AAIC 2014

COPENHAGEN – Detection of tau neurofibrillary tangles in the brain via PET imaging highly correlates with memory decline and could serve as an accurate way to identify individuals at high risk of Alzheimer’s disease and track disease progression, according to the results of a prospective study.

In a group of cognitively normal elderly subjects, PET imaging with an investigational tau-specific radioligand showed a significant association between increased tau binding and progressive memory decline over 3 years. A second study found that increased binding effectively discriminated cognitively normal subjects from those with mild cognitive impairment (MCI) and Alzheimer’s dementia.

The studies hold great promise for the future of Alzheimer’s drug development, Dr. Keith Johnson said at the Alzheimer’s Association International Conference 2014.

"At this early stage of tau PET imaging, we do think we are able to visualize the second of the two cardinal pathologic processes," said Dr. Johnson, codirector of the Neuroimaging Program of the Massachusetts Alzheimer’s Disease Research Center at Harvard University, Cambridge, Mass. "Our initial findings indicate that the spread of tau to widespread cortical regions, in the presence of amyloid plaques, may be the smoking gun – the sign that indicates cognitive impairment is either imminent or underway."

The compound, [¹⁸F]T807, is being developed by Avid Radiopharmaceuticals, a subsidiary of Eli Lilly.

The first study by Dr. Johnson and his colleagues looked at [¹⁸F]T807 binding in a group of 56 cognitively normal subjects with a mean age of 72 years. All were members of the Harvard Aging Brain Study. The ongoing project tracks amyloid-beta deposition with PET imaging, as well as other Alzheimer’s biomarkers, in a group of cognitively normal, healthy subjects. Each participant also undergoes an annual test of cognition.

Dr. Johnson’s investigation examined the relationship between tau binding and memory performance as assessed retrospectively with the six-trial Selective Reminding Test over a median 3-year period. The linear regression model controlled for amyloid-beta plaque burden, age, and education.

Over the study period, the investigators found a highly significant relationship between memory performance and [¹⁸F]T807 binding in the entorhinal cortex (P less than .008) and the inferior temporal cortex (P less than .006). Amyloid-beta binding was significantly associated with tau binding in both regions.

When the model included tau and amyloid-beta plaque burden, the relationship between memory performance and inferior temporal tau burden remained significant in the inferior temporal region, whereas memory performance was no longer associated with tau binding in the entorhinal cortex. The amyloid burden was a significant, independent predictor of memory decline in both models.

The second study demonstrated the ligand’s ability to discriminate between normal and impaired memory. This study cohort comprised 51 individuals (mean age, 74 years); 40 were cognitively normal, 6 had MCI, and 5 had Alzheimer’s disease. They also underwent both tau and amyloid-beta PET imaging.

Among the cognitively normal subjects, [¹⁸F]T807 uptake was concentrated in the hippocampus. It varied considerably in the temporal allocortex, and occurred at low levels in the neocortex.

Compared with the cognitively normal subjects, the MCI and Alzheimer’s patients showed significantly greater binding in the neocortical regions, particularly in the temporal and occipital lobes. Binding extended into the parietal and frontal regions in patients with advanced symptoms.

Among all subjects, those with greater entorhinal binding performed significantly worse on a measure of delayed recall. Worse memory performance was also associated with higher amyloid-beta binding.

"We saw a progressive increase in cortical tau going from the normal subjects to those with Alzheimer’s dementia, and this pattern was different from amyloid," Dr. Johnson said. "The amyloid plaques were more diffuse and appeared at an earlier stage than the tau tangles. Our hypothesis is that the tau appears closer to the action, indicating incident cognitive impairment. It shows that these are the people who have or are about to have cognitive impairment, while the amyloid scan shows a much earlier stage of the pathology."

Although these studies are preliminary, they show that tau imaging may benefit research as much as amyloid imaging has, Dr. Johnson said.

"Ten years ago, amyloid plaque detection changed much of what we do in Alzheimer’s research, enabling us to identify the pathology years before any symptoms develop. It’s had a huge impact on drug development, allowing us to focus in on the right people for research cohorts. Unfortunately, amyloid has only been half of the story."

This new ability to see tau neurofibrillary tangles in vivo "should eventually enable us to more efficiently develop preventive therapies and even treatments for the actual symptoms," he said.

Dr. Johnson has been an adviser or consultant for Siemens Healthcare Diagnostics, Genzyme, and Piramal Healthcare. He has received research funding from Avid Radiopharmaceuticals, Eli Lilly, and other companies.

[email protected]

On Twitter @alz_gal

COPENHAGEN – Detection of tau neurofibrillary tangles in the brain via PET imaging highly correlates with memory decline and could serve as an accurate way to identify individuals at high risk of Alzheimer’s disease and track disease progression, according to the results of a prospective study.

In a group of cognitively normal elderly subjects, PET imaging with an investigational tau-specific radioligand showed a significant association between increased tau binding and progressive memory decline over 3 years. A second study found that increased binding effectively discriminated cognitively normal subjects from those with mild cognitive impairment (MCI) and Alzheimer’s dementia.

The studies hold great promise for the future of Alzheimer’s drug development, Dr. Keith Johnson said at the Alzheimer’s Association International Conference 2014.

"At this early stage of tau PET imaging, we do think we are able to visualize the second of the two cardinal pathologic processes," said Dr. Johnson, codirector of the Neuroimaging Program of the Massachusetts Alzheimer’s Disease Research Center at Harvard University, Cambridge, Mass. "Our initial findings indicate that the spread of tau to widespread cortical regions, in the presence of amyloid plaques, may be the smoking gun – the sign that indicates cognitive impairment is either imminent or underway."

The compound, [¹⁸F]T807, is being developed by Avid Radiopharmaceuticals, a subsidiary of Eli Lilly.

The first study by Dr. Johnson and his colleagues looked at [¹⁸F]T807 binding in a group of 56 cognitively normal subjects with a mean age of 72 years. All were members of the Harvard Aging Brain Study. The ongoing project tracks amyloid-beta deposition with PET imaging, as well as other Alzheimer’s biomarkers, in a group of cognitively normal, healthy subjects. Each participant also undergoes an annual test of cognition.

Dr. Johnson’s investigation examined the relationship between tau binding and memory performance as assessed retrospectively with the six-trial Selective Reminding Test over a median 3-year period. The linear regression model controlled for amyloid-beta plaque burden, age, and education.

Over the study period, the investigators found a highly significant relationship between memory performance and [¹⁸F]T807 binding in the entorhinal cortex (P less than .008) and the inferior temporal cortex (P less than .006). Amyloid-beta binding was significantly associated with tau binding in both regions.

When the model included tau and amyloid-beta plaque burden, the relationship between memory performance and inferior temporal tau burden remained significant in the inferior temporal region, whereas memory performance was no longer associated with tau binding in the entorhinal cortex. The amyloid burden was a significant, independent predictor of memory decline in both models.

The second study demonstrated the ligand’s ability to discriminate between normal and impaired memory. This study cohort comprised 51 individuals (mean age, 74 years); 40 were cognitively normal, 6 had MCI, and 5 had Alzheimer’s disease. They also underwent both tau and amyloid-beta PET imaging.

Among the cognitively normal subjects, [¹⁸F]T807 uptake was concentrated in the hippocampus. It varied considerably in the temporal allocortex, and occurred at low levels in the neocortex.

Compared with the cognitively normal subjects, the MCI and Alzheimer’s patients showed significantly greater binding in the neocortical regions, particularly in the temporal and occipital lobes. Binding extended into the parietal and frontal regions in patients with advanced symptoms.

Among all subjects, those with greater entorhinal binding performed significantly worse on a measure of delayed recall. Worse memory performance was also associated with higher amyloid-beta binding.

"We saw a progressive increase in cortical tau going from the normal subjects to those with Alzheimer’s dementia, and this pattern was different from amyloid," Dr. Johnson said. "The amyloid plaques were more diffuse and appeared at an earlier stage than the tau tangles. Our hypothesis is that the tau appears closer to the action, indicating incident cognitive impairment. It shows that these are the people who have or are about to have cognitive impairment, while the amyloid scan shows a much earlier stage of the pathology."

Although these studies are preliminary, they show that tau imaging may benefit research as much as amyloid imaging has, Dr. Johnson said.

"Ten years ago, amyloid plaque detection changed much of what we do in Alzheimer’s research, enabling us to identify the pathology years before any symptoms develop. It’s had a huge impact on drug development, allowing us to focus in on the right people for research cohorts. Unfortunately, amyloid has only been half of the story."

This new ability to see tau neurofibrillary tangles in vivo "should eventually enable us to more efficiently develop preventive therapies and even treatments for the actual symptoms," he said.

Dr. Johnson has been an adviser or consultant for Siemens Healthcare Diagnostics, Genzyme, and Piramal Healthcare. He has received research funding from Avid Radiopharmaceuticals, Eli Lilly, and other companies.

[email protected]

On Twitter @alz_gal

COPENHAGEN – Detection of tau neurofibrillary tangles in the brain via PET imaging highly correlates with memory decline and could serve as an accurate way to identify individuals at high risk of Alzheimer’s disease and track disease progression, according to the results of a prospective study.

In a group of cognitively normal elderly subjects, PET imaging with an investigational tau-specific radioligand showed a significant association between increased tau binding and progressive memory decline over 3 years. A second study found that increased binding effectively discriminated cognitively normal subjects from those with mild cognitive impairment (MCI) and Alzheimer’s dementia.

The studies hold great promise for the future of Alzheimer’s drug development, Dr. Keith Johnson said at the Alzheimer’s Association International Conference 2014.

"At this early stage of tau PET imaging, we do think we are able to visualize the second of the two cardinal pathologic processes," said Dr. Johnson, codirector of the Neuroimaging Program of the Massachusetts Alzheimer’s Disease Research Center at Harvard University, Cambridge, Mass. "Our initial findings indicate that the spread of tau to widespread cortical regions, in the presence of amyloid plaques, may be the smoking gun – the sign that indicates cognitive impairment is either imminent or underway."

The compound, [¹⁸F]T807, is being developed by Avid Radiopharmaceuticals, a subsidiary of Eli Lilly.

The first study by Dr. Johnson and his colleagues looked at [¹⁸F]T807 binding in a group of 56 cognitively normal subjects with a mean age of 72 years. All were members of the Harvard Aging Brain Study. The ongoing project tracks amyloid-beta deposition with PET imaging, as well as other Alzheimer’s biomarkers, in a group of cognitively normal, healthy subjects. Each participant also undergoes an annual test of cognition.

Dr. Johnson’s investigation examined the relationship between tau binding and memory performance as assessed retrospectively with the six-trial Selective Reminding Test over a median 3-year period. The linear regression model controlled for amyloid-beta plaque burden, age, and education.

Over the study period, the investigators found a highly significant relationship between memory performance and [¹⁸F]T807 binding in the entorhinal cortex (P less than .008) and the inferior temporal cortex (P less than .006). Amyloid-beta binding was significantly associated with tau binding in both regions.

When the model included tau and amyloid-beta plaque burden, the relationship between memory performance and inferior temporal tau burden remained significant in the inferior temporal region, whereas memory performance was no longer associated with tau binding in the entorhinal cortex. The amyloid burden was a significant, independent predictor of memory decline in both models.

The second study demonstrated the ligand’s ability to discriminate between normal and impaired memory. This study cohort comprised 51 individuals (mean age, 74 years); 40 were cognitively normal, 6 had MCI, and 5 had Alzheimer’s disease. They also underwent both tau and amyloid-beta PET imaging.

Among the cognitively normal subjects, [¹⁸F]T807 uptake was concentrated in the hippocampus. It varied considerably in the temporal allocortex, and occurred at low levels in the neocortex.

Compared with the cognitively normal subjects, the MCI and Alzheimer’s patients showed significantly greater binding in the neocortical regions, particularly in the temporal and occipital lobes. Binding extended into the parietal and frontal regions in patients with advanced symptoms.

Among all subjects, those with greater entorhinal binding performed significantly worse on a measure of delayed recall. Worse memory performance was also associated with higher amyloid-beta binding.

"We saw a progressive increase in cortical tau going from the normal subjects to those with Alzheimer’s dementia, and this pattern was different from amyloid," Dr. Johnson said. "The amyloid plaques were more diffuse and appeared at an earlier stage than the tau tangles. Our hypothesis is that the tau appears closer to the action, indicating incident cognitive impairment. It shows that these are the people who have or are about to have cognitive impairment, while the amyloid scan shows a much earlier stage of the pathology."

Although these studies are preliminary, they show that tau imaging may benefit research as much as amyloid imaging has, Dr. Johnson said.

"Ten years ago, amyloid plaque detection changed much of what we do in Alzheimer’s research, enabling us to identify the pathology years before any symptoms develop. It’s had a huge impact on drug development, allowing us to focus in on the right people for research cohorts. Unfortunately, amyloid has only been half of the story."

This new ability to see tau neurofibrillary tangles in vivo "should eventually enable us to more efficiently develop preventive therapies and even treatments for the actual symptoms," he said.

Dr. Johnson has been an adviser or consultant for Siemens Healthcare Diagnostics, Genzyme, and Piramal Healthcare. He has received research funding from Avid Radiopharmaceuticals, Eli Lilly, and other companies.

[email protected]

On Twitter @alz_gal

COPENHAGEN – TDP-43, a protein that has been associated with neurodegenerative diseases such as dementia and amyotrophic lateral sclerosis, could also be contributing to brain shrinkage in Alzheimer’s disease, adding another potential biomarker and treatment target for the disease, according to researchers at the Mayo Clinic.

The study of brain scans for 133 patients with Alzheimer’s disease diagnosed at autopsy revealed that TAR DNA binding protein of 43 kDa, or TDP-43, was associated with faster rates of hippocampal and cortical atrophy. The protein was also associated with memory loss and clinical features associated with the disease, said Jennifer L. Whitwell, Ph.D., of the Mayo Clinic, Rochester, Minn., who presented the study at the annual Alzheimer’s Association International Conference.

Michele Sullivan/Frontline Medical News

The results suggest that TDP-43 could be a target for treatment and should be considered in future studies and clinical trials, Dr. Whitwell said. "Can we target TDP-43 and try to slow down the disease processes?" she asked. "If we can remove it or prevent it from accumulating, perhaps we could slow down the rate of hippocampal loss."

Dr. Whitwell is part of Dr. Keith Josephs’s team at the Mayo Clinic. The group recently showed that the protein was present in almost 60% of 342 Alzheimer’s disease brains they studied using the Mayo Clinic neuropathological database (Acta Neuropathol. 2014;127:811-24).

They found that TDP-43–positive subjects were 10 times more likely to be cognitively impaired at death, compared with TDP-43–negative individuals. (Some patients had normal cognition at death.) Resilient cognition seemed to be almost nonexistent in the presence of TDP-43, Dr. Whitwell said. Also, the protein seemed to have a greater effect in Braak stage IV and V than with stage VI.

In a longitudinal analysis of the same 342 subjects, the team analyzed the data for 133 individuals who had two MRIs before death, separated by a mean interval of 3.4 years. There was a mean of 3.7 years between the repeat scan at the time of death. They looked for presence of TDP-43 and tau neurofibrillary tangle burden in the hippocampus and the lateral temporal cortex, an area affected in Alzheimer’s disease. They then measured the rates of hippocampal and cortical atrophy and tried to decide if the shrinkage was driven by TDP-43, tau, or both.

The average age of death was 82 years, and the population was split almost evenly by sex.

The results showed that the presence of TDP-43 was significantly associated with volume loss at the hippocampus, while tau showed no such association.

In the cortex, both TDP-43 and tau were associated with the rate of volume change, although tau showed a stronger association (P less than .0001 for tau vs. P = .01 for TDP-43). Also, the rate of cortical atrophy was strongly associated with age of death, while the rate of hippocampus shrinkage wasn’t. The investigators adjusted their models for other features found in the brains patients with Alzheimer’s disease, such as the presence of amyloid-beta plaques and Lewy bodies, Dr. Whitwell said.

The findings "would suggest that [TDP-43] might be a new target," said Ralph Nixon, Ph.D., chair of the Alzheimer’s Association Medical and Scientific Advisory Council, in a comment on the association’s website. "This might be one of the missing factors that we’ve been looking for, for quite some time, any it maybe a hopeful prospect for a new biomarker."

The study was funded by the National Institute on Aging. Dr. Whitwell and Dr. Nixon had no financial disclosures.

[email protected]

On Twitter @naseemmiller

COPENHAGEN – TDP-43, a protein that has been associated with neurodegenerative diseases such as dementia and amyotrophic lateral sclerosis, could also be contributing to brain shrinkage in Alzheimer’s disease, adding another potential biomarker and treatment target for the disease, according to researchers at the Mayo Clinic.

The study of brain scans for 133 patients with Alzheimer’s disease diagnosed at autopsy revealed that TAR DNA binding protein of 43 kDa, or TDP-43, was associated with faster rates of hippocampal and cortical atrophy. The protein was also associated with memory loss and clinical features associated with the disease, said Jennifer L. Whitwell, Ph.D., of the Mayo Clinic, Rochester, Minn., who presented the study at the annual Alzheimer’s Association International Conference.

Michele Sullivan/Frontline Medical News

The results suggest that TDP-43 could be a target for treatment and should be considered in future studies and clinical trials, Dr. Whitwell said. "Can we target TDP-43 and try to slow down the disease processes?" she asked. "If we can remove it or prevent it from accumulating, perhaps we could slow down the rate of hippocampal loss."

Dr. Whitwell is part of Dr. Keith Josephs’s team at the Mayo Clinic. The group recently showed that the protein was present in almost 60% of 342 Alzheimer’s disease brains they studied using the Mayo Clinic neuropathological database (Acta Neuropathol. 2014;127:811-24).

They found that TDP-43–positive subjects were 10 times more likely to be cognitively impaired at death, compared with TDP-43–negative individuals. (Some patients had normal cognition at death.) Resilient cognition seemed to be almost nonexistent in the presence of TDP-43, Dr. Whitwell said. Also, the protein seemed to have a greater effect in Braak stage IV and V than with stage VI.

In a longitudinal analysis of the same 342 subjects, the team analyzed the data for 133 individuals who had two MRIs before death, separated by a mean interval of 3.4 years. There was a mean of 3.7 years between the repeat scan at the time of death. They looked for presence of TDP-43 and tau neurofibrillary tangle burden in the hippocampus and the lateral temporal cortex, an area affected in Alzheimer’s disease. They then measured the rates of hippocampal and cortical atrophy and tried to decide if the shrinkage was driven by TDP-43, tau, or both.

The average age of death was 82 years, and the population was split almost evenly by sex.

The results showed that the presence of TDP-43 was significantly associated with volume loss at the hippocampus, while tau showed no such association.

In the cortex, both TDP-43 and tau were associated with the rate of volume change, although tau showed a stronger association (P less than .0001 for tau vs. P = .01 for TDP-43). Also, the rate of cortical atrophy was strongly associated with age of death, while the rate of hippocampus shrinkage wasn’t. The investigators adjusted their models for other features found in the brains patients with Alzheimer’s disease, such as the presence of amyloid-beta plaques and Lewy bodies, Dr. Whitwell said.

The findings "would suggest that [TDP-43] might be a new target," said Ralph Nixon, Ph.D., chair of the Alzheimer’s Association Medical and Scientific Advisory Council, in a comment on the association’s website. "This might be one of the missing factors that we’ve been looking for, for quite some time, any it maybe a hopeful prospect for a new biomarker."

The study was funded by the National Institute on Aging. Dr. Whitwell and Dr. Nixon had no financial disclosures.

[email protected]

On Twitter @naseemmiller

COPENHAGEN – TDP-43, a protein that has been associated with neurodegenerative diseases such as dementia and amyotrophic lateral sclerosis, could also be contributing to brain shrinkage in Alzheimer’s disease, adding another potential biomarker and treatment target for the disease, according to researchers at the Mayo Clinic.

The study of brain scans for 133 patients with Alzheimer’s disease diagnosed at autopsy revealed that TAR DNA binding protein of 43 kDa, or TDP-43, was associated with faster rates of hippocampal and cortical atrophy. The protein was also associated with memory loss and clinical features associated with the disease, said Jennifer L. Whitwell, Ph.D., of the Mayo Clinic, Rochester, Minn., who presented the study at the annual Alzheimer’s Association International Conference.

Michele Sullivan/Frontline Medical News

The results suggest that TDP-43 could be a target for treatment and should be considered in future studies and clinical trials, Dr. Whitwell said. "Can we target TDP-43 and try to slow down the disease processes?" she asked. "If we can remove it or prevent it from accumulating, perhaps we could slow down the rate of hippocampal loss."

Dr. Whitwell is part of Dr. Keith Josephs’s team at the Mayo Clinic. The group recently showed that the protein was present in almost 60% of 342 Alzheimer’s disease brains they studied using the Mayo Clinic neuropathological database (Acta Neuropathol. 2014;127:811-24).

They found that TDP-43–positive subjects were 10 times more likely to be cognitively impaired at death, compared with TDP-43–negative individuals. (Some patients had normal cognition at death.) Resilient cognition seemed to be almost nonexistent in the presence of TDP-43, Dr. Whitwell said. Also, the protein seemed to have a greater effect in Braak stage IV and V than with stage VI.

In a longitudinal analysis of the same 342 subjects, the team analyzed the data for 133 individuals who had two MRIs before death, separated by a mean interval of 3.4 years. There was a mean of 3.7 years between the repeat scan at the time of death. They looked for presence of TDP-43 and tau neurofibrillary tangle burden in the hippocampus and the lateral temporal cortex, an area affected in Alzheimer’s disease. They then measured the rates of hippocampal and cortical atrophy and tried to decide if the shrinkage was driven by TDP-43, tau, or both.

The average age of death was 82 years, and the population was split almost evenly by sex.

The results showed that the presence of TDP-43 was significantly associated with volume loss at the hippocampus, while tau showed no such association.

In the cortex, both TDP-43 and tau were associated with the rate of volume change, although tau showed a stronger association (P less than .0001 for tau vs. P = .01 for TDP-43). Also, the rate of cortical atrophy was strongly associated with age of death, while the rate of hippocampus shrinkage wasn’t. The investigators adjusted their models for other features found in the brains patients with Alzheimer’s disease, such as the presence of amyloid-beta plaques and Lewy bodies, Dr. Whitwell said.

The findings "would suggest that [TDP-43] might be a new target," said Ralph Nixon, Ph.D., chair of the Alzheimer’s Association Medical and Scientific Advisory Council, in a comment on the association’s website. "This might be one of the missing factors that we’ve been looking for, for quite some time, any it maybe a hopeful prospect for a new biomarker."

The study was funded by the National Institute on Aging. Dr. Whitwell and Dr. Nixon had no financial disclosures.

[email protected]

On Twitter @naseemmiller

COPENHAGEN – Losing a spouse has been associated with the broken heart syndrome and other adverse health outcomes, but the loss seems to have a paradoxical effect on the development of dementia.

An analysis of a large national database showed that individuals who had a mild cognitive impairment (MCI) and lost a spouse developed dementia significantly later than did those who hadn’t lose a spouse.

"Initially, we said this can’t be right," Dr. Bryan K. Woodruff of the Mayo Clinic in Scottsdale, Ariz., said in an interview at the annual meeting of the Alzheimer’s Association International Conference.

"But what we think is happening is when somebody loses their spouse and they’ve got MCI, that individual isn’t going to continue to live independently, so we think extended family is coming in and recognizing that this person needs more help now that the spouse is gone, getting them into assisted living or other arrangements. And the married couple continues to plug along without getting extended support," said Dr. Woodruff.

The finding hints at the need for mobilizing more support for married couples, too, Dr. Woodruff said. "This needs to start at the MCI stage, to increase support for the MCI person and also the spouse."

Dr. Woodruff and his colleagues selected 3,783 married individuals with MCI using the National Alzheimer’s Coordinating Center (NACC) database from September 2005 to September 2013. The subjects were enrolled in a National Institute of Aging-Alzheimer’s Disease Center, and stayed in the study for up to 7.5 years. Those who were divorced or separated were excluded, and so were those without follow-up.

Of the remaining 2,457 individuals, 134 were widowed and the rest stayed married. A total of 1,078 developed dementia.

At first visit, the widowed individuals were significantly more often older, female, a carrier of the apolipoprotein E epsilon-4 (APOE epsilon-4) allele, and less educated.

Results showed that the median age of dementia onset in the widowed group was 92 years, compared with 83 years in the married group (hazard ratio, 0.36; 95% confidence interval, 0.26-0.48; P less than .001). Adjustment for sex, presence of an APOE epsilon-4 allele, and age did not substantially affect the hazard ratio calculated for the risk of dementia after losing a spouse, the authors wrote.

Aside from the possible effect of additional support after loss of a spouse, the authors also wondered if the findings could be the result of selection bias "if the excluded widowed subject with MCI developed dementia at a younger age."

Dr. Woodruff and his associates ran another analysis on the same database, focusing on individuals who had normal cognitive function. This time, both groups, married or widowed, developed dementia around the same age, showing that "loss of spouse does not predict earlier development of dementia," among those with normal cognition, the authors wrote in their poster.

In the second analysis, there were 6,088 individuals who were married and cognitively normal at entry. Those who were divorced or separated were excluded, and so were those with no follow-up.

Of the remaining 4,446 subjects, 398 were widowed, and the rest remained married. Overall, 218 individuals developed dementia.

Both groups developed dementia at 96 years of age. Adjustments for sex, age, and presence of APOE epsilon-4 allele did not increase the hazard ratio for loss of a spouse, according to the authors.

"The absence of a "widowhood effect" may reflect increased resilience in individuals who elect to participate in such research studies, or could be result of selection bias if excluded subjects developed dementia at a younger age," the authors wrote. "Alternatively, the impact of widowhood may lessen with age, noting the advanced age of this sample," they added.

A recent study also found that loss of a spouse didn’t increase the risk of dementia, "yet women demonstrate a seemingly temporary decline in executive function following the death of a partner" (Am. J. Epidemiol. 2014;179:674-83)

Dr. Woodruff and his colleagues are planning to conduct the studies in community settings to find out if the results can be replicated.

Dr. Woodruff had no financial disclosures.

[email protected]

On Twitter @naseemmiller

COPENHAGEN – Losing a spouse has been associated with the broken heart syndrome and other adverse health outcomes, but the loss seems to have a paradoxical effect on the development of dementia.

An analysis of a large national database showed that individuals who had a mild cognitive impairment (MCI) and lost a spouse developed dementia significantly later than did those who hadn’t lose a spouse.

"Initially, we said this can’t be right," Dr. Bryan K. Woodruff of the Mayo Clinic in Scottsdale, Ariz., said in an interview at the annual meeting of the Alzheimer’s Association International Conference.

"But what we think is happening is when somebody loses their spouse and they’ve got MCI, that individual isn’t going to continue to live independently, so we think extended family is coming in and recognizing that this person needs more help now that the spouse is gone, getting them into assisted living or other arrangements. And the married couple continues to plug along without getting extended support," said Dr. Woodruff.

The finding hints at the need for mobilizing more support for married couples, too, Dr. Woodruff said. "This needs to start at the MCI stage, to increase support for the MCI person and also the spouse."

Dr. Woodruff and his colleagues selected 3,783 married individuals with MCI using the National Alzheimer’s Coordinating Center (NACC) database from September 2005 to September 2013. The subjects were enrolled in a National Institute of Aging-Alzheimer’s Disease Center, and stayed in the study for up to 7.5 years. Those who were divorced or separated were excluded, and so were those without follow-up.

Of the remaining 2,457 individuals, 134 were widowed and the rest stayed married. A total of 1,078 developed dementia.

At first visit, the widowed individuals were significantly more often older, female, a carrier of the apolipoprotein E epsilon-4 (APOE epsilon-4) allele, and less educated.

Results showed that the median age of dementia onset in the widowed group was 92 years, compared with 83 years in the married group (hazard ratio, 0.36; 95% confidence interval, 0.26-0.48; P less than .001). Adjustment for sex, presence of an APOE epsilon-4 allele, and age did not substantially affect the hazard ratio calculated for the risk of dementia after losing a spouse, the authors wrote.

Aside from the possible effect of additional support after loss of a spouse, the authors also wondered if the findings could be the result of selection bias "if the excluded widowed subject with MCI developed dementia at a younger age."

Dr. Woodruff and his associates ran another analysis on the same database, focusing on individuals who had normal cognitive function. This time, both groups, married or widowed, developed dementia around the same age, showing that "loss of spouse does not predict earlier development of dementia," among those with normal cognition, the authors wrote in their poster.

In the second analysis, there were 6,088 individuals who were married and cognitively normal at entry. Those who were divorced or separated were excluded, and so were those with no follow-up.

Of the remaining 4,446 subjects, 398 were widowed, and the rest remained married. Overall, 218 individuals developed dementia.

Both groups developed dementia at 96 years of age. Adjustments for sex, age, and presence of APOE epsilon-4 allele did not increase the hazard ratio for loss of a spouse, according to the authors.

"The absence of a "widowhood effect" may reflect increased resilience in individuals who elect to participate in such research studies, or could be result of selection bias if excluded subjects developed dementia at a younger age," the authors wrote. "Alternatively, the impact of widowhood may lessen with age, noting the advanced age of this sample," they added.

A recent study also found that loss of a spouse didn’t increase the risk of dementia, "yet women demonstrate a seemingly temporary decline in executive function following the death of a partner" (Am. J. Epidemiol. 2014;179:674-83)

Dr. Woodruff and his colleagues are planning to conduct the studies in community settings to find out if the results can be replicated.

Dr. Woodruff had no financial disclosures.

[email protected]

On Twitter @naseemmiller

COPENHAGEN – Losing a spouse has been associated with the broken heart syndrome and other adverse health outcomes, but the loss seems to have a paradoxical effect on the development of dementia.

An analysis of a large national database showed that individuals who had a mild cognitive impairment (MCI) and lost a spouse developed dementia significantly later than did those who hadn’t lose a spouse.

"Initially, we said this can’t be right," Dr. Bryan K. Woodruff of the Mayo Clinic in Scottsdale, Ariz., said in an interview at the annual meeting of the Alzheimer’s Association International Conference.

"But what we think is happening is when somebody loses their spouse and they’ve got MCI, that individual isn’t going to continue to live independently, so we think extended family is coming in and recognizing that this person needs more help now that the spouse is gone, getting them into assisted living or other arrangements. And the married couple continues to plug along without getting extended support," said Dr. Woodruff.

The finding hints at the need for mobilizing more support for married couples, too, Dr. Woodruff said. "This needs to start at the MCI stage, to increase support for the MCI person and also the spouse."

Dr. Woodruff and his colleagues selected 3,783 married individuals with MCI using the National Alzheimer’s Coordinating Center (NACC) database from September 2005 to September 2013. The subjects were enrolled in a National Institute of Aging-Alzheimer’s Disease Center, and stayed in the study for up to 7.5 years. Those who were divorced or separated were excluded, and so were those without follow-up.

Of the remaining 2,457 individuals, 134 were widowed and the rest stayed married. A total of 1,078 developed dementia.

At first visit, the widowed individuals were significantly more often older, female, a carrier of the apolipoprotein E epsilon-4 (APOE epsilon-4) allele, and less educated.

Results showed that the median age of dementia onset in the widowed group was 92 years, compared with 83 years in the married group (hazard ratio, 0.36; 95% confidence interval, 0.26-0.48; P less than .001). Adjustment for sex, presence of an APOE epsilon-4 allele, and age did not substantially affect the hazard ratio calculated for the risk of dementia after losing a spouse, the authors wrote.

Aside from the possible effect of additional support after loss of a spouse, the authors also wondered if the findings could be the result of selection bias "if the excluded widowed subject with MCI developed dementia at a younger age."

Dr. Woodruff and his associates ran another analysis on the same database, focusing on individuals who had normal cognitive function. This time, both groups, married or widowed, developed dementia around the same age, showing that "loss of spouse does not predict earlier development of dementia," among those with normal cognition, the authors wrote in their poster.

In the second analysis, there were 6,088 individuals who were married and cognitively normal at entry. Those who were divorced or separated were excluded, and so were those with no follow-up.

Of the remaining 4,446 subjects, 398 were widowed, and the rest remained married. Overall, 218 individuals developed dementia.

Both groups developed dementia at 96 years of age. Adjustments for sex, age, and presence of APOE epsilon-4 allele did not increase the hazard ratio for loss of a spouse, according to the authors.

"The absence of a "widowhood effect" may reflect increased resilience in individuals who elect to participate in such research studies, or could be result of selection bias if excluded subjects developed dementia at a younger age," the authors wrote. "Alternatively, the impact of widowhood may lessen with age, noting the advanced age of this sample," they added.

A recent study also found that loss of a spouse didn’t increase the risk of dementia, "yet women demonstrate a seemingly temporary decline in executive function following the death of a partner" (Am. J. Epidemiol. 2014;179:674-83)

Dr. Woodruff and his colleagues are planning to conduct the studies in community settings to find out if the results can be replicated.

Dr. Woodruff had no financial disclosures.

[email protected]

On Twitter @naseemmiller

COPENHAGEN – When it comes to treatment of hypertension, perhaps not all age groups should be treated equally, according to findings from a study of very elderly patients.

The 90+ Study, which analyzed data from 625 dementia-free participants, showed that developing high blood pressure in the 80s and 90s was associated with a reduced risk of developing dementia, researchers reported at the Alzheimer’s Association’s International Conference.

They also found that as the participants’ blood pressure level increased, their risk of dementia decreased. Results remained the same after researchers adjusted for hypertension medication and history of stroke or heart disease.

The findings are important because people who are in their 80s and 90s are among the fastest growing segments of the U.S. population, said Maria M. Corrada, Sc.D., an epidemiologist at the University of California, Irvine.

In a video interview, Dr. Corrada explains the research findings and the implications for clinical practice.

[email protected]

On Twitter @naseemmiller

COPENHAGEN – When it comes to treatment of hypertension, perhaps not all age groups should be treated equally, according to findings from a study of very elderly patients.

The 90+ Study, which analyzed data from 625 dementia-free participants, showed that developing high blood pressure in the 80s and 90s was associated with a reduced risk of developing dementia, researchers reported at the Alzheimer’s Association’s International Conference.

They also found that as the participants’ blood pressure level increased, their risk of dementia decreased. Results remained the same after researchers adjusted for hypertension medication and history of stroke or heart disease.

The findings are important because people who are in their 80s and 90s are among the fastest growing segments of the U.S. population, said Maria M. Corrada, Sc.D., an epidemiologist at the University of California, Irvine.

In a video interview, Dr. Corrada explains the research findings and the implications for clinical practice.

[email protected]

On Twitter @naseemmiller

COPENHAGEN – When it comes to treatment of hypertension, perhaps not all age groups should be treated equally, according to findings from a study of very elderly patients.

The 90+ Study, which analyzed data from 625 dementia-free participants, showed that developing high blood pressure in the 80s and 90s was associated with a reduced risk of developing dementia, researchers reported at the Alzheimer’s Association’s International Conference.

They also found that as the participants’ blood pressure level increased, their risk of dementia decreased. Results remained the same after researchers adjusted for hypertension medication and history of stroke or heart disease.

The findings are important because people who are in their 80s and 90s are among the fastest growing segments of the U.S. population, said Maria M. Corrada, Sc.D., an epidemiologist at the University of California, Irvine.

In a video interview, Dr. Corrada explains the research findings and the implications for clinical practice.

[email protected]

On Twitter @naseemmiller

COPENHAGEN – When it comes to treatment of hypertension, perhaps not all age groups should be treated equally, according to findings from a study of very elderly patients.

The 90+ Study, which analyzed data from 625 dementia-free participants, showed that developing high blood pressure in the 80s and 90s was associated with a reduced risk of developing dementia, researchers reported at the Alzheimer’s Association’s International Conference.

They also found that as the participants’ blood pressure level increased, their risk of dementia decreased. Results remained the same after researchers adjusted for hypertension medication and history of stroke or heart disease.

The findings are important because people who are in their 80s and 90s are among the fastest growing segments of the U.S. population, said Maria M. Corrada, Sc.D., an epidemiologist at the University of California, Irvine.

In a video interview, Dr. Corrada explains the research findings and the implications for clinical practice.

[email protected]

On Twitter @naseemmiller

COPENHAGEN – When it comes to treatment of hypertension, perhaps not all age groups should be treated equally, according to findings from a study of very elderly patients.

The 90+ Study, which analyzed data from 625 dementia-free participants, showed that developing high blood pressure in the 80s and 90s was associated with a reduced risk of developing dementia, researchers reported at the Alzheimer’s Association’s International Conference.

They also found that as the participants’ blood pressure level increased, their risk of dementia decreased. Results remained the same after researchers adjusted for hypertension medication and history of stroke or heart disease.

The findings are important because people who are in their 80s and 90s are among the fastest growing segments of the U.S. population, said Maria M. Corrada, Sc.D., an epidemiologist at the University of California, Irvine.

In a video interview, Dr. Corrada explains the research findings and the implications for clinical practice.

[email protected]

On Twitter @naseemmiller

COPENHAGEN – When it comes to treatment of hypertension, perhaps not all age groups should be treated equally, according to findings from a study of very elderly patients.

The 90+ Study, which analyzed data from 625 dementia-free participants, showed that developing high blood pressure in the 80s and 90s was associated with a reduced risk of developing dementia, researchers reported at the Alzheimer’s Association’s International Conference.

They also found that as the participants’ blood pressure level increased, their risk of dementia decreased. Results remained the same after researchers adjusted for hypertension medication and history of stroke or heart disease.

The findings are important because people who are in their 80s and 90s are among the fastest growing segments of the U.S. population, said Maria M. Corrada, Sc.D., an epidemiologist at the University of California, Irvine.

In a video interview, Dr. Corrada explains the research findings and the implications for clinical practice.

[email protected]

On Twitter @naseemmiller

COPENHAGEN – When older adults who were at risk of Alzheimer’s disease adopted more healthful lifestyles, including diet and exercise, their cognitive performance improved, according to findings from a 2-year randomized, controlled trial.

The study is yet more proof that "it’s never too late to adopt a healthful lifestyle," said Dr. Ralph A. Nixon, chair of the Alzheimer’s Association Medical and Scientific Advisory Council.

The multimodal intervention study, called the Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER), added nutritional guidance, physical exercise, cognitive training, and vascular risk factor management to the treatment of half of 1,260 participants who were between ages 60 and 77 years. The other half of participants received regular health advice.

To their surprise, researchers achieved their primary outcome – improvement in cognitive performance – within 2 years. In fact, the benefit was significant in all cognitive domains, including memory, executive function, and psychomotor speed, compared with the control group.

Only 11% of the participants dropped out. There were no serious adverse events.

This is the first long-term study to assess the impact of simultaneous improvement of several lifestyle factors on elderly cognition, the investigators said. The researchers are now conducting cost analysis, and they plan to follow the patients for 7 years to assess the longer-term effect of the interventions.

The findings demonstrate that multidomain intervention is feasible and can reduce the risk of cognitive impairment among the at-risk elderly population, said the study’s lead investigator, Dr. Miia Kivipelto. She hopes that this proof-of-concept study becomes a model for future programs in this group.

In a video interview, Dr. Kivipelto, a professor at the Karolinska Institute in Stockholm, discusses the study’s findings and its implications for clinical practice.

[email protected]

On Twitter @naseemmiller

COPENHAGEN – When older adults who were at risk of Alzheimer’s disease adopted more healthful lifestyles, including diet and exercise, their cognitive performance improved, according to findings from a 2-year randomized, controlled trial.

The study is yet more proof that "it’s never too late to adopt a healthful lifestyle," said Dr. Ralph A. Nixon, chair of the Alzheimer’s Association Medical and Scientific Advisory Council.

The multimodal intervention study, called the Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER), added nutritional guidance, physical exercise, cognitive training, and vascular risk factor management to the treatment of half of 1,260 participants who were between ages 60 and 77 years. The other half of participants received regular health advice.

To their surprise, researchers achieved their primary outcome – improvement in cognitive performance – within 2 years. In fact, the benefit was significant in all cognitive domains, including memory, executive function, and psychomotor speed, compared with the control group.

Only 11% of the participants dropped out. There were no serious adverse events.

This is the first long-term study to assess the impact of simultaneous improvement of several lifestyle factors on elderly cognition, the investigators said. The researchers are now conducting cost analysis, and they plan to follow the patients for 7 years to assess the longer-term effect of the interventions.

The findings demonstrate that multidomain intervention is feasible and can reduce the risk of cognitive impairment among the at-risk elderly population, said the study’s lead investigator, Dr. Miia Kivipelto. She hopes that this proof-of-concept study becomes a model for future programs in this group.

In a video interview, Dr. Kivipelto, a professor at the Karolinska Institute in Stockholm, discusses the study’s findings and its implications for clinical practice.

[email protected]

On Twitter @naseemmiller

COPENHAGEN – When older adults who were at risk of Alzheimer’s disease adopted more healthful lifestyles, including diet and exercise, their cognitive performance improved, according to findings from a 2-year randomized, controlled trial.

The study is yet more proof that "it’s never too late to adopt a healthful lifestyle," said Dr. Ralph A. Nixon, chair of the Alzheimer’s Association Medical and Scientific Advisory Council.

The multimodal intervention study, called the Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER), added nutritional guidance, physical exercise, cognitive training, and vascular risk factor management to the treatment of half of 1,260 participants who were between ages 60 and 77 years. The other half of participants received regular health advice.

To their surprise, researchers achieved their primary outcome – improvement in cognitive performance – within 2 years. In fact, the benefit was significant in all cognitive domains, including memory, executive function, and psychomotor speed, compared with the control group.

Only 11% of the participants dropped out. There were no serious adverse events.

This is the first long-term study to assess the impact of simultaneous improvement of several lifestyle factors on elderly cognition, the investigators said. The researchers are now conducting cost analysis, and they plan to follow the patients for 7 years to assess the longer-term effect of the interventions.

The findings demonstrate that multidomain intervention is feasible and can reduce the risk of cognitive impairment among the at-risk elderly population, said the study’s lead investigator, Dr. Miia Kivipelto. She hopes that this proof-of-concept study becomes a model for future programs in this group.

In a video interview, Dr. Kivipelto, a professor at the Karolinska Institute in Stockholm, discusses the study’s findings and its implications for clinical practice.

[email protected]

On Twitter @naseemmiller

COPENHAGEN – More than 1 in 10 community-dwelling dementia patients had firearms in their homes, and many of those patients suffered from delusions, hallucinations, or depression, a study of nearly 500 Midwestern patients revealed.

"This combination of a growing elderly population and guns presents some very concerning public health issues," said study investigator Jason Hsieh, a fourth-year medical student at Cleveland Clinic Lerner College of Medicine. "First and foremost, they have the highest suicide rate of any population segment, and a firearm in the home is the most common method of carrying out that act. Dementia patients are also victims of a high rate of homicide, most committed by family members or caregivers."

The inexorable personality changes that develop as disease progresses – aggression, hallucinations, and paranoid delusions – also make the combination of dementia and a loaded weapon an extraordinarily bad one, Mr. Hsieh said.

National statistics already identify gun ownership as fairly high among U.S. elders: As many as 27% own at least one. And those who do have a firearm at home are likely to have more than one – up to six, in fact, according to the National Rifle Association. But a not-insignificant proportion of those senior citizens also have diagnosed dementia disorders, and this combination should be ringing a very loud alarm bell for doctors, families, and communities, Mr. Hsieh said at the Alzheimer’s Association International Conference 2014.

Mr. Hsieh and his colleagues conducted a chart review of 495 patients who underwent initial evaluation for cognitive impairment at an outpatient memory clinic at the Cleveland Clinic. Of these, 89 (18%) lived in a home with a gun; 70% of that group (62) had a formal diagnosis of Alzheimer’s or another dementia disorder.

Associated mental disorders were common in the group with dementia. More than half (33) had delusions, 15 had hallucinations, and nearly all (57) had a diagnosed depression or endorsed depressive symptoms during their evaluation.

The delusions and hallucinations were likely to be paranoid (73% and 47%, respectively). Charts also included descriptions of aggressive behavior – some of which included firing weapons in the house and through open windows. Family members also reported some patients who repeatedly asked for their gun in order to commit suicide.

The unsettling combination is a difficult knot for U.S. doctors, Mr. Hsieh said.

"Doctors have no legal right here to remove weapons from the home," he said. "The only thing we can do is try to identify if one exists and encourage family members and carers to consider removing it or at least store it locked and unloaded in an inaccessible location."

Mr. Hsieh had no financial disclosures.

[email protected]

On Twitter @alz_gal

COPENHAGEN – More than 1 in 10 community-dwelling dementia patients had firearms in their homes, and many of those patients suffered from delusions, hallucinations, or depression, a study of nearly 500 Midwestern patients revealed.

"This combination of a growing elderly population and guns presents some very concerning public health issues," said study investigator Jason Hsieh, a fourth-year medical student at Cleveland Clinic Lerner College of Medicine. "First and foremost, they have the highest suicide rate of any population segment, and a firearm in the home is the most common method of carrying out that act. Dementia patients are also victims of a high rate of homicide, most committed by family members or caregivers."

The inexorable personality changes that develop as disease progresses – aggression, hallucinations, and paranoid delusions – also make the combination of dementia and a loaded weapon an extraordinarily bad one, Mr. Hsieh said.

National statistics already identify gun ownership as fairly high among U.S. elders: As many as 27% own at least one. And those who do have a firearm at home are likely to have more than one – up to six, in fact, according to the National Rifle Association. But a not-insignificant proportion of those senior citizens also have diagnosed dementia disorders, and this combination should be ringing a very loud alarm bell for doctors, families, and communities, Mr. Hsieh said at the Alzheimer’s Association International Conference 2014.

Mr. Hsieh and his colleagues conducted a chart review of 495 patients who underwent initial evaluation for cognitive impairment at an outpatient memory clinic at the Cleveland Clinic. Of these, 89 (18%) lived in a home with a gun; 70% of that group (62) had a formal diagnosis of Alzheimer’s or another dementia disorder.

Associated mental disorders were common in the group with dementia. More than half (33) had delusions, 15 had hallucinations, and nearly all (57) had a diagnosed depression or endorsed depressive symptoms during their evaluation.

The delusions and hallucinations were likely to be paranoid (73% and 47%, respectively). Charts also included descriptions of aggressive behavior – some of which included firing weapons in the house and through open windows. Family members also reported some patients who repeatedly asked for their gun in order to commit suicide.

The unsettling combination is a difficult knot for U.S. doctors, Mr. Hsieh said.

"Doctors have no legal right here to remove weapons from the home," he said. "The only thing we can do is try to identify if one exists and encourage family members and carers to consider removing it or at least store it locked and unloaded in an inaccessible location."

Mr. Hsieh had no financial disclosures.

[email protected]

On Twitter @alz_gal

COPENHAGEN – More than 1 in 10 community-dwelling dementia patients had firearms in their homes, and many of those patients suffered from delusions, hallucinations, or depression, a study of nearly 500 Midwestern patients revealed.

"This combination of a growing elderly population and guns presents some very concerning public health issues," said study investigator Jason Hsieh, a fourth-year medical student at Cleveland Clinic Lerner College of Medicine. "First and foremost, they have the highest suicide rate of any population segment, and a firearm in the home is the most common method of carrying out that act. Dementia patients are also victims of a high rate of homicide, most committed by family members or caregivers."

The inexorable personality changes that develop as disease progresses – aggression, hallucinations, and paranoid delusions – also make the combination of dementia and a loaded weapon an extraordinarily bad one, Mr. Hsieh said.

National statistics already identify gun ownership as fairly high among U.S. elders: As many as 27% own at least one. And those who do have a firearm at home are likely to have more than one – up to six, in fact, according to the National Rifle Association. But a not-insignificant proportion of those senior citizens also have diagnosed dementia disorders, and this combination should be ringing a very loud alarm bell for doctors, families, and communities, Mr. Hsieh said at the Alzheimer’s Association International Conference 2014.

Mr. Hsieh and his colleagues conducted a chart review of 495 patients who underwent initial evaluation for cognitive impairment at an outpatient memory clinic at the Cleveland Clinic. Of these, 89 (18%) lived in a home with a gun; 70% of that group (62) had a formal diagnosis of Alzheimer’s or another dementia disorder.

Associated mental disorders were common in the group with dementia. More than half (33) had delusions, 15 had hallucinations, and nearly all (57) had a diagnosed depression or endorsed depressive symptoms during their evaluation.

The delusions and hallucinations were likely to be paranoid (73% and 47%, respectively). Charts also included descriptions of aggressive behavior – some of which included firing weapons in the house and through open windows. Family members also reported some patients who repeatedly asked for their gun in order to commit suicide.

The unsettling combination is a difficult knot for U.S. doctors, Mr. Hsieh said.

"Doctors have no legal right here to remove weapons from the home," he said. "The only thing we can do is try to identify if one exists and encourage family members and carers to consider removing it or at least store it locked and unloaded in an inaccessible location."

Mr. Hsieh had no financial disclosures.

[email protected]

On Twitter @alz_gal

COPENHAGEN – A new study revealing the presence of firearms in the homes of more than 12% of community-dwelling dementia patients in the Midwest highlights a difficult situation for physicians treating such patients.

"Doctors have no legal right here to remove weapons from the home," noted study investigator Jason Hsieh, a fourth-year medical student at Cleveland Clinic Lerner College of Medicine. "The only thing we can do is try to identify if one exists, and encourage family members and caregivers to consider removing it or at least store it locked and unloaded in an inaccessible location."

In a video interview at the Alzheimer’s Association International Conference 2014, Mr. Hsieh discussed the study’s findings and the strategies physicians might use to keep their community-dwelling patients with dementia safe.

[email protected]

On Twitter @alz_gal

COPENHAGEN – A new study revealing the presence of firearms in the homes of more than 12% of community-dwelling dementia patients in the Midwest highlights a difficult situation for physicians treating such patients.

"Doctors have no legal right here to remove weapons from the home," noted study investigator Jason Hsieh, a fourth-year medical student at Cleveland Clinic Lerner College of Medicine. "The only thing we can do is try to identify if one exists, and encourage family members and caregivers to consider removing it or at least store it locked and unloaded in an inaccessible location."

In a video interview at the Alzheimer’s Association International Conference 2014, Mr. Hsieh discussed the study’s findings and the strategies physicians might use to keep their community-dwelling patients with dementia safe.

[email protected]

On Twitter @alz_gal

COPENHAGEN – A new study revealing the presence of firearms in the homes of more than 12% of community-dwelling dementia patients in the Midwest highlights a difficult situation for physicians treating such patients.

"Doctors have no legal right here to remove weapons from the home," noted study investigator Jason Hsieh, a fourth-year medical student at Cleveland Clinic Lerner College of Medicine. "The only thing we can do is try to identify if one exists, and encourage family members and caregivers to consider removing it or at least store it locked and unloaded in an inaccessible location."

In a video interview at the Alzheimer’s Association International Conference 2014, Mr. Hsieh discussed the study’s findings and the strategies physicians might use to keep their community-dwelling patients with dementia safe.

[email protected]

On Twitter @alz_gal

COPENHAGEN – Almost half of patients with mild cognitive impairment progressed to dementia within 1 year of undergoing either arthroplasty or coronary angiography, according to a small Australian study.

Baseline cognitive impairment appeared to be the main driver of progression, increasing the risk more than sevenfold – significantly more than age or heart attack, Lisbeth Evered, Ph.D., said at the annual Alzheimer’s Association International Conference.

"After 12 months, 42% met the criteria for dementia," said Dr. Evered, a researcher at the University of Melbourne. "The expected annual progression from mild cognitive impairment [MCI] to dementia would be about 10%-12% per year."

Her study included 67 patients with a mean age of 70 years. All had MCI at baseline, with a mean score of 23 on the Mini-Mental State Exam (MMSE). They underwent either arthroplasty (26 patients) or coronary angiography (41 patients).

A year after surgery, about 34% of the arthroplasty patients and 46% of the angiography patients had progressed to dementia. Baseline cognitive impairment was the only factor significantly associated with the change.

Postsurgical cognitive decline, both transient and long lasting, is a well-documented phenomenon, with studies going back to the late 1800s. Although the causative link isn’t entirely clear, anesthetics have long been implicated, said Dr. Evered. In animal models, some anesthesia drugs do seem to precipitate an Alzheimer’s-like amyloidosis and tau hyperphosphorylation.

More recent animal data suggest that inflammation might be a powerful influence.

"When a patient has surgery with a general anesthetic, they experience peripheral inflammation," Dr. Evered explained. "In a healthy normal brain, there’s plenty of cognitive reserve, and although there might be some cognitive decline afterward, the person won’t really notice and will certainly recover."

In a vulnerable brain, however, the inflammation may be amplified and may cause significant collateral damage that accelerates cognitive decline. "The problem is, we don’t know why they are vulnerable or what we might do about it," she noted.

The best approach now is to routinely assess cognition before surgery and monitor it afterward, Dr. Evered explained. "Then, the perioperative period is not something occurring in isolation," she noted. "We will be better able to identify those at risk and implement strategies to improve their outcomes."

In a video interview, Dr. Evered and Dr. Brendan Silbert of St. Vincent’s Hospital, Melbourne, discuss the study and its implications.

Dr. Evered had no financial disclosures

[email protected]

On Twitter @alz_gal

COPENHAGEN – Almost half of patients with mild cognitive impairment progressed to dementia within 1 year of undergoing either arthroplasty or coronary angiography, according to a small Australian study.

Baseline cognitive impairment appeared to be the main driver of progression, increasing the risk more than sevenfold – significantly more than age or heart attack, Lisbeth Evered, Ph.D., said at the annual Alzheimer’s Association International Conference.

"After 12 months, 42% met the criteria for dementia," said Dr. Evered, a researcher at the University of Melbourne. "The expected annual progression from mild cognitive impairment [MCI] to dementia would be about 10%-12% per year."

Her study included 67 patients with a mean age of 70 years. All had MCI at baseline, with a mean score of 23 on the Mini-Mental State Exam (MMSE). They underwent either arthroplasty (26 patients) or coronary angiography (41 patients).

A year after surgery, about 34% of the arthroplasty patients and 46% of the angiography patients had progressed to dementia. Baseline cognitive impairment was the only factor significantly associated with the change.

Postsurgical cognitive decline, both transient and long lasting, is a well-documented phenomenon, with studies going back to the late 1800s. Although the causative link isn’t entirely clear, anesthetics have long been implicated, said Dr. Evered. In animal models, some anesthesia drugs do seem to precipitate an Alzheimer’s-like amyloidosis and tau hyperphosphorylation.

More recent animal data suggest that inflammation might be a powerful influence.

"When a patient has surgery with a general anesthetic, they experience peripheral inflammation," Dr. Evered explained. "In a healthy normal brain, there’s plenty of cognitive reserve, and although there might be some cognitive decline afterward, the person won’t really notice and will certainly recover."

In a vulnerable brain, however, the inflammation may be amplified and may cause significant collateral damage that accelerates cognitive decline. "The problem is, we don’t know why they are vulnerable or what we might do about it," she noted.

The best approach now is to routinely assess cognition before surgery and monitor it afterward, Dr. Evered explained. "Then, the perioperative period is not something occurring in isolation," she noted. "We will be better able to identify those at risk and implement strategies to improve their outcomes."

In a video interview, Dr. Evered and Dr. Brendan Silbert of St. Vincent’s Hospital, Melbourne, discuss the study and its implications.

Dr. Evered had no financial disclosures

[email protected]

On Twitter @alz_gal

COPENHAGEN – Almost half of patients with mild cognitive impairment progressed to dementia within 1 year of undergoing either arthroplasty or coronary angiography, according to a small Australian study.

Baseline cognitive impairment appeared to be the main driver of progression, increasing the risk more than sevenfold – significantly more than age or heart attack, Lisbeth Evered, Ph.D., said at the annual Alzheimer’s Association International Conference.

"After 12 months, 42% met the criteria for dementia," said Dr. Evered, a researcher at the University of Melbourne. "The expected annual progression from mild cognitive impairment [MCI] to dementia would be about 10%-12% per year."

Her study included 67 patients with a mean age of 70 years. All had MCI at baseline, with a mean score of 23 on the Mini-Mental State Exam (MMSE). They underwent either arthroplasty (26 patients) or coronary angiography (41 patients).

A year after surgery, about 34% of the arthroplasty patients and 46% of the angiography patients had progressed to dementia. Baseline cognitive impairment was the only factor significantly associated with the change.

Postsurgical cognitive decline, both transient and long lasting, is a well-documented phenomenon, with studies going back to the late 1800s. Although the causative link isn’t entirely clear, anesthetics have long been implicated, said Dr. Evered. In animal models, some anesthesia drugs do seem to precipitate an Alzheimer’s-like amyloidosis and tau hyperphosphorylation.

More recent animal data suggest that inflammation might be a powerful influence.

"When a patient has surgery with a general anesthetic, they experience peripheral inflammation," Dr. Evered explained. "In a healthy normal brain, there’s plenty of cognitive reserve, and although there might be some cognitive decline afterward, the person won’t really notice and will certainly recover."

In a vulnerable brain, however, the inflammation may be amplified and may cause significant collateral damage that accelerates cognitive decline. "The problem is, we don’t know why they are vulnerable or what we might do about it," she noted.

The best approach now is to routinely assess cognition before surgery and monitor it afterward, Dr. Evered explained. "Then, the perioperative period is not something occurring in isolation," she noted. "We will be better able to identify those at risk and implement strategies to improve their outcomes."

In a video interview, Dr. Evered and Dr. Brendan Silbert of St. Vincent’s Hospital, Melbourne, discuss the study and its implications.

Dr. Evered had no financial disclosures

[email protected]

On Twitter @alz_gal