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Corder EH, Ervin JF, Lockhart E, et al. Cardiovascular damage in Alzheimer disease: autopsy findings from the Bryan ADRC. J Biomed Biotechnol. 2005;2005(2):189-97doi: 10.1155/JBB.2005.189.
Corder, E. H., Ervin, J. F., Lockhart, E., Szymanski, M. H., Schmechel, D. E., & Hulette, C. M. (2005). Cardiovascular damage in Alzheimer disease: autopsy findings from the Bryan ADRC. Journal of biomedicine & biotechnology, 2005(2), 189-97. https://doi.org/10.1155/JBB.2005.189
Corder, Elizabeth H, et al. "Cardiovascular damage in Alzheimer disease: autopsy findings from the Bryan ADRC." Journal of biomedicine & biotechnology vol. 2005,2 (2005): 189-97. doi: https://doi.org/10.1155/JBB.2005.189
Corder EH, Ervin JF, Lockhart E, Szymanski MH, Schmechel DE, Hulette CM. Cardiovascular damage in Alzheimer disease: autopsy findings from the Bryan ADRC. J Biomed Biotechnol. 2005 Jun 30;2005(2):189-97. doi: 10.1155/JBB.2005.189. PMID: 16046825; PMCID: PMC1184050.
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J Biomed Biotechnol. 2005 Jun 30;2005(2):189-97. doi: 10.1155/JBB.2005.189.

Cardiovascular damage in Alzheimer disease: autopsy findings from the Bryan ADRC.

Journal of biomedicine & biotechnology

Elizabeth H Corder, John F Ervin, Evelyn Lockhart, Mari H Szymanski, Donald E Schmechel, Christine M Hulette

Affiliations

  1. Center for Demographic Studies, Duke University, 2117 Campus Drive, Box 90408, Durham, NC 27708-0408, USA.

PMID: 16046825 PMCID: PMC1184050 DOI: 10.1155/JBB.2005.189

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 APOE epsilon 4 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 APOE epsilon 4. 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 epsilon 4 contributes directly to heart valve and myocardial damage.

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