BioMed Research International

BioMed Research International / 2005 / Article
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Data Mining in Genomics and Proteomics

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Research article | Open Access

Volume 2005 |Article ID 709642 | https://doi.org/10.1155/JBB.2005.189

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", BioMed Research International, vol. 2005, Article ID 709642, 9 pages, 2005. https://doi.org/10.1155/JBB.2005.189

Cardiovascular Damage in Alzheimer Disease: Autopsy Findings From the Bryan ADRC

Received07 Jun 2004
Revised29 Nov 2004
Accepted07 Dec 2004

Abstract

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.

Copyright © 2005 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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