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BOSTON – Daytime sleepiness in cognitively intact older adults was significantly associated with subsequent neuroimaging evidence of brain amyloid deposition, according to a data analysis presented at the annual meeting of the Associated Professional Sleep Societies.
Self-reported regular nappers were also more likely to have brain amyloid on subsequent imaging, compared with non-nappers, but this difference just missed statistical significance.
Alzheimer’s disease is characterized by extracellular beta-amyloid deposition and intraneuronal neurofibrillary tangles. In 2009, researchers at Washington University in St. Louis showed that sleep restriction promoted beta-amyloid deposition in a mouse model of Alzheimer’s disease. (Kang et al. Science. 2009).
Complementing these findings, Adam P. Spira, PhD, and his colleagues from John’s Hopkins University, Baltimore, previously published a study showing that self-reported sleep duration and poorer sleep quality were associated with greater beta-amyloid deposition in cognitively normal adults. (Spira et al. JAMA Neurology, 2013).
This new study by Dr. Spira and his colleagues sought to look at the link between excessive daytime sleepiness (EDS)/napping in older adults and beta-amyloid burden 15 years later as determined by positron emission tomography (PET) scanning. EDS, defined as a level of sleepiness during the day sufficient to interfere with daily activities, is a common manifestation of sleep disorders, in particular sleep disordered breathing, and is tied to cognitive impairment and accidents.
In unadjusted analyses, participants with EDS were beyond three times more likely to be beta-amyloid+ (odds ratio, 3.37), compared with those who did not meet criteria for EDS. This finding remained significant after adjustment for age, body mass index, and education level (OR, 2.59).
Nappers had an almost twofold greater odds of being beta-amyloid+ than non-nappers after adjustment, but this difference was not statistically meaningful (multivariate adjusted odds ratio, 1.82).
The researchers analyzed data on 124 participants drawn from the National Institute of Aging’s Baltimore Longitudinal Study of Aging (BLSA), the longest-running study of human aging in the U.S. The mean age of these patients at baseline was 60.1 years, and 50.8% of the sample was female. All participants were determined to be cognitively normal at baseline.
At the beginning of the study, participants were asked about their daytime sleepiness and napping habits. Those who reported often being drowsy or falling asleep during the daytime when they preferred to be awake were considered to having EDS. Those who napped once or twice a week or more were considered nappers.
About one-quarter of participants (24.4%) reported EDS, and 28.5% identified themselves as regular nappers. An average of 15.7 years later, participants completed Pittsburgh Compound B PET imaging, at which time 34.7% were deemed beta-amyloid+.
“We were kind of shocked that a single question with a yes/no response was robustly associated with [beta-amyloid] status that many years later,” reported Dr. Spira.
Still unknown, he added, is whether there is utility in quantifying or screening for preclinical Alzheimer’s disease risk using sleep variables. Also unclear is how EDS itself might drive beta-amyloid deposition. “What is likely to be happening here is something like sleep disordered breathing – which has been linked to cognitive impairment and dementia and has been linked to [Alzheimer’s disease] biomarkers – is driving this association,” he speculated.
“We have to keep in mind that even the people at baseline, even though they were cognitively normal, may have had some beta-amyloid deposition, which might have contributed to their EDS,” said Dr. Spira.
Dr. Spira intends to conduct a prospective study using laboratory-based sleep testing (polysomnography) and repeated measures of brain amyloid to clarify whether sleep disordered breathing or other factors were driving the association he found.
Dr. Spira reported having no financial disclosures. This study was supported by grants from the National Institute on Aging.
BOSTON – Daytime sleepiness in cognitively intact older adults was significantly associated with subsequent neuroimaging evidence of brain amyloid deposition, according to a data analysis presented at the annual meeting of the Associated Professional Sleep Societies.
Self-reported regular nappers were also more likely to have brain amyloid on subsequent imaging, compared with non-nappers, but this difference just missed statistical significance.
Alzheimer’s disease is characterized by extracellular beta-amyloid deposition and intraneuronal neurofibrillary tangles. In 2009, researchers at Washington University in St. Louis showed that sleep restriction promoted beta-amyloid deposition in a mouse model of Alzheimer’s disease. (Kang et al. Science. 2009).
Complementing these findings, Adam P. Spira, PhD, and his colleagues from John’s Hopkins University, Baltimore, previously published a study showing that self-reported sleep duration and poorer sleep quality were associated with greater beta-amyloid deposition in cognitively normal adults. (Spira et al. JAMA Neurology, 2013).
This new study by Dr. Spira and his colleagues sought to look at the link between excessive daytime sleepiness (EDS)/napping in older adults and beta-amyloid burden 15 years later as determined by positron emission tomography (PET) scanning. EDS, defined as a level of sleepiness during the day sufficient to interfere with daily activities, is a common manifestation of sleep disorders, in particular sleep disordered breathing, and is tied to cognitive impairment and accidents.
In unadjusted analyses, participants with EDS were beyond three times more likely to be beta-amyloid+ (odds ratio, 3.37), compared with those who did not meet criteria for EDS. This finding remained significant after adjustment for age, body mass index, and education level (OR, 2.59).
Nappers had an almost twofold greater odds of being beta-amyloid+ than non-nappers after adjustment, but this difference was not statistically meaningful (multivariate adjusted odds ratio, 1.82).
The researchers analyzed data on 124 participants drawn from the National Institute of Aging’s Baltimore Longitudinal Study of Aging (BLSA), the longest-running study of human aging in the U.S. The mean age of these patients at baseline was 60.1 years, and 50.8% of the sample was female. All participants were determined to be cognitively normal at baseline.
At the beginning of the study, participants were asked about their daytime sleepiness and napping habits. Those who reported often being drowsy or falling asleep during the daytime when they preferred to be awake were considered to having EDS. Those who napped once or twice a week or more were considered nappers.
About one-quarter of participants (24.4%) reported EDS, and 28.5% identified themselves as regular nappers. An average of 15.7 years later, participants completed Pittsburgh Compound B PET imaging, at which time 34.7% were deemed beta-amyloid+.
“We were kind of shocked that a single question with a yes/no response was robustly associated with [beta-amyloid] status that many years later,” reported Dr. Spira.
Still unknown, he added, is whether there is utility in quantifying or screening for preclinical Alzheimer’s disease risk using sleep variables. Also unclear is how EDS itself might drive beta-amyloid deposition. “What is likely to be happening here is something like sleep disordered breathing – which has been linked to cognitive impairment and dementia and has been linked to [Alzheimer’s disease] biomarkers – is driving this association,” he speculated.
“We have to keep in mind that even the people at baseline, even though they were cognitively normal, may have had some beta-amyloid deposition, which might have contributed to their EDS,” said Dr. Spira.
Dr. Spira intends to conduct a prospective study using laboratory-based sleep testing (polysomnography) and repeated measures of brain amyloid to clarify whether sleep disordered breathing or other factors were driving the association he found.
Dr. Spira reported having no financial disclosures. This study was supported by grants from the National Institute on Aging.
BOSTON – Daytime sleepiness in cognitively intact older adults was significantly associated with subsequent neuroimaging evidence of brain amyloid deposition, according to a data analysis presented at the annual meeting of the Associated Professional Sleep Societies.
Self-reported regular nappers were also more likely to have brain amyloid on subsequent imaging, compared with non-nappers, but this difference just missed statistical significance.
Alzheimer’s disease is characterized by extracellular beta-amyloid deposition and intraneuronal neurofibrillary tangles. In 2009, researchers at Washington University in St. Louis showed that sleep restriction promoted beta-amyloid deposition in a mouse model of Alzheimer’s disease. (Kang et al. Science. 2009).
Complementing these findings, Adam P. Spira, PhD, and his colleagues from John’s Hopkins University, Baltimore, previously published a study showing that self-reported sleep duration and poorer sleep quality were associated with greater beta-amyloid deposition in cognitively normal adults. (Spira et al. JAMA Neurology, 2013).
This new study by Dr. Spira and his colleagues sought to look at the link between excessive daytime sleepiness (EDS)/napping in older adults and beta-amyloid burden 15 years later as determined by positron emission tomography (PET) scanning. EDS, defined as a level of sleepiness during the day sufficient to interfere with daily activities, is a common manifestation of sleep disorders, in particular sleep disordered breathing, and is tied to cognitive impairment and accidents.
In unadjusted analyses, participants with EDS were beyond three times more likely to be beta-amyloid+ (odds ratio, 3.37), compared with those who did not meet criteria for EDS. This finding remained significant after adjustment for age, body mass index, and education level (OR, 2.59).
Nappers had an almost twofold greater odds of being beta-amyloid+ than non-nappers after adjustment, but this difference was not statistically meaningful (multivariate adjusted odds ratio, 1.82).
The researchers analyzed data on 124 participants drawn from the National Institute of Aging’s Baltimore Longitudinal Study of Aging (BLSA), the longest-running study of human aging in the U.S. The mean age of these patients at baseline was 60.1 years, and 50.8% of the sample was female. All participants were determined to be cognitively normal at baseline.
At the beginning of the study, participants were asked about their daytime sleepiness and napping habits. Those who reported often being drowsy or falling asleep during the daytime when they preferred to be awake were considered to having EDS. Those who napped once or twice a week or more were considered nappers.
About one-quarter of participants (24.4%) reported EDS, and 28.5% identified themselves as regular nappers. An average of 15.7 years later, participants completed Pittsburgh Compound B PET imaging, at which time 34.7% were deemed beta-amyloid+.
“We were kind of shocked that a single question with a yes/no response was robustly associated with [beta-amyloid] status that many years later,” reported Dr. Spira.
Still unknown, he added, is whether there is utility in quantifying or screening for preclinical Alzheimer’s disease risk using sleep variables. Also unclear is how EDS itself might drive beta-amyloid deposition. “What is likely to be happening here is something like sleep disordered breathing – which has been linked to cognitive impairment and dementia and has been linked to [Alzheimer’s disease] biomarkers – is driving this association,” he speculated.
“We have to keep in mind that even the people at baseline, even though they were cognitively normal, may have had some beta-amyloid deposition, which might have contributed to their EDS,” said Dr. Spira.
Dr. Spira intends to conduct a prospective study using laboratory-based sleep testing (polysomnography) and repeated measures of brain amyloid to clarify whether sleep disordered breathing or other factors were driving the association he found.
Dr. Spira reported having no financial disclosures. This study was supported by grants from the National Institute on Aging.
AT SLEEP 2017
Key clinical point: Cognitively normal older adults who reported excessive sleepiness or napping were more likely, at follow-up 15 years later, to have brain amyloid deposition, one of the hallmarks of Alzheimer’s disease.
Major finding: Compared with those who did not report excessive daytime sleepiness, those who did were more than three times more likely to have beta-amyloid deposition on PET imaging more than 15 years later.
Data source: The data analysis included 124 participants in the Baltimore Longitudinal Study of Aging who were queried on their sleep habits and then underwent PET imaging more than 15 years later.
Disclosures: Dr. Spira reported having no financial disclosures. This study was supported by grants from the National Institute on Aging.