At baseline and after 6 months, they completed neuropsychological tests and behavioral rating scales. The Attention Network Test assessed attention, and the N-back test was used to assess working memory. The Tests of Primary Mental Abilities assessed fluid intelligence. Risky decision-making was tested using the Roulettes Task.
Fruit and nuts
Participants also completed the Strengths and Difficulties Questionnaire, which provided a total score of problem behavior. Teachers filled out the ADHD DSM-IV form list to provide additional information about ADHD behaviors.
The intervention group received 30 grams/day of raw California walnut kernels to incorporate into their daily diet. It is estimated that this walnut contains about 9 g of ALA per 100 g.
All participants received a seasonal fruit calendar and were asked to eat at least one piece of seasonal fruit daily.
Parents reported their child’s daily walnut consumption, with adherence defined as 100 or more days of eating walnuts during the 6-month period.
All main analyses were based on an intention-to-treat method (participants were analyzed according to their original group assignment, regardless of their adherence to the intervention).
The researchers also conducted a secondary per-protocol analysis, comparing the intervention and control groups to estimate the effect if all participants had adhered to their assigned intervention. They censored data for participants who reported eating walnuts for less than 100 days during the 6-month trial period.
Secondary outcomes included changes in height, weight, waist circumference, and BMI, as well as red blood cell proportions of omega-3 fatty acids (DHA, EPA, and ALA) at baseline and after 6 months.
Adherence counts
Most participants had “medium” or “high” levels of adherence to the Mediterranean diet, with “no meaningful differences” at baseline between the intervention and control groups in lifestyle characteristics or mean scores in all primary endpoints.
In the ITT analysis, there were no statistically significant differences in primary outcomes between the groups following the intervention. As for secondary outcomes, the RBC ALA significantly increased in the walnuts group but not the control group (coefficient, 0.04%; 95% confidence interval, 0.03%-0.06%; P < .0001).
However, there were differences in primary outcomes between the groups in the per-protocol analysis: The adherence-adjusted effect on improvement in attention score was −11.26 ms; 95% CI, −19.92 to −2.60; P = .011) for the intervention versus the control group.
The per-protocol analysis showed other differences: an improvement in fluid intelligence score (1.78; 95% CI, 0.90 - 2.67; P < .0001) and a reduction in ADHD symptom score (−2.18; 95% CI, −3.70 to −0.67; P = .0050).
“Overall, no significant differences were found in the intervention group in relation to the control group,” Dr. Julvez said in a news release. “But if the adherence factor is considered, then positive results are observed, since participants who most closely followed the guidelines – in terms of the recommended dose of walnuts and the number of days of consumption – did show improvements in the neuropsychological functions evaluated.”
Adolescence “is a time of great biological changes. Hormonal transformation occurs, which in turn is responsible for stimulating the synaptic growth of the frontal lobe,” he continued, adding that this brain region “enables neuropsychological maturation of more complex emotional and cognitive functions.”
“Neurons that are well nourished with these types of fatty acids will be able to grow and form new, stronger synapses,” he said.
Food as medicine
Uma Naidoo, MD, director of nutritional and lifestyle psychiatry at Massachusetts General Hospital, Boston, “commends” the researchers for conducting an RCT with a “robust” sample size and said she is “excited to see research like this furthering functional nutrition for mental health,” as she believes that “food is medicine.”
Dr. Naidoo, a professional chef, nutritional biologist, and author of the book “This Is Your Brain on Food,” said the findings “align” with her own approach to nutritional psychiatry and are also “in line” with her clinical practice.
However, although these results are “promising,” more research is needed across more diverse populations to “make sure these results are truly generalizable,” said Dr. Naidoo, a faculty member at Harvard Medical School, Boston, who was not involved with the study.
She “envisions a future where the research is so advanced that we can ‘dose’ these healthy whole foods for specific psychiatric symptoms and conditions.”
This study was supported by Instituto de Salud Carlos III (co-funded by European Union Regional Development Fund “A way to make Europe”). The California Walnut Commission has given support by supplying the walnuts for free for the Walnuts Smart Snack Dietary Intervention Trial. Dr. Julvez holds a Miguel Servet-II contract awarded by the Instituto de Salud Carlos III (co-funded by European Union Social Fund). The other authors’ disclosures are listed in the original article. Dr. Naidoo reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, new research shows. Adolescents who consumed walnuts for at least 100 days showed improved sustained attention and fluid intelligence as well as a reduction in symptoms of attension deficit hyperactivity disorder, compared with matched controls who did not consume the nuts. However, there were no statistically significant changes between the groups in other parameters, such as working memory and executive function.
Clinicians should advise adolescents “to eat a handful of walnuts three times a week for the rest of their lives. They may have a healthier brain with better cognitive function,” said senior investigator Jordi Julvez, PhD, group leader at the Institute of Health Research Pere Virgili, Barcelona, and associated researcher at the Barcelona Institute for Global Health.
The study was published online in eClinicalMedicine.
Rich source of omega-3s
Adolescence is “a period of refinement of brain connectivity and complex behaviors,” the investigators noted.
Previous research suggests polyunsaturated fatty acids are key in central nervous system architecture and function during times of neural development, with three specific PUFAs playing an “essential developmental role.”
Two omega-3 fatty acids – docosahexaenoic acid and eicosapentaenoic acid – are PUFAs that must be obtained through diet, mainly from seafood. Walnuts are “among the richest sources” of plant-derived omega-3 fatty acids, particularly alpha-linolenic acid (ALA), a precursor for longer-chain EPA and DHA.
ALA independently “has positive effects on brain function and plasticity,” the authors wrote. In addition, walnut constituents – particularly polyphenols and other bioactive compounds – “may act synergistically with ALA to foster brain health.”
Earlier small studies have found positive associations between walnut consumption and cognitive function in children, adolescents, and young adults, but to date, no randomized controlled trial has focused on the effect of walnut consumption on adolescent neuropsychological function.
The researchers studied 771 healthy adolescents (aged 11-16 years, mean age 14) drawn from 12 Spanish high schools. Participants were instructed to follow healthy eating recommendations and were randomly assigned 1:1 to the intervention (n = 386) or the control group (n = 385).
At baseline and after 6 months, they completed neuropsychological tests and behavioral rating scales. The Attention Network Test assessed attention, and the N-back test was used to assess working memory. The Tests of Primary Mental Abilities assessed fluid intelligence. Risky decision-making was tested using the Roulettes Task.
Fruit and nuts
Participants also completed the Strengths and Difficulties Questionnaire, which provided a total score of problem behavior. Teachers filled out the ADHD DSM-IV form list to provide additional information about ADHD behaviors.
The intervention group received 30 grams/day of raw California walnut kernels to incorporate into their daily diet. It is estimated that this walnut contains about 9 g of ALA per 100 g.
All participants received a seasonal fruit calendar and were asked to eat at least one piece of seasonal fruit daily.
Parents reported their child’s daily walnut consumption, with adherence defined as 100 or more days of eating walnuts during the 6-month period.
All main analyses were based on an intention-to-treat method (participants were analyzed according to their original group assignment, regardless of their adherence to the intervention).
The researchers also conducted a secondary per-protocol analysis, comparing the intervention and control groups to estimate the effect if all participants had adhered to their assigned intervention. They censored data for participants who reported eating walnuts for less than 100 days during the 6-month trial period.
Secondary outcomes included changes in height, weight, waist circumference, and BMI, as well as red blood cell proportions of omega-3 fatty acids (DHA, EPA, and ALA) at baseline and after 6 months.
Adherence counts
Most participants had “medium” or “high” levels of adherence to the Mediterranean diet, with “no meaningful differences” at baseline between the intervention and control groups in lifestyle characteristics or mean scores in all primary endpoints.
In the ITT analysis, there were no statistically significant differences in primary outcomes between the groups following the intervention. As for secondary outcomes, the RBC ALA significantly increased in the walnuts group but not the control group (coefficient, 0.04%; 95% confidence interval, 0.03%-0.06%; P < .0001).
However, there were differences in primary outcomes between the groups in the per-protocol analysis: The adherence-adjusted effect on improvement in attention score was −11.26 ms; 95% CI, −19.92 to −2.60; P = .011) for the intervention versus the control group.
The per-protocol analysis showed other differences: an improvement in fluid intelligence score (1.78; 95% CI, 0.90 - 2.67; P < .0001) and a reduction in ADHD symptom score (−2.18; 95% CI, −3.70 to −0.67; P = .0050).
“Overall, no significant differences were found in the intervention group in relation to the control group,” Dr. Julvez said in a news release. “But if the adherence factor is considered, then positive results are observed, since participants who most closely followed the guidelines – in terms of the recommended dose of walnuts and the number of days of consumption – did show improvements in the neuropsychological functions evaluated.”
Adolescence “is a time of great biological changes. Hormonal transformation occurs, which in turn is responsible for stimulating the synaptic growth of the frontal lobe,” he continued, adding that this brain region “enables neuropsychological maturation of more complex emotional and cognitive functions.”
“Neurons that are well nourished with these types of fatty acids will be able to grow and form new, stronger synapses,” he said.
Food as medicine
Uma Naidoo, MD, director of nutritional and lifestyle psychiatry at Massachusetts General Hospital, Boston, “commends” the researchers for conducting an RCT with a “robust” sample size and said she is “excited to see research like this furthering functional nutrition for mental health,” as she believes that “food is medicine.”
Dr. Naidoo, a professional chef, nutritional biologist, and author of the book “This Is Your Brain on Food,” said the findings “align” with her own approach to nutritional psychiatry and are also “in line” with her clinical practice.
However, although these results are “promising,” more research is needed across more diverse populations to “make sure these results are truly generalizable,” said Dr. Naidoo, a faculty member at Harvard Medical School, Boston, who was not involved with the study.
She “envisions a future where the research is so advanced that we can ‘dose’ these healthy whole foods for specific psychiatric symptoms and conditions.”
This study was supported by Instituto de Salud Carlos III (co-funded by European Union Regional Development Fund “A way to make Europe”). The California Walnut Commission has given support by supplying the walnuts for free for the Walnuts Smart Snack Dietary Intervention Trial. Dr. Julvez holds a Miguel Servet-II contract awarded by the Instituto de Salud Carlos III (co-funded by European Union Social Fund). The other authors’ disclosures are listed in the original article. Dr. Naidoo reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM ECLINICALMEDICINE
Ablation for atrial fibrillation may protect the aging brain
BOSTON – , new research suggests.
Investigators found adults who had previously undergone catheter ablation were significantly less likely to be cognitively impaired during the 2-year study period, compared with those who receive medical management alone.
“Catheter ablation is intended to stop atrial fibrillation and restore the normal rhythm of the heart. By doing so, there is an improved cerebral hemodynamic profile,” said Bahadar S. Srichawla, DO, department of neurology, University of Massachusetts, Worcester.
“Thus, long-term cognitive outcomes may be improved due to improved blood flow to the brain by restoring the normal rhythm of the heart,” he added.
This research was presented at the 2023 annual meeting of the American Academy of Neurology.
Heart-brain connection
The study involved 887 older adults (mean age 75; 49% women) with atrial fibrillation participating in the SAGE-AF (Systematic Assessment of Geriatric Elements) study. A total of 193 (22%) participants underwent catheter ablation prior to enrollment. These individuals more frequently had an implantable cardiac device (46% vs. 28%, P < .001) and persistent atrial fibrillation (31% vs. 23%, P < .05).
Cognitive function was assessed using the Montreal Cognitive Assessment (MoCA) tool at baseline and 1 and 2 years, with cognitive impairment defined as a MoCA score of 23 or below. Individuals who had catheter ablation had an average MoCA score of 25, compared with an average score of 23 in those who didn’t have catheter ablation.
After adjusting for potential confounding factors such as heart disease, renal disease, sleep apnea, and atrial fibrillation risk score, those who underwent catheter ablation were 36% less likely to develop cognitive impairment over 2 years than those who were treated only with medication (adjusted odds ratio, 0.64; 95% CI, 0.46-0.88).
During his presentation, Dr. Srichawla noted there is a hypothesis that individuals who are anticoagulated with warfarin may be prone to cerebral microbleeds and may be more cognitively impaired over time.
However, in a subgroup analysis, “cognitive function was similar at 2-year follow-up in those anticoagulated with warfarin, compared with all other anticoagulants. However, it should be noted that in this study, a direct head-to-head comparison was not done,” Dr. Srichawla told attendees.
“In patients with atrial fibrillation, catheter ablation should be discussed as a potential treatment strategy, particularly in patients who have or are at risk for cognitive decline and dementia,” Dr. Srichawla said.
Intriguing findings
Commenting on the research, Percy Griffin, PhD, Alzheimer’s Association director of scientific engagement, said the study is “intriguing and adds to what we know from previous research connecting cardiovascular and cognitive health.”
“However, there are limitations to this study,” Dr. Griffin said, “including its predominantly White cohort and the use of only neuropsychiatric testing to diagnose dementia. More research is needed to fully understand the impact of atrial fibrillation on cognitive outcomes in all people.”
“It’s well known that the heart and the brain are intimately connected. Individuals experiencing any cardiovascular issues should speak to their doctor,” Dr. Griffin added.
Shaheen Lakhan, MD, PhD, a neurologist and researcher in Boston, agreed. “If you ever get up too quickly and feel woozy, that is your brain not getting enough blood flow and you are getting all the warning signs to correct that – or else! Similarly, with atrial fibrillation, the heart is contracting, but not effectively pumping blood to the brain,” he said.
“This line of research shows that correcting the abnormal heart rhythm by zapping the faulty circuit with a catheter is actually better for your brain health than just taking medications alone,” added Dr. Lakhan, who was not involved with the study.
The study had no commercial funding. Dr. Srichawla, Dr. Griffin, and Dr. Lakhan report no relevant financial relationships.
A version of this article first appeared on Medscape.com.
BOSTON – , new research suggests.
Investigators found adults who had previously undergone catheter ablation were significantly less likely to be cognitively impaired during the 2-year study period, compared with those who receive medical management alone.
“Catheter ablation is intended to stop atrial fibrillation and restore the normal rhythm of the heart. By doing so, there is an improved cerebral hemodynamic profile,” said Bahadar S. Srichawla, DO, department of neurology, University of Massachusetts, Worcester.
“Thus, long-term cognitive outcomes may be improved due to improved blood flow to the brain by restoring the normal rhythm of the heart,” he added.
This research was presented at the 2023 annual meeting of the American Academy of Neurology.
Heart-brain connection
The study involved 887 older adults (mean age 75; 49% women) with atrial fibrillation participating in the SAGE-AF (Systematic Assessment of Geriatric Elements) study. A total of 193 (22%) participants underwent catheter ablation prior to enrollment. These individuals more frequently had an implantable cardiac device (46% vs. 28%, P < .001) and persistent atrial fibrillation (31% vs. 23%, P < .05).
Cognitive function was assessed using the Montreal Cognitive Assessment (MoCA) tool at baseline and 1 and 2 years, with cognitive impairment defined as a MoCA score of 23 or below. Individuals who had catheter ablation had an average MoCA score of 25, compared with an average score of 23 in those who didn’t have catheter ablation.
After adjusting for potential confounding factors such as heart disease, renal disease, sleep apnea, and atrial fibrillation risk score, those who underwent catheter ablation were 36% less likely to develop cognitive impairment over 2 years than those who were treated only with medication (adjusted odds ratio, 0.64; 95% CI, 0.46-0.88).
During his presentation, Dr. Srichawla noted there is a hypothesis that individuals who are anticoagulated with warfarin may be prone to cerebral microbleeds and may be more cognitively impaired over time.
However, in a subgroup analysis, “cognitive function was similar at 2-year follow-up in those anticoagulated with warfarin, compared with all other anticoagulants. However, it should be noted that in this study, a direct head-to-head comparison was not done,” Dr. Srichawla told attendees.
“In patients with atrial fibrillation, catheter ablation should be discussed as a potential treatment strategy, particularly in patients who have or are at risk for cognitive decline and dementia,” Dr. Srichawla said.
Intriguing findings
Commenting on the research, Percy Griffin, PhD, Alzheimer’s Association director of scientific engagement, said the study is “intriguing and adds to what we know from previous research connecting cardiovascular and cognitive health.”
“However, there are limitations to this study,” Dr. Griffin said, “including its predominantly White cohort and the use of only neuropsychiatric testing to diagnose dementia. More research is needed to fully understand the impact of atrial fibrillation on cognitive outcomes in all people.”
“It’s well known that the heart and the brain are intimately connected. Individuals experiencing any cardiovascular issues should speak to their doctor,” Dr. Griffin added.
Shaheen Lakhan, MD, PhD, a neurologist and researcher in Boston, agreed. “If you ever get up too quickly and feel woozy, that is your brain not getting enough blood flow and you are getting all the warning signs to correct that – or else! Similarly, with atrial fibrillation, the heart is contracting, but not effectively pumping blood to the brain,” he said.
“This line of research shows that correcting the abnormal heart rhythm by zapping the faulty circuit with a catheter is actually better for your brain health than just taking medications alone,” added Dr. Lakhan, who was not involved with the study.
The study had no commercial funding. Dr. Srichawla, Dr. Griffin, and Dr. Lakhan report no relevant financial relationships.
A version of this article first appeared on Medscape.com.
BOSTON – , new research suggests.
Investigators found adults who had previously undergone catheter ablation were significantly less likely to be cognitively impaired during the 2-year study period, compared with those who receive medical management alone.
“Catheter ablation is intended to stop atrial fibrillation and restore the normal rhythm of the heart. By doing so, there is an improved cerebral hemodynamic profile,” said Bahadar S. Srichawla, DO, department of neurology, University of Massachusetts, Worcester.
“Thus, long-term cognitive outcomes may be improved due to improved blood flow to the brain by restoring the normal rhythm of the heart,” he added.
This research was presented at the 2023 annual meeting of the American Academy of Neurology.
Heart-brain connection
The study involved 887 older adults (mean age 75; 49% women) with atrial fibrillation participating in the SAGE-AF (Systematic Assessment of Geriatric Elements) study. A total of 193 (22%) participants underwent catheter ablation prior to enrollment. These individuals more frequently had an implantable cardiac device (46% vs. 28%, P < .001) and persistent atrial fibrillation (31% vs. 23%, P < .05).
Cognitive function was assessed using the Montreal Cognitive Assessment (MoCA) tool at baseline and 1 and 2 years, with cognitive impairment defined as a MoCA score of 23 or below. Individuals who had catheter ablation had an average MoCA score of 25, compared with an average score of 23 in those who didn’t have catheter ablation.
After adjusting for potential confounding factors such as heart disease, renal disease, sleep apnea, and atrial fibrillation risk score, those who underwent catheter ablation were 36% less likely to develop cognitive impairment over 2 years than those who were treated only with medication (adjusted odds ratio, 0.64; 95% CI, 0.46-0.88).
During his presentation, Dr. Srichawla noted there is a hypothesis that individuals who are anticoagulated with warfarin may be prone to cerebral microbleeds and may be more cognitively impaired over time.
However, in a subgroup analysis, “cognitive function was similar at 2-year follow-up in those anticoagulated with warfarin, compared with all other anticoagulants. However, it should be noted that in this study, a direct head-to-head comparison was not done,” Dr. Srichawla told attendees.
“In patients with atrial fibrillation, catheter ablation should be discussed as a potential treatment strategy, particularly in patients who have or are at risk for cognitive decline and dementia,” Dr. Srichawla said.
Intriguing findings
Commenting on the research, Percy Griffin, PhD, Alzheimer’s Association director of scientific engagement, said the study is “intriguing and adds to what we know from previous research connecting cardiovascular and cognitive health.”
“However, there are limitations to this study,” Dr. Griffin said, “including its predominantly White cohort and the use of only neuropsychiatric testing to diagnose dementia. More research is needed to fully understand the impact of atrial fibrillation on cognitive outcomes in all people.”
“It’s well known that the heart and the brain are intimately connected. Individuals experiencing any cardiovascular issues should speak to their doctor,” Dr. Griffin added.
Shaheen Lakhan, MD, PhD, a neurologist and researcher in Boston, agreed. “If you ever get up too quickly and feel woozy, that is your brain not getting enough blood flow and you are getting all the warning signs to correct that – or else! Similarly, with atrial fibrillation, the heart is contracting, but not effectively pumping blood to the brain,” he said.
“This line of research shows that correcting the abnormal heart rhythm by zapping the faulty circuit with a catheter is actually better for your brain health than just taking medications alone,” added Dr. Lakhan, who was not involved with the study.
The study had no commercial funding. Dr. Srichawla, Dr. Griffin, and Dr. Lakhan report no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM AAN 2023
The amazing brain
Last week, unbeknownst to most people, Dayton, Ohio, hosted the world championships of Winter Drumline. It’s a combination of percussion instruments, dance, and music, with a storyline. Think of it as a very fast-paced half-time show, with only percussion, in 6 minutes or less.
My daughter fell in love with it her second year of high school, and has participated in it through college. Her specialty is the pit – marimba, vibraphone, xylophone. This gives our house a cruise ship atmosphere when she comes home to practice on weekends.
Over the years my wife and I have gone to many of her shows and competitions, streamed others online, and always been amazed by the variety of costumes, choreography, music numbers, and overall themes different teams come up with. We’ve seen shows based on 1930s detective fiction, ocean life, westerns, science fiction, toxic waste, emotions, relationships, flamenco, pirate ships, and many others.
And, as always, I marvel at the human brain.
Only 2-3 pounds but still an amazing thing. The capacity for imagination is endless, and one of the things that got us where we are today. The ability to see things that don’t exist yet, and work out the details on how to get there. The pyramids, Petra, the Great Wall, flight, the steam engine, landing on the moon, the ISS. And, of course, Winter Drumline.
It’s a uniquely (as far as we know) human capacity. To look at a rock and envision what it might be carved into. To look at Jupiter and think of a way to get a probe there. To sit in an empty gym and imagine the floor covered with dozens of percussion instruments and their players, imagining what each will be playing and doing at a given moment.
It’s really a remarkable capacity when you think about it. I’m sure it originally began as a way to figure out where you might find shelter or food, or simply to outwit the other tribe. But it’s become so much more than that. Someone envisioned every movie you see, book you read, and the computer I’m writing this on.
In his 1968 novelization of “2001: A Space Odyssey” Arthur C. Clarke described the thoughts of the unknown civilization that had left the Monolith behind for us as “in all the galaxy they had found nothing more precious than Mind.”
I’d agree with that. Even after 30 years of learning about the 2-3 pounds of semi-solid tissue we all carry upstairs, and doing my best to treat its malfunctions, I’ve never ceased to be amazed by it.
I hope I always will be.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
Last week, unbeknownst to most people, Dayton, Ohio, hosted the world championships of Winter Drumline. It’s a combination of percussion instruments, dance, and music, with a storyline. Think of it as a very fast-paced half-time show, with only percussion, in 6 minutes or less.
My daughter fell in love with it her second year of high school, and has participated in it through college. Her specialty is the pit – marimba, vibraphone, xylophone. This gives our house a cruise ship atmosphere when she comes home to practice on weekends.
Over the years my wife and I have gone to many of her shows and competitions, streamed others online, and always been amazed by the variety of costumes, choreography, music numbers, and overall themes different teams come up with. We’ve seen shows based on 1930s detective fiction, ocean life, westerns, science fiction, toxic waste, emotions, relationships, flamenco, pirate ships, and many others.
And, as always, I marvel at the human brain.
Only 2-3 pounds but still an amazing thing. The capacity for imagination is endless, and one of the things that got us where we are today. The ability to see things that don’t exist yet, and work out the details on how to get there. The pyramids, Petra, the Great Wall, flight, the steam engine, landing on the moon, the ISS. And, of course, Winter Drumline.
It’s a uniquely (as far as we know) human capacity. To look at a rock and envision what it might be carved into. To look at Jupiter and think of a way to get a probe there. To sit in an empty gym and imagine the floor covered with dozens of percussion instruments and their players, imagining what each will be playing and doing at a given moment.
It’s really a remarkable capacity when you think about it. I’m sure it originally began as a way to figure out where you might find shelter or food, or simply to outwit the other tribe. But it’s become so much more than that. Someone envisioned every movie you see, book you read, and the computer I’m writing this on.
In his 1968 novelization of “2001: A Space Odyssey” Arthur C. Clarke described the thoughts of the unknown civilization that had left the Monolith behind for us as “in all the galaxy they had found nothing more precious than Mind.”
I’d agree with that. Even after 30 years of learning about the 2-3 pounds of semi-solid tissue we all carry upstairs, and doing my best to treat its malfunctions, I’ve never ceased to be amazed by it.
I hope I always will be.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
Last week, unbeknownst to most people, Dayton, Ohio, hosted the world championships of Winter Drumline. It’s a combination of percussion instruments, dance, and music, with a storyline. Think of it as a very fast-paced half-time show, with only percussion, in 6 minutes or less.
My daughter fell in love with it her second year of high school, and has participated in it through college. Her specialty is the pit – marimba, vibraphone, xylophone. This gives our house a cruise ship atmosphere when she comes home to practice on weekends.
Over the years my wife and I have gone to many of her shows and competitions, streamed others online, and always been amazed by the variety of costumes, choreography, music numbers, and overall themes different teams come up with. We’ve seen shows based on 1930s detective fiction, ocean life, westerns, science fiction, toxic waste, emotions, relationships, flamenco, pirate ships, and many others.
And, as always, I marvel at the human brain.
Only 2-3 pounds but still an amazing thing. The capacity for imagination is endless, and one of the things that got us where we are today. The ability to see things that don’t exist yet, and work out the details on how to get there. The pyramids, Petra, the Great Wall, flight, the steam engine, landing on the moon, the ISS. And, of course, Winter Drumline.
It’s a uniquely (as far as we know) human capacity. To look at a rock and envision what it might be carved into. To look at Jupiter and think of a way to get a probe there. To sit in an empty gym and imagine the floor covered with dozens of percussion instruments and their players, imagining what each will be playing and doing at a given moment.
It’s really a remarkable capacity when you think about it. I’m sure it originally began as a way to figure out where you might find shelter or food, or simply to outwit the other tribe. But it’s become so much more than that. Someone envisioned every movie you see, book you read, and the computer I’m writing this on.
In his 1968 novelization of “2001: A Space Odyssey” Arthur C. Clarke described the thoughts of the unknown civilization that had left the Monolith behind for us as “in all the galaxy they had found nothing more precious than Mind.”
I’d agree with that. Even after 30 years of learning about the 2-3 pounds of semi-solid tissue we all carry upstairs, and doing my best to treat its malfunctions, I’ve never ceased to be amazed by it.
I hope I always will be.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
Early menopause, delayed HT tied to Alzheimer’s pathology
Investigators found elevated levels of tau protein in the brains of women who initiated HT more than 5 years after menopause onset, while those who started the therapy earlier had normal levels.
Tau levels were also higher in women who started menopause before age 45, either naturally or following surgery, but only in those who already had high levels of beta-amyloid.
The findings were published online in JAMA Neurology.
Hotly debated
Previous research has suggested the timing of menopause and HT initiation may be associated with AD. However, the current research is the first to suggest tau deposition may explain that link.
“There have been a lot of conflicting findings around whether HT induces risk for Alzheimer’s disease dementia or not, and – at least in our hands – our observational evidence suggests that any risk is fairly limited to those rarer cases when women might delay their initiation of HT considerably,” senior investigator Rachel Buckley, PhD, assistant investigator in neurology at Massachusetts General Hospital and assistant professor of neurology at Harvard Medical School, Boston, told this news organization.
The link between HT, dementia, and cognitive decline has been hotly debated since the initial release of findings from the Women’s Health Initiative Memory Study, reported 20 years ago.
Since then, dozens of studies have yielded conflicting evidence about HT and AD risk, with some showing a protective effect and others showing the treatment may increase AD risk.
For this study, researchers analyzed data from 292 cognitively unimpaired participants (66.1% female) in the Wisconsin Registry for Alzheimer Prevention. About half of the women had received HT.
Women had higher levels of tau measured on PET imaging than age-matched males, even after adjustment for APOE status and other potential confounders.
Higher tau levels were found in those with an earlier age at menopause (P < .001) and HT use (P = .008) compared with male sex; later menopause onset; or HT nonuse – but only in patients who also had a higher beta-amyloid burden.
Late initiation of HT (> 5 years following age at menopause) was associated with higher tau compared with early initiation (P = .001), regardless of amyloid levels.
Surprising finding
Although researchers expected to find that surgical history (specifically oophorectomy) might have a greater impact on risk, that wasn’t the case.
“Given that bilateral oophorectomy involves the removal of both ovaries, and the immediate ceasing of estrogen production, I had expected this to be the primary driver of higher tau levels,” Dr. Buckley said. “But early age at menopause – regardless of whether the genesis was natural or surgical – seemed to have similar impacts.”
These findings are the latest from Dr. Buckley’s group that indicate that women tend to have higher levels of tau than men, regardless of preexisting amyloid burden in the brain.
“We see this in healthy older women, women with dementia, and even in postmortem cases,” Dr. Buckley said. “It really remains to be seen whether women tend to accumulate tau faster in the brain than men, or whether this is simply a one-shot phenomenon that we see in observational studies at the baseline.”
“One could really flip this finding on its head and suggest that women are truly resilient to the disease,” she continued. “That is, they can hold much more tau in their brain and remain well enough to be studied, unlike men.”
Among the study’s limitations is that the data were collected at a single time point and did not include information on subsequent Alzheimer’s diagnosis or cognitive decline.
“It is important to remember that the participants in this study were not as representative of the general population in the United States, so we cannot extrapolate our findings to women from a range of socioeconomic, racial and ethnic backgrounds or education levels,” she said.
The study’s observational design left researchers unable to demonstrate causation. What’s more, the findings don’t support the assertion that hormone therapy may protect against AD, Dr. Buckley added.
“I would more confidently say that evidence from our work, and that of many others, seems to suggest that HT initiated around the time of menopause may be benign – not providing benefit or risk, at least in the context of Alzheimer’s disease risk,” she said.
Another important takeaway from the study, Dr. Buckley said, is that not all women are at high risk for AD.
“Often the headlines might make you think that most women are destined to progress to dementia, but this simply is not the case,” Dr. Buckley said. “We are now starting to really drill down on what might elevate risk for AD in women and use this information to better inform clinical trials and doctors on how best to think about treating these higher-risk groups.”
New mechanism?
Commenting on the findings, Pauline Maki, PhD, professor of psychiatry, psychology and obstetrics & gynecology at the University of Illinois at Chicago, called the study “interesting.”
“It identifies a new mechanism in humans that could underlie a possible link between sex hormones and dementia,” Dr. Maki said.
However, Dr. Maki noted that the study wasn’t randomized and information about menopause onset was self-reported.
“We must remember that many of the hypotheses about hormone therapy and brain health that came from observational studies were not validated in randomized trials, including the hypothesis that hormone therapy prevents dementia,” she said.
The findings don’t resolve the debate over hormone therapy and AD risk and point to the need for randomized, prospective studies on the topic, Dr. Maki added. Still, she said, they underscore the gender disparity in AD risk.
“It’s a good reminder to clinicians that women have a higher lifetime risk of Alzheimer’s disease and should be advised on factors that might lower their risk,” she said.
The study was funded by the National Institutes of Health. Dr. Buckley reports no relevant financial conflicts. Dr. Maki serves on the advisory boards for Astellas, Bayer, Johnson & Johnson, consults for Pfizer and Mithra, and has equity in Estrigenix, Midi-Health, and Alloy.
A version of this article originally appeared on Medscape.com.
Investigators found elevated levels of tau protein in the brains of women who initiated HT more than 5 years after menopause onset, while those who started the therapy earlier had normal levels.
Tau levels were also higher in women who started menopause before age 45, either naturally or following surgery, but only in those who already had high levels of beta-amyloid.
The findings were published online in JAMA Neurology.
Hotly debated
Previous research has suggested the timing of menopause and HT initiation may be associated with AD. However, the current research is the first to suggest tau deposition may explain that link.
“There have been a lot of conflicting findings around whether HT induces risk for Alzheimer’s disease dementia or not, and – at least in our hands – our observational evidence suggests that any risk is fairly limited to those rarer cases when women might delay their initiation of HT considerably,” senior investigator Rachel Buckley, PhD, assistant investigator in neurology at Massachusetts General Hospital and assistant professor of neurology at Harvard Medical School, Boston, told this news organization.
The link between HT, dementia, and cognitive decline has been hotly debated since the initial release of findings from the Women’s Health Initiative Memory Study, reported 20 years ago.
Since then, dozens of studies have yielded conflicting evidence about HT and AD risk, with some showing a protective effect and others showing the treatment may increase AD risk.
For this study, researchers analyzed data from 292 cognitively unimpaired participants (66.1% female) in the Wisconsin Registry for Alzheimer Prevention. About half of the women had received HT.
Women had higher levels of tau measured on PET imaging than age-matched males, even after adjustment for APOE status and other potential confounders.
Higher tau levels were found in those with an earlier age at menopause (P < .001) and HT use (P = .008) compared with male sex; later menopause onset; or HT nonuse – but only in patients who also had a higher beta-amyloid burden.
Late initiation of HT (> 5 years following age at menopause) was associated with higher tau compared with early initiation (P = .001), regardless of amyloid levels.
Surprising finding
Although researchers expected to find that surgical history (specifically oophorectomy) might have a greater impact on risk, that wasn’t the case.
“Given that bilateral oophorectomy involves the removal of both ovaries, and the immediate ceasing of estrogen production, I had expected this to be the primary driver of higher tau levels,” Dr. Buckley said. “But early age at menopause – regardless of whether the genesis was natural or surgical – seemed to have similar impacts.”
These findings are the latest from Dr. Buckley’s group that indicate that women tend to have higher levels of tau than men, regardless of preexisting amyloid burden in the brain.
“We see this in healthy older women, women with dementia, and even in postmortem cases,” Dr. Buckley said. “It really remains to be seen whether women tend to accumulate tau faster in the brain than men, or whether this is simply a one-shot phenomenon that we see in observational studies at the baseline.”
“One could really flip this finding on its head and suggest that women are truly resilient to the disease,” she continued. “That is, they can hold much more tau in their brain and remain well enough to be studied, unlike men.”
Among the study’s limitations is that the data were collected at a single time point and did not include information on subsequent Alzheimer’s diagnosis or cognitive decline.
“It is important to remember that the participants in this study were not as representative of the general population in the United States, so we cannot extrapolate our findings to women from a range of socioeconomic, racial and ethnic backgrounds or education levels,” she said.
The study’s observational design left researchers unable to demonstrate causation. What’s more, the findings don’t support the assertion that hormone therapy may protect against AD, Dr. Buckley added.
“I would more confidently say that evidence from our work, and that of many others, seems to suggest that HT initiated around the time of menopause may be benign – not providing benefit or risk, at least in the context of Alzheimer’s disease risk,” she said.
Another important takeaway from the study, Dr. Buckley said, is that not all women are at high risk for AD.
“Often the headlines might make you think that most women are destined to progress to dementia, but this simply is not the case,” Dr. Buckley said. “We are now starting to really drill down on what might elevate risk for AD in women and use this information to better inform clinical trials and doctors on how best to think about treating these higher-risk groups.”
New mechanism?
Commenting on the findings, Pauline Maki, PhD, professor of psychiatry, psychology and obstetrics & gynecology at the University of Illinois at Chicago, called the study “interesting.”
“It identifies a new mechanism in humans that could underlie a possible link between sex hormones and dementia,” Dr. Maki said.
However, Dr. Maki noted that the study wasn’t randomized and information about menopause onset was self-reported.
“We must remember that many of the hypotheses about hormone therapy and brain health that came from observational studies were not validated in randomized trials, including the hypothesis that hormone therapy prevents dementia,” she said.
The findings don’t resolve the debate over hormone therapy and AD risk and point to the need for randomized, prospective studies on the topic, Dr. Maki added. Still, she said, they underscore the gender disparity in AD risk.
“It’s a good reminder to clinicians that women have a higher lifetime risk of Alzheimer’s disease and should be advised on factors that might lower their risk,” she said.
The study was funded by the National Institutes of Health. Dr. Buckley reports no relevant financial conflicts. Dr. Maki serves on the advisory boards for Astellas, Bayer, Johnson & Johnson, consults for Pfizer and Mithra, and has equity in Estrigenix, Midi-Health, and Alloy.
A version of this article originally appeared on Medscape.com.
Investigators found elevated levels of tau protein in the brains of women who initiated HT more than 5 years after menopause onset, while those who started the therapy earlier had normal levels.
Tau levels were also higher in women who started menopause before age 45, either naturally or following surgery, but only in those who already had high levels of beta-amyloid.
The findings were published online in JAMA Neurology.
Hotly debated
Previous research has suggested the timing of menopause and HT initiation may be associated with AD. However, the current research is the first to suggest tau deposition may explain that link.
“There have been a lot of conflicting findings around whether HT induces risk for Alzheimer’s disease dementia or not, and – at least in our hands – our observational evidence suggests that any risk is fairly limited to those rarer cases when women might delay their initiation of HT considerably,” senior investigator Rachel Buckley, PhD, assistant investigator in neurology at Massachusetts General Hospital and assistant professor of neurology at Harvard Medical School, Boston, told this news organization.
The link between HT, dementia, and cognitive decline has been hotly debated since the initial release of findings from the Women’s Health Initiative Memory Study, reported 20 years ago.
Since then, dozens of studies have yielded conflicting evidence about HT and AD risk, with some showing a protective effect and others showing the treatment may increase AD risk.
For this study, researchers analyzed data from 292 cognitively unimpaired participants (66.1% female) in the Wisconsin Registry for Alzheimer Prevention. About half of the women had received HT.
Women had higher levels of tau measured on PET imaging than age-matched males, even after adjustment for APOE status and other potential confounders.
Higher tau levels were found in those with an earlier age at menopause (P < .001) and HT use (P = .008) compared with male sex; later menopause onset; or HT nonuse – but only in patients who also had a higher beta-amyloid burden.
Late initiation of HT (> 5 years following age at menopause) was associated with higher tau compared with early initiation (P = .001), regardless of amyloid levels.
Surprising finding
Although researchers expected to find that surgical history (specifically oophorectomy) might have a greater impact on risk, that wasn’t the case.
“Given that bilateral oophorectomy involves the removal of both ovaries, and the immediate ceasing of estrogen production, I had expected this to be the primary driver of higher tau levels,” Dr. Buckley said. “But early age at menopause – regardless of whether the genesis was natural or surgical – seemed to have similar impacts.”
These findings are the latest from Dr. Buckley’s group that indicate that women tend to have higher levels of tau than men, regardless of preexisting amyloid burden in the brain.
“We see this in healthy older women, women with dementia, and even in postmortem cases,” Dr. Buckley said. “It really remains to be seen whether women tend to accumulate tau faster in the brain than men, or whether this is simply a one-shot phenomenon that we see in observational studies at the baseline.”
“One could really flip this finding on its head and suggest that women are truly resilient to the disease,” she continued. “That is, they can hold much more tau in their brain and remain well enough to be studied, unlike men.”
Among the study’s limitations is that the data were collected at a single time point and did not include information on subsequent Alzheimer’s diagnosis or cognitive decline.
“It is important to remember that the participants in this study were not as representative of the general population in the United States, so we cannot extrapolate our findings to women from a range of socioeconomic, racial and ethnic backgrounds or education levels,” she said.
The study’s observational design left researchers unable to demonstrate causation. What’s more, the findings don’t support the assertion that hormone therapy may protect against AD, Dr. Buckley added.
“I would more confidently say that evidence from our work, and that of many others, seems to suggest that HT initiated around the time of menopause may be benign – not providing benefit or risk, at least in the context of Alzheimer’s disease risk,” she said.
Another important takeaway from the study, Dr. Buckley said, is that not all women are at high risk for AD.
“Often the headlines might make you think that most women are destined to progress to dementia, but this simply is not the case,” Dr. Buckley said. “We are now starting to really drill down on what might elevate risk for AD in women and use this information to better inform clinical trials and doctors on how best to think about treating these higher-risk groups.”
New mechanism?
Commenting on the findings, Pauline Maki, PhD, professor of psychiatry, psychology and obstetrics & gynecology at the University of Illinois at Chicago, called the study “interesting.”
“It identifies a new mechanism in humans that could underlie a possible link between sex hormones and dementia,” Dr. Maki said.
However, Dr. Maki noted that the study wasn’t randomized and information about menopause onset was self-reported.
“We must remember that many of the hypotheses about hormone therapy and brain health that came from observational studies were not validated in randomized trials, including the hypothesis that hormone therapy prevents dementia,” she said.
The findings don’t resolve the debate over hormone therapy and AD risk and point to the need for randomized, prospective studies on the topic, Dr. Maki added. Still, she said, they underscore the gender disparity in AD risk.
“It’s a good reminder to clinicians that women have a higher lifetime risk of Alzheimer’s disease and should be advised on factors that might lower their risk,” she said.
The study was funded by the National Institutes of Health. Dr. Buckley reports no relevant financial conflicts. Dr. Maki serves on the advisory boards for Astellas, Bayer, Johnson & Johnson, consults for Pfizer and Mithra, and has equity in Estrigenix, Midi-Health, and Alloy.
A version of this article originally appeared on Medscape.com.
FROM JAMA NEUROLOGY
Mediterranean diet improves cognition in MS
due to a potential neuroprotective mechanism, according to findings of a study that was released early, ahead of presentation at the annual meting of the American Academy of Neurology.
“We were most surprised by the magnitude of the results,” said Ilana Katz Sand, MD, associate professor of neurology at the Corinne Goldsmith Dickinson Center for MS at Mount Sinai in New York. “We hypothesized a significant association between Mediterranean diet and cognition in MS, but we did not anticipate the 20% absolute difference, particularly because we rigorously controlled the demographic and health-related factors, like socioeconomic status, body mass index, and exercise habits.”
The Mediterranean diet consists of predominately vegetables, fruits, legumes, fish, and healthy fats while minimizing the consumption of dairy products, meats, and saturated acids. Previous literature has drawn an association between diet and MS symptomology, notably with regard to the Mediterranean diet. These studies indicated a connection between thalamic volume in patients with early MS as well as objectively captured MS-related disability. In this study, researchers have continued their investigation by exploring how the Mediterranean diet affects cognition.
In this cross-sectional observational study, investigators evaluated 563 people with MS ranging in age from 18 to 65 years (n = 563; 71% women; aged 44.2 ± 11.3 years). To accomplish this task, researchers conducted a retrospective chart review capturing data from patients with MS who had undergone neurobehavioral screenings. Qualifying subjects completed the Mediterranean Diet Adherence Screener (MEDAS) to determine the extent to which they adhered to the Mediterranean diet. A 14-item questionnaire, MEDAS assess a person’s usual intake of healthful foods such as vegetables and olive oil, as well as minimization of unhealthy foods such as butter and red meat. They also completed an analogue of the CICMAS cognitive battery comprised of a composite of Symbol Digit Modalities Test, Hopkins Verbal Learning Test, Revised, and CANTAB Paired Associate Learning.
Researchers evaluated patient-reported outcomes adjusted based on demographics (i.e., age, sex, race, ethnicity, and socioeconomic status) and health-related factors. These elements included body mass index, exercise, sleep disturbance, hypertension, diabetes, hyperlipidemia, and smoking.
The study excluded patients who had another primary neurological condition in addition to MS (n = 24), serious psychiatric illness such as schizophrenia (n = 5) or clinical relapse within 6 weeks (n = 2), or missing data (n = 13).
Based on the diet scores, investigators stratified participants into four groups. Those with the scores ranging from 0 to 4 were classified into the lowest group, while scores of 9 or greater qualified participants for the high group.
Investigators observed a significant association between a higher Mediterranean diet score and condition in the population sampled. They found a mean z-score of –0.67 (0.95). In addition, a higher MEDAS proved an independent indicator of better cognition (B = 0.08 [95% confidence interval (CI), 0.05, 0.11], beta = 0.20, P < .001). In fact, a high MEDAS independently correlated to a 20% lower risk for cognitive impairment (odds ratio [OR] = .80 {95% CI, 0.73, 0.89}, P < .001). Ultimately, the study’s findings demonstrated MEDAS served as the strongest health-related indicator of z-score and cognitive impairment. Moreover, dietary modification based on effect suggested stronger associations between diet and cognition with progressive disease as opposed to relapsing disease, as noted by the relationship between the z-score and cognition.
“Further research is needed,” Dr. Katz Sand said. “But because the progressive phenotype reflects more prominent neurodegeneration, the greater observed effect size in those with progressive MS suggests a potential neuroprotective mechanism.”
This study was funded in part by an Irma T. Hirschl/Monique Weill-Caulier Research Award to Dr. Katz Sand. Dr. Katz Sand and coauthors also received funding from the National Multiple Sclerosis Society.
due to a potential neuroprotective mechanism, according to findings of a study that was released early, ahead of presentation at the annual meting of the American Academy of Neurology.
“We were most surprised by the magnitude of the results,” said Ilana Katz Sand, MD, associate professor of neurology at the Corinne Goldsmith Dickinson Center for MS at Mount Sinai in New York. “We hypothesized a significant association between Mediterranean diet and cognition in MS, but we did not anticipate the 20% absolute difference, particularly because we rigorously controlled the demographic and health-related factors, like socioeconomic status, body mass index, and exercise habits.”
The Mediterranean diet consists of predominately vegetables, fruits, legumes, fish, and healthy fats while minimizing the consumption of dairy products, meats, and saturated acids. Previous literature has drawn an association between diet and MS symptomology, notably with regard to the Mediterranean diet. These studies indicated a connection between thalamic volume in patients with early MS as well as objectively captured MS-related disability. In this study, researchers have continued their investigation by exploring how the Mediterranean diet affects cognition.
In this cross-sectional observational study, investigators evaluated 563 people with MS ranging in age from 18 to 65 years (n = 563; 71% women; aged 44.2 ± 11.3 years). To accomplish this task, researchers conducted a retrospective chart review capturing data from patients with MS who had undergone neurobehavioral screenings. Qualifying subjects completed the Mediterranean Diet Adherence Screener (MEDAS) to determine the extent to which they adhered to the Mediterranean diet. A 14-item questionnaire, MEDAS assess a person’s usual intake of healthful foods such as vegetables and olive oil, as well as minimization of unhealthy foods such as butter and red meat. They also completed an analogue of the CICMAS cognitive battery comprised of a composite of Symbol Digit Modalities Test, Hopkins Verbal Learning Test, Revised, and CANTAB Paired Associate Learning.
Researchers evaluated patient-reported outcomes adjusted based on demographics (i.e., age, sex, race, ethnicity, and socioeconomic status) and health-related factors. These elements included body mass index, exercise, sleep disturbance, hypertension, diabetes, hyperlipidemia, and smoking.
The study excluded patients who had another primary neurological condition in addition to MS (n = 24), serious psychiatric illness such as schizophrenia (n = 5) or clinical relapse within 6 weeks (n = 2), or missing data (n = 13).
Based on the diet scores, investigators stratified participants into four groups. Those with the scores ranging from 0 to 4 were classified into the lowest group, while scores of 9 or greater qualified participants for the high group.
Investigators observed a significant association between a higher Mediterranean diet score and condition in the population sampled. They found a mean z-score of –0.67 (0.95). In addition, a higher MEDAS proved an independent indicator of better cognition (B = 0.08 [95% confidence interval (CI), 0.05, 0.11], beta = 0.20, P < .001). In fact, a high MEDAS independently correlated to a 20% lower risk for cognitive impairment (odds ratio [OR] = .80 {95% CI, 0.73, 0.89}, P < .001). Ultimately, the study’s findings demonstrated MEDAS served as the strongest health-related indicator of z-score and cognitive impairment. Moreover, dietary modification based on effect suggested stronger associations between diet and cognition with progressive disease as opposed to relapsing disease, as noted by the relationship between the z-score and cognition.
“Further research is needed,” Dr. Katz Sand said. “But because the progressive phenotype reflects more prominent neurodegeneration, the greater observed effect size in those with progressive MS suggests a potential neuroprotective mechanism.”
This study was funded in part by an Irma T. Hirschl/Monique Weill-Caulier Research Award to Dr. Katz Sand. Dr. Katz Sand and coauthors also received funding from the National Multiple Sclerosis Society.
due to a potential neuroprotective mechanism, according to findings of a study that was released early, ahead of presentation at the annual meting of the American Academy of Neurology.
“We were most surprised by the magnitude of the results,” said Ilana Katz Sand, MD, associate professor of neurology at the Corinne Goldsmith Dickinson Center for MS at Mount Sinai in New York. “We hypothesized a significant association between Mediterranean diet and cognition in MS, but we did not anticipate the 20% absolute difference, particularly because we rigorously controlled the demographic and health-related factors, like socioeconomic status, body mass index, and exercise habits.”
The Mediterranean diet consists of predominately vegetables, fruits, legumes, fish, and healthy fats while minimizing the consumption of dairy products, meats, and saturated acids. Previous literature has drawn an association between diet and MS symptomology, notably with regard to the Mediterranean diet. These studies indicated a connection between thalamic volume in patients with early MS as well as objectively captured MS-related disability. In this study, researchers have continued their investigation by exploring how the Mediterranean diet affects cognition.
In this cross-sectional observational study, investigators evaluated 563 people with MS ranging in age from 18 to 65 years (n = 563; 71% women; aged 44.2 ± 11.3 years). To accomplish this task, researchers conducted a retrospective chart review capturing data from patients with MS who had undergone neurobehavioral screenings. Qualifying subjects completed the Mediterranean Diet Adherence Screener (MEDAS) to determine the extent to which they adhered to the Mediterranean diet. A 14-item questionnaire, MEDAS assess a person’s usual intake of healthful foods such as vegetables and olive oil, as well as minimization of unhealthy foods such as butter and red meat. They also completed an analogue of the CICMAS cognitive battery comprised of a composite of Symbol Digit Modalities Test, Hopkins Verbal Learning Test, Revised, and CANTAB Paired Associate Learning.
Researchers evaluated patient-reported outcomes adjusted based on demographics (i.e., age, sex, race, ethnicity, and socioeconomic status) and health-related factors. These elements included body mass index, exercise, sleep disturbance, hypertension, diabetes, hyperlipidemia, and smoking.
The study excluded patients who had another primary neurological condition in addition to MS (n = 24), serious psychiatric illness such as schizophrenia (n = 5) or clinical relapse within 6 weeks (n = 2), or missing data (n = 13).
Based on the diet scores, investigators stratified participants into four groups. Those with the scores ranging from 0 to 4 were classified into the lowest group, while scores of 9 or greater qualified participants for the high group.
Investigators observed a significant association between a higher Mediterranean diet score and condition in the population sampled. They found a mean z-score of –0.67 (0.95). In addition, a higher MEDAS proved an independent indicator of better cognition (B = 0.08 [95% confidence interval (CI), 0.05, 0.11], beta = 0.20, P < .001). In fact, a high MEDAS independently correlated to a 20% lower risk for cognitive impairment (odds ratio [OR] = .80 {95% CI, 0.73, 0.89}, P < .001). Ultimately, the study’s findings demonstrated MEDAS served as the strongest health-related indicator of z-score and cognitive impairment. Moreover, dietary modification based on effect suggested stronger associations between diet and cognition with progressive disease as opposed to relapsing disease, as noted by the relationship between the z-score and cognition.
“Further research is needed,” Dr. Katz Sand said. “But because the progressive phenotype reflects more prominent neurodegeneration, the greater observed effect size in those with progressive MS suggests a potential neuroprotective mechanism.”
This study was funded in part by an Irma T. Hirschl/Monique Weill-Caulier Research Award to Dr. Katz Sand. Dr. Katz Sand and coauthors also received funding from the National Multiple Sclerosis Society.
FROM AAN 2023
Obstructive sleep apnea linked to early cognitive decline
In a pilot study out of King’s College London, participants with severe OSA experienced worse executive functioning as well as social and emotional recognition versus healthy controls.
Major risk factors for OSA include obesity, high blood pressure, smoking, high cholesterol, and being middle-aged or older. Because some researchers have hypothesized that cognitive deficits could be driven by such comorbidities, the study investigators recruited middle-aged men with no medical comorbidities.
“Traditionally, we were more concerned with sleep apnea’s metabolic and cardiovascular comorbidities, and indeed, when cognitive deficits were demonstrated, most were attributed to them, and yet, our patients and their partners/families commonly tell us differently,” lead investigator Ivana Rosenzweig, MD, PhD, of King’s College London, who is also a consultant in sleep medicine and neuropsychiatry at Guy’s and St Thomas’ Hospital, London, said in an interview.
“Our findings provide a very important first step towards challenging the long-standing dogma that sleep apnea has little to do with the brain – apart from causing sleepiness – and that it is a predominantly nonneuro/psychiatric illness,” added Dr. Rosenzweig.
The findings were published online in Frontiers in Sleep.
Brain changes
The researchers wanted to understand how OSA may be linked to cognitive decline in the absence of cardiovascular and metabolic conditions.
To accomplish this, the investigators studied 27 men between the ages of 35 and 70 with a new diagnosis of mild to severe OSA without any comorbidities (16 with mild OSA and 11 with severe OSA). They also studied a control group of seven men matched for age, body mass index, and education level.
The team tested participants’ cognitive performance using the Cambridge Neuropsychological Test Automated Battery and found that the most significant deficits for the OSA group, compared with controls, were in areas of visual matching ability (P < .0001), short-term visual recognition memory, nonverbal patterns, executive functioning and attentional set-shifting (P < .001), psychomotor functioning, and social cognition and emotional recognition (P < .05).
On the latter two tests, impaired participants were less likely to accurately identify the emotion on computer-generated faces. Those with mild OSA performed better than those with severe OSA on these tasks, but rarely worse than controls.
Dr. Rosenzweig noted that the findings were one-of-a-kind because of the recruitment of patients with OSA who were otherwise healthy and nonobese, “something one rarely sees in the sleep clinic, where we commonly encounter patients with already developed comorbidities.
“In order to truly revolutionize the treatment for our patients, it is important to understand how much the accompanying comorbidities, such as systemic hypertension, obesity, diabetes, hyperlipidemia, and other various serious cardiovascular and metabolic diseases and how much the illness itself may shape the demonstrated cognitive deficits,” she said.
She also said that “it is widely agreed that medical problems in middle age may predispose to increased prevalence of dementia in later years.
Moreover, the very link between sleep apnea and Alzheimer’s, vascular and mixed dementia is increasingly demonstrated,” said Dr. Rosenzweig.
Although women typically have a lower prevalence of OSA than men, Dr. Rosenzweig said women were not included in the study “because we are too complex. As a lifelong feminist it pains me to say this, but to get any authoritative answer on our physiology, we need decent funding in place so that we can take into account all the intricacies of the changes of our sleep, physiology, and metabolism.
“While there is always lots of noise about how important it is to answer these questions, there are only very limited funds available for the sleep research,” she added.
Dr. Rosenzweig’s future research will focus on the potential link between OSA and neuroinflammation.
In a comment, Liza Ashbrook, MD, associate professor of neurology at the University of California, San Francisco, said the findings “add to the growing list of negative health consequences associated with sleep apnea.”
She said that, if the cognitive changes found in the study are, in fact, caused by OSA, it is unclear whether they are the beginning of long-term cognitive changes or a symptom of fragmented sleep that may be reversible.
Dr. Ashbrook said she would be interested in seeing research on understanding the effect of OSA treatment on the affected cognitive domains.
The study was funded by the Wellcome Trust. No relevant financial relationships were reported.
A version of this article originally appeared on Medscape.com.
In a pilot study out of King’s College London, participants with severe OSA experienced worse executive functioning as well as social and emotional recognition versus healthy controls.
Major risk factors for OSA include obesity, high blood pressure, smoking, high cholesterol, and being middle-aged or older. Because some researchers have hypothesized that cognitive deficits could be driven by such comorbidities, the study investigators recruited middle-aged men with no medical comorbidities.
“Traditionally, we were more concerned with sleep apnea’s metabolic and cardiovascular comorbidities, and indeed, when cognitive deficits were demonstrated, most were attributed to them, and yet, our patients and their partners/families commonly tell us differently,” lead investigator Ivana Rosenzweig, MD, PhD, of King’s College London, who is also a consultant in sleep medicine and neuropsychiatry at Guy’s and St Thomas’ Hospital, London, said in an interview.
“Our findings provide a very important first step towards challenging the long-standing dogma that sleep apnea has little to do with the brain – apart from causing sleepiness – and that it is a predominantly nonneuro/psychiatric illness,” added Dr. Rosenzweig.
The findings were published online in Frontiers in Sleep.
Brain changes
The researchers wanted to understand how OSA may be linked to cognitive decline in the absence of cardiovascular and metabolic conditions.
To accomplish this, the investigators studied 27 men between the ages of 35 and 70 with a new diagnosis of mild to severe OSA without any comorbidities (16 with mild OSA and 11 with severe OSA). They also studied a control group of seven men matched for age, body mass index, and education level.
The team tested participants’ cognitive performance using the Cambridge Neuropsychological Test Automated Battery and found that the most significant deficits for the OSA group, compared with controls, were in areas of visual matching ability (P < .0001), short-term visual recognition memory, nonverbal patterns, executive functioning and attentional set-shifting (P < .001), psychomotor functioning, and social cognition and emotional recognition (P < .05).
On the latter two tests, impaired participants were less likely to accurately identify the emotion on computer-generated faces. Those with mild OSA performed better than those with severe OSA on these tasks, but rarely worse than controls.
Dr. Rosenzweig noted that the findings were one-of-a-kind because of the recruitment of patients with OSA who were otherwise healthy and nonobese, “something one rarely sees in the sleep clinic, where we commonly encounter patients with already developed comorbidities.
“In order to truly revolutionize the treatment for our patients, it is important to understand how much the accompanying comorbidities, such as systemic hypertension, obesity, diabetes, hyperlipidemia, and other various serious cardiovascular and metabolic diseases and how much the illness itself may shape the demonstrated cognitive deficits,” she said.
She also said that “it is widely agreed that medical problems in middle age may predispose to increased prevalence of dementia in later years.
Moreover, the very link between sleep apnea and Alzheimer’s, vascular and mixed dementia is increasingly demonstrated,” said Dr. Rosenzweig.
Although women typically have a lower prevalence of OSA than men, Dr. Rosenzweig said women were not included in the study “because we are too complex. As a lifelong feminist it pains me to say this, but to get any authoritative answer on our physiology, we need decent funding in place so that we can take into account all the intricacies of the changes of our sleep, physiology, and metabolism.
“While there is always lots of noise about how important it is to answer these questions, there are only very limited funds available for the sleep research,” she added.
Dr. Rosenzweig’s future research will focus on the potential link between OSA and neuroinflammation.
In a comment, Liza Ashbrook, MD, associate professor of neurology at the University of California, San Francisco, said the findings “add to the growing list of negative health consequences associated with sleep apnea.”
She said that, if the cognitive changes found in the study are, in fact, caused by OSA, it is unclear whether they are the beginning of long-term cognitive changes or a symptom of fragmented sleep that may be reversible.
Dr. Ashbrook said she would be interested in seeing research on understanding the effect of OSA treatment on the affected cognitive domains.
The study was funded by the Wellcome Trust. No relevant financial relationships were reported.
A version of this article originally appeared on Medscape.com.
In a pilot study out of King’s College London, participants with severe OSA experienced worse executive functioning as well as social and emotional recognition versus healthy controls.
Major risk factors for OSA include obesity, high blood pressure, smoking, high cholesterol, and being middle-aged or older. Because some researchers have hypothesized that cognitive deficits could be driven by such comorbidities, the study investigators recruited middle-aged men with no medical comorbidities.
“Traditionally, we were more concerned with sleep apnea’s metabolic and cardiovascular comorbidities, and indeed, when cognitive deficits were demonstrated, most were attributed to them, and yet, our patients and their partners/families commonly tell us differently,” lead investigator Ivana Rosenzweig, MD, PhD, of King’s College London, who is also a consultant in sleep medicine and neuropsychiatry at Guy’s and St Thomas’ Hospital, London, said in an interview.
“Our findings provide a very important first step towards challenging the long-standing dogma that sleep apnea has little to do with the brain – apart from causing sleepiness – and that it is a predominantly nonneuro/psychiatric illness,” added Dr. Rosenzweig.
The findings were published online in Frontiers in Sleep.
Brain changes
The researchers wanted to understand how OSA may be linked to cognitive decline in the absence of cardiovascular and metabolic conditions.
To accomplish this, the investigators studied 27 men between the ages of 35 and 70 with a new diagnosis of mild to severe OSA without any comorbidities (16 with mild OSA and 11 with severe OSA). They also studied a control group of seven men matched for age, body mass index, and education level.
The team tested participants’ cognitive performance using the Cambridge Neuropsychological Test Automated Battery and found that the most significant deficits for the OSA group, compared with controls, were in areas of visual matching ability (P < .0001), short-term visual recognition memory, nonverbal patterns, executive functioning and attentional set-shifting (P < .001), psychomotor functioning, and social cognition and emotional recognition (P < .05).
On the latter two tests, impaired participants were less likely to accurately identify the emotion on computer-generated faces. Those with mild OSA performed better than those with severe OSA on these tasks, but rarely worse than controls.
Dr. Rosenzweig noted that the findings were one-of-a-kind because of the recruitment of patients with OSA who were otherwise healthy and nonobese, “something one rarely sees in the sleep clinic, where we commonly encounter patients with already developed comorbidities.
“In order to truly revolutionize the treatment for our patients, it is important to understand how much the accompanying comorbidities, such as systemic hypertension, obesity, diabetes, hyperlipidemia, and other various serious cardiovascular and metabolic diseases and how much the illness itself may shape the demonstrated cognitive deficits,” she said.
She also said that “it is widely agreed that medical problems in middle age may predispose to increased prevalence of dementia in later years.
Moreover, the very link between sleep apnea and Alzheimer’s, vascular and mixed dementia is increasingly demonstrated,” said Dr. Rosenzweig.
Although women typically have a lower prevalence of OSA than men, Dr. Rosenzweig said women were not included in the study “because we are too complex. As a lifelong feminist it pains me to say this, but to get any authoritative answer on our physiology, we need decent funding in place so that we can take into account all the intricacies of the changes of our sleep, physiology, and metabolism.
“While there is always lots of noise about how important it is to answer these questions, there are only very limited funds available for the sleep research,” she added.
Dr. Rosenzweig’s future research will focus on the potential link between OSA and neuroinflammation.
In a comment, Liza Ashbrook, MD, associate professor of neurology at the University of California, San Francisco, said the findings “add to the growing list of negative health consequences associated with sleep apnea.”
She said that, if the cognitive changes found in the study are, in fact, caused by OSA, it is unclear whether they are the beginning of long-term cognitive changes or a symptom of fragmented sleep that may be reversible.
Dr. Ashbrook said she would be interested in seeing research on understanding the effect of OSA treatment on the affected cognitive domains.
The study was funded by the Wellcome Trust. No relevant financial relationships were reported.
A version of this article originally appeared on Medscape.com.
FROM FRONTIERS IN SLEEP
Food insecurity linked to more rapid cognitive decline in seniors
Food insecurity is linked to a more rapid decline in executive function in older adults, a new study shows.
The findings were reported just weeks after a pandemic-era expansion in Supplemental Nutrition Assistance Program benefits ended, leading to less food assistance for about 5 million people over age 60 who participate in the program.
“Even though we found only a very small association between food insecurity and executive function, it’s still meaningful, because food insecurity is something we can prevent,” lead investigator Boeun Kim, PhD, MPH, RN, postdoctoral fellow at Johns Hopkins University School of Nursing, Baltimore, told this news organization.
The findings were published online in JAMA Network Open.
National data
The number of Americans over 60 with food insecurity has more than doubled since 2007, with an estimated 5.2 million older adults reporting food insecurity in 2020.
Prior studies have linked malnutrition and food insecurity to a decline in cognitive function. Participating in food assistance programs such as SNAP is associated with slower memory decline in older adults.
However, to date, there has been no longitudinal study that has used data from a nationally representative sample of older Americans, which, Dr. Kim said, could limit generalizability of the findings.
To address that issue, investigators analyzed data from 3,037 participants in the National Health and Aging Trends Study, which includes community dwellers age 65 and older who receive Medicare.
Participants reported food insecurity over 7 years, from 2012 to 2019. Data on immediate memory, delayed memory, and executive function were from 2013 to 2020.
Food insecurity was defined as going without groceries due to limited ability or social support; a lack of hot meals related to functional limitation or no help; going without eating because of the inability to feed oneself or no available support; skipping meals due to insufficient food or money; or skipping meals for 5 days or more.
Immediate and delayed recall were assessed using a 10-item word-list memory task, and executive function was measured using a clock drawing test. Each year’s cognitive functions were linked to the prior year’s food insecurity data.
Over 7 years, 417 people, or 12.1%, experienced food insecurity at least once.
Those with food insecurity were more likely to be older, female, part of racial and ethnic minority groups, living alone, obese, and have a lower income and educational attainment, depressive symptoms, social isolation and disability, compared with those without food insecurity.
After adjusting for age, sex, race/ethnicity, educational level, income, marital status, body mass index, functional disability, social isolation, and other potential confounders, researchers found that food insecurity was associated with a more rapid decline in executive function (mean difference in annual change in executive function score, −0.04; 95% confidence interval, −0.09 to −0.003).
Food insecurity was not associated with baseline cognitive function scores or changes in immediate or delayed recall.
“Clinicians should be aware of the experience of food insecurity and the higher risk of cognitive decline so maybe they could do universal screening and refer people with food insecurity to programs that can help them access nutritious meals,” Dr. Kim said.
A sign of other problems?
Thomas Vidic, MD, said food insecurity often goes hand-in-hand with lack of medication adherence, lack of regular medical care, and a host of other issues. Dr. Vidic is a neurologist at the Elkhart Clinic, Ind., and an adjunct clinical professor of neurology at Indiana University.
“When a person has food insecurity, they likely have other problems, and they’re going to degenerate faster,” said Dr. Vidic, who was not part of the study. “This is one important component, and it’s one more way of getting a handle on people who are failing.”
Dr. Vidic, who has dealt with the issue of food insecurity with his own patients, said he suspects the self-report nature of the study may hide the true scale of the problem.
“I suspect the numbers might actually be higher,” he said, adding that the study fills a gap in the literature with a large, nationally representative sample.
“We’re looking for issues to help with the elderly as far as what can we do to keep dementia from progressing,” he said. “There are some things that make sense, but we’ve never had this kind of data before.”
The study was funded by the National Institute on Aging. Dr. Kim and Dr. Vidic have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Food insecurity is linked to a more rapid decline in executive function in older adults, a new study shows.
The findings were reported just weeks after a pandemic-era expansion in Supplemental Nutrition Assistance Program benefits ended, leading to less food assistance for about 5 million people over age 60 who participate in the program.
“Even though we found only a very small association between food insecurity and executive function, it’s still meaningful, because food insecurity is something we can prevent,” lead investigator Boeun Kim, PhD, MPH, RN, postdoctoral fellow at Johns Hopkins University School of Nursing, Baltimore, told this news organization.
The findings were published online in JAMA Network Open.
National data
The number of Americans over 60 with food insecurity has more than doubled since 2007, with an estimated 5.2 million older adults reporting food insecurity in 2020.
Prior studies have linked malnutrition and food insecurity to a decline in cognitive function. Participating in food assistance programs such as SNAP is associated with slower memory decline in older adults.
However, to date, there has been no longitudinal study that has used data from a nationally representative sample of older Americans, which, Dr. Kim said, could limit generalizability of the findings.
To address that issue, investigators analyzed data from 3,037 participants in the National Health and Aging Trends Study, which includes community dwellers age 65 and older who receive Medicare.
Participants reported food insecurity over 7 years, from 2012 to 2019. Data on immediate memory, delayed memory, and executive function were from 2013 to 2020.
Food insecurity was defined as going without groceries due to limited ability or social support; a lack of hot meals related to functional limitation or no help; going without eating because of the inability to feed oneself or no available support; skipping meals due to insufficient food or money; or skipping meals for 5 days or more.
Immediate and delayed recall were assessed using a 10-item word-list memory task, and executive function was measured using a clock drawing test. Each year’s cognitive functions were linked to the prior year’s food insecurity data.
Over 7 years, 417 people, or 12.1%, experienced food insecurity at least once.
Those with food insecurity were more likely to be older, female, part of racial and ethnic minority groups, living alone, obese, and have a lower income and educational attainment, depressive symptoms, social isolation and disability, compared with those without food insecurity.
After adjusting for age, sex, race/ethnicity, educational level, income, marital status, body mass index, functional disability, social isolation, and other potential confounders, researchers found that food insecurity was associated with a more rapid decline in executive function (mean difference in annual change in executive function score, −0.04; 95% confidence interval, −0.09 to −0.003).
Food insecurity was not associated with baseline cognitive function scores or changes in immediate or delayed recall.
“Clinicians should be aware of the experience of food insecurity and the higher risk of cognitive decline so maybe they could do universal screening and refer people with food insecurity to programs that can help them access nutritious meals,” Dr. Kim said.
A sign of other problems?
Thomas Vidic, MD, said food insecurity often goes hand-in-hand with lack of medication adherence, lack of regular medical care, and a host of other issues. Dr. Vidic is a neurologist at the Elkhart Clinic, Ind., and an adjunct clinical professor of neurology at Indiana University.
“When a person has food insecurity, they likely have other problems, and they’re going to degenerate faster,” said Dr. Vidic, who was not part of the study. “This is one important component, and it’s one more way of getting a handle on people who are failing.”
Dr. Vidic, who has dealt with the issue of food insecurity with his own patients, said he suspects the self-report nature of the study may hide the true scale of the problem.
“I suspect the numbers might actually be higher,” he said, adding that the study fills a gap in the literature with a large, nationally representative sample.
“We’re looking for issues to help with the elderly as far as what can we do to keep dementia from progressing,” he said. “There are some things that make sense, but we’ve never had this kind of data before.”
The study was funded by the National Institute on Aging. Dr. Kim and Dr. Vidic have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Food insecurity is linked to a more rapid decline in executive function in older adults, a new study shows.
The findings were reported just weeks after a pandemic-era expansion in Supplemental Nutrition Assistance Program benefits ended, leading to less food assistance for about 5 million people over age 60 who participate in the program.
“Even though we found only a very small association between food insecurity and executive function, it’s still meaningful, because food insecurity is something we can prevent,” lead investigator Boeun Kim, PhD, MPH, RN, postdoctoral fellow at Johns Hopkins University School of Nursing, Baltimore, told this news organization.
The findings were published online in JAMA Network Open.
National data
The number of Americans over 60 with food insecurity has more than doubled since 2007, with an estimated 5.2 million older adults reporting food insecurity in 2020.
Prior studies have linked malnutrition and food insecurity to a decline in cognitive function. Participating in food assistance programs such as SNAP is associated with slower memory decline in older adults.
However, to date, there has been no longitudinal study that has used data from a nationally representative sample of older Americans, which, Dr. Kim said, could limit generalizability of the findings.
To address that issue, investigators analyzed data from 3,037 participants in the National Health and Aging Trends Study, which includes community dwellers age 65 and older who receive Medicare.
Participants reported food insecurity over 7 years, from 2012 to 2019. Data on immediate memory, delayed memory, and executive function were from 2013 to 2020.
Food insecurity was defined as going without groceries due to limited ability or social support; a lack of hot meals related to functional limitation or no help; going without eating because of the inability to feed oneself or no available support; skipping meals due to insufficient food or money; or skipping meals for 5 days or more.
Immediate and delayed recall were assessed using a 10-item word-list memory task, and executive function was measured using a clock drawing test. Each year’s cognitive functions were linked to the prior year’s food insecurity data.
Over 7 years, 417 people, or 12.1%, experienced food insecurity at least once.
Those with food insecurity were more likely to be older, female, part of racial and ethnic minority groups, living alone, obese, and have a lower income and educational attainment, depressive symptoms, social isolation and disability, compared with those without food insecurity.
After adjusting for age, sex, race/ethnicity, educational level, income, marital status, body mass index, functional disability, social isolation, and other potential confounders, researchers found that food insecurity was associated with a more rapid decline in executive function (mean difference in annual change in executive function score, −0.04; 95% confidence interval, −0.09 to −0.003).
Food insecurity was not associated with baseline cognitive function scores or changes in immediate or delayed recall.
“Clinicians should be aware of the experience of food insecurity and the higher risk of cognitive decline so maybe they could do universal screening and refer people with food insecurity to programs that can help them access nutritious meals,” Dr. Kim said.
A sign of other problems?
Thomas Vidic, MD, said food insecurity often goes hand-in-hand with lack of medication adherence, lack of regular medical care, and a host of other issues. Dr. Vidic is a neurologist at the Elkhart Clinic, Ind., and an adjunct clinical professor of neurology at Indiana University.
“When a person has food insecurity, they likely have other problems, and they’re going to degenerate faster,” said Dr. Vidic, who was not part of the study. “This is one important component, and it’s one more way of getting a handle on people who are failing.”
Dr. Vidic, who has dealt with the issue of food insecurity with his own patients, said he suspects the self-report nature of the study may hide the true scale of the problem.
“I suspect the numbers might actually be higher,” he said, adding that the study fills a gap in the literature with a large, nationally representative sample.
“We’re looking for issues to help with the elderly as far as what can we do to keep dementia from progressing,” he said. “There are some things that make sense, but we’ve never had this kind of data before.”
The study was funded by the National Institute on Aging. Dr. Kim and Dr. Vidic have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Urban green and blue spaces linked to less psychological distress
The findings of the study, which was released ahead of its scheduled presentation at the annual meeting of the American Academy of Neurology, build on a growing understanding of the relationship between types and qualities of urban environments and dementia risk.
Adithya Vegaraju, a student at Washington State University, Spokane, led the study, which looked at data from the Washington State Behavioral Risk Factor Surveillance System to assess prevalence of serious psychological distress among 42,980 Washington state residents aged 65 and over.
The data, collected between 2011 and 2019, used a self-reported questionnaire to determine serious psychological distress, which is defined as a level of mental distress considered debilitating enough to warrant treatment.
Mr. Vegaraju and his coauthor Solmaz Amiri, DDes, also of Washington State University, used ZIP codes, along with U.S. census data, to approximate the urban adults’ proximity to green and blue spaces.
After controlling for potential confounders of age, sex, ethnicity, education, and marital status, the investigators found that people living within half a mile of green or blue spaces had a 17% lower risk of experiencing serious psychological distress, compared with people living farther from these spaces, the investigators said in a news release.
Implications for cognitive decline and dementia?
Psychological distress in adults has been linked in population-based longitudinal studies to later cognitive decline and dementia. One study in older adults found the risk of dementia to be more than 50% higher among adults aged 50-70 with persistent depression. Blue and green spaces have also been investigated in relation to neurodegenerative disease among older adults; a 2022 study looking at data from some 62 million Medicare beneficiaries found those living in areas with more vegetation saw lower risk of hospitalizations for Alzheimer’s disease and related dementias.
“Since we lack effective prevention methods or treatments for mild cognitive impairment and dementia, we need to get creative in how we look at these issues,” Dr. Amiri commented in a press statement about her and Mr. Vegaraju’s findings. “Our hope is that this study showing better mental health among people living close to parks and water will trigger other studies about how these benefits work and whether this proximity can help prevent or delay mild cognitive impairment and dementia.”
The investigators acknowledged that their findings were limited by reliance on a self-reported measure of psychological distress.
A bidirectional connection with depression and dementia
In a comment, Anjum Hajat, PhD, an epidemiologist at University of Washington School of Public Health in Seattle who has also studied the relationship between green space and dementia risk in older adults, noted some further apparent limitations of the new study, for which only an abstract was available at publication.
“It has been shown that people with depression are at higher risk for dementia, but the opposite is also true,” Dr. Hajat commented. “Those with dementia are more likely to develop depression. This bidirectionality makes this study abstract difficult to interpret since the study is based on cross-sectional data: Individuals are not followed over time to see which develops first, dementia or depression.”
Additionally, Dr. Hajat noted, the data used to determine proximity to green and blue spaces did not allow for the calculation of precise distances between subjects’ homes and these spaces.
Mr. Vegaraju and Dr. Amiri’s study had no outside support, and the investigators declared no conflicts of interest. Dr. Hajat declared no conflicts of interest.
The findings of the study, which was released ahead of its scheduled presentation at the annual meeting of the American Academy of Neurology, build on a growing understanding of the relationship between types and qualities of urban environments and dementia risk.
Adithya Vegaraju, a student at Washington State University, Spokane, led the study, which looked at data from the Washington State Behavioral Risk Factor Surveillance System to assess prevalence of serious psychological distress among 42,980 Washington state residents aged 65 and over.
The data, collected between 2011 and 2019, used a self-reported questionnaire to determine serious psychological distress, which is defined as a level of mental distress considered debilitating enough to warrant treatment.
Mr. Vegaraju and his coauthor Solmaz Amiri, DDes, also of Washington State University, used ZIP codes, along with U.S. census data, to approximate the urban adults’ proximity to green and blue spaces.
After controlling for potential confounders of age, sex, ethnicity, education, and marital status, the investigators found that people living within half a mile of green or blue spaces had a 17% lower risk of experiencing serious psychological distress, compared with people living farther from these spaces, the investigators said in a news release.
Implications for cognitive decline and dementia?
Psychological distress in adults has been linked in population-based longitudinal studies to later cognitive decline and dementia. One study in older adults found the risk of dementia to be more than 50% higher among adults aged 50-70 with persistent depression. Blue and green spaces have also been investigated in relation to neurodegenerative disease among older adults; a 2022 study looking at data from some 62 million Medicare beneficiaries found those living in areas with more vegetation saw lower risk of hospitalizations for Alzheimer’s disease and related dementias.
“Since we lack effective prevention methods or treatments for mild cognitive impairment and dementia, we need to get creative in how we look at these issues,” Dr. Amiri commented in a press statement about her and Mr. Vegaraju’s findings. “Our hope is that this study showing better mental health among people living close to parks and water will trigger other studies about how these benefits work and whether this proximity can help prevent or delay mild cognitive impairment and dementia.”
The investigators acknowledged that their findings were limited by reliance on a self-reported measure of psychological distress.
A bidirectional connection with depression and dementia
In a comment, Anjum Hajat, PhD, an epidemiologist at University of Washington School of Public Health in Seattle who has also studied the relationship between green space and dementia risk in older adults, noted some further apparent limitations of the new study, for which only an abstract was available at publication.
“It has been shown that people with depression are at higher risk for dementia, but the opposite is also true,” Dr. Hajat commented. “Those with dementia are more likely to develop depression. This bidirectionality makes this study abstract difficult to interpret since the study is based on cross-sectional data: Individuals are not followed over time to see which develops first, dementia or depression.”
Additionally, Dr. Hajat noted, the data used to determine proximity to green and blue spaces did not allow for the calculation of precise distances between subjects’ homes and these spaces.
Mr. Vegaraju and Dr. Amiri’s study had no outside support, and the investigators declared no conflicts of interest. Dr. Hajat declared no conflicts of interest.
The findings of the study, which was released ahead of its scheduled presentation at the annual meeting of the American Academy of Neurology, build on a growing understanding of the relationship between types and qualities of urban environments and dementia risk.
Adithya Vegaraju, a student at Washington State University, Spokane, led the study, which looked at data from the Washington State Behavioral Risk Factor Surveillance System to assess prevalence of serious psychological distress among 42,980 Washington state residents aged 65 and over.
The data, collected between 2011 and 2019, used a self-reported questionnaire to determine serious psychological distress, which is defined as a level of mental distress considered debilitating enough to warrant treatment.
Mr. Vegaraju and his coauthor Solmaz Amiri, DDes, also of Washington State University, used ZIP codes, along with U.S. census data, to approximate the urban adults’ proximity to green and blue spaces.
After controlling for potential confounders of age, sex, ethnicity, education, and marital status, the investigators found that people living within half a mile of green or blue spaces had a 17% lower risk of experiencing serious psychological distress, compared with people living farther from these spaces, the investigators said in a news release.
Implications for cognitive decline and dementia?
Psychological distress in adults has been linked in population-based longitudinal studies to later cognitive decline and dementia. One study in older adults found the risk of dementia to be more than 50% higher among adults aged 50-70 with persistent depression. Blue and green spaces have also been investigated in relation to neurodegenerative disease among older adults; a 2022 study looking at data from some 62 million Medicare beneficiaries found those living in areas with more vegetation saw lower risk of hospitalizations for Alzheimer’s disease and related dementias.
“Since we lack effective prevention methods or treatments for mild cognitive impairment and dementia, we need to get creative in how we look at these issues,” Dr. Amiri commented in a press statement about her and Mr. Vegaraju’s findings. “Our hope is that this study showing better mental health among people living close to parks and water will trigger other studies about how these benefits work and whether this proximity can help prevent or delay mild cognitive impairment and dementia.”
The investigators acknowledged that their findings were limited by reliance on a self-reported measure of psychological distress.
A bidirectional connection with depression and dementia
In a comment, Anjum Hajat, PhD, an epidemiologist at University of Washington School of Public Health in Seattle who has also studied the relationship between green space and dementia risk in older adults, noted some further apparent limitations of the new study, for which only an abstract was available at publication.
“It has been shown that people with depression are at higher risk for dementia, but the opposite is also true,” Dr. Hajat commented. “Those with dementia are more likely to develop depression. This bidirectionality makes this study abstract difficult to interpret since the study is based on cross-sectional data: Individuals are not followed over time to see which develops first, dementia or depression.”
Additionally, Dr. Hajat noted, the data used to determine proximity to green and blue spaces did not allow for the calculation of precise distances between subjects’ homes and these spaces.
Mr. Vegaraju and Dr. Amiri’s study had no outside support, and the investigators declared no conflicts of interest. Dr. Hajat declared no conflicts of interest.
FROM AAN 2023