Cardiovascular Damage in Alzheimer Disease: Autopsy Findings From the Bryan ADRC
Autopsy information on cardiovascular damage was investigated for pathologically confirmed Alzheimer disease (AD) patients (n=84) and non-AD control patients (n=60). The 51 relevant items were entered into a grade-of-membership model to describe vascular damage in AD. Five latent groups were identif...
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doaj-0ba7613df7754a6f954c87d70acaa3332020-11-24T22:09:36ZengHindawi LimitedJournal of Biomedicine and Biotechnology1110-72431110-72512005-01-012005218919710.1155/JBB.2005.189Cardiovascular Damage in Alzheimer Disease: Autopsy Findings From the Bryan ADRCElizabeth H. Corder0John F. Ervin1Evelyn Lockhart2Mari H. Szymanski3Donald E. Schmechel4Christine M. Hulette5Center for Demographic Studies, Duke University, 2117 Campus Drive, Box 90408, Durham, NC 27708-0408, USADivision of Neurology, Duke University Medical Center, Durham, NC 27710, USADivision of Pathology, Duke University Medical Center, Durham, NC 27710, USADivision of Neurology, Duke University Medical Center, Durham, NC 27710, USADivision of Pathology, Duke University Medical Center, Durham, NC 27710, USADivision of Neurology, Duke University Medical Center, Durham, NC 27710, USAAutopsy information on cardiovascular damage was investigated for pathologically confirmed Alzheimer disease (AD) patients (n=84) and non-AD control patients (n=60). The 51 relevant items were entered into a grade-of-membership model to describe vascular damage in AD. Five latent groups were identified “I: early-onset AD,” “II: controls, cancer,” “III: controls, extensive atherosclerosis,” “IV: late-onset AD, male,” and “V: late-onset AD, female.” Expectedly, Groups IV and V had elevated APOEε4 frequency. Unexpectedly, there was limited atherosclerosis and frequent myocardial valve and ventricular damage. The findings do not indicate a strong relationship between atherosclerosis and AD, although both are associated with the APOEε4. Instead, autopsy findings of extensive atherosclerosis were associated with possible, not probable or definite AD, and premature death. They are consistent with the hypothesis that brain hypoperfusion contributes to dementia, possibly to AD pathogenesis, and raise the possibility that the APOE allele ε4 contributes directly to heart valve and myocardial damage.http://dx.doi.org/10.1155/JBB.2005.189 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Elizabeth H. Corder John F. Ervin Evelyn Lockhart Mari H. Szymanski Donald E. Schmechel Christine M. Hulette |
spellingShingle |
Elizabeth H. Corder John F. Ervin Evelyn Lockhart Mari H. Szymanski Donald E. Schmechel Christine M. Hulette Cardiovascular Damage in Alzheimer Disease: Autopsy Findings From the Bryan ADRC Journal of Biomedicine and Biotechnology |
author_facet |
Elizabeth H. Corder John F. Ervin Evelyn Lockhart Mari H. Szymanski Donald E. Schmechel Christine M. Hulette |
author_sort |
Elizabeth H. Corder |
title |
Cardiovascular Damage in Alzheimer Disease: Autopsy Findings From the Bryan ADRC |
title_short |
Cardiovascular Damage in Alzheimer Disease: Autopsy Findings From the Bryan ADRC |
title_full |
Cardiovascular Damage in Alzheimer Disease: Autopsy Findings From the Bryan ADRC |
title_fullStr |
Cardiovascular Damage in Alzheimer Disease: Autopsy Findings From the Bryan ADRC |
title_full_unstemmed |
Cardiovascular Damage in Alzheimer Disease: Autopsy Findings From the Bryan ADRC |
title_sort |
cardiovascular damage in alzheimer disease: autopsy findings from the bryan adrc |
publisher |
Hindawi Limited |
series |
Journal of Biomedicine and Biotechnology |
issn |
1110-7243 1110-7251 |
publishDate |
2005-01-01 |
description |
Autopsy information on cardiovascular damage was investigated for pathologically confirmed Alzheimer disease (AD) patients (n=84) and non-AD control patients (n=60). The 51 relevant items were entered into a grade-of-membership model to describe vascular damage in AD. Five latent groups were identified “I: early-onset AD,” “II: controls, cancer,” “III: controls, extensive atherosclerosis,” “IV: late-onset AD, male,” and “V:
late-onset AD, female.” Expectedly, Groups IV and V had elevated APOEε4 frequency. Unexpectedly, there was limited atherosclerosis and frequent myocardial valve and ventricular damage. The findings do not indicate a strong relationship between atherosclerosis and AD, although both are
associated with the APOEε4. Instead, autopsy findings of extensive atherosclerosis were associated with possible, not probable or definite AD, and premature death. They are consistent with the hypothesis that brain hypoperfusion contributes to dementia, possibly to AD pathogenesis, and raise the possibility that the APOE allele ε4 contributes directly to heart valve and myocardial damage. |
url |
http://dx.doi.org/10.1155/JBB.2005.189 |
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