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

Author:

Corder Elizabeth H.1,Ervin John F.2,Lockhart Evelyn3,Szymanski Mari H.2,Schmechel Donald E.34,Hulette Christine M.235

Affiliation:

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

2. Division of Neurology, Duke University Medical Center, Durham, NC 27710, USA

3. Division of Pathology, Duke University Medical Center, Durham, NC 27710, USA

4. Division of Neurobiology, Duke University Medical Center, Durham, NC 27710, USA

5. Soybean Genomics and Improvement Laboratory, USDA-ARS, Beltsville, MD 20705, USA

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 elevatedAPOEε4frequency. 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 theAPOEε4. 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 theAPOEalleleε4contributes directly to heart valve and myocardial damage.

Funder

National Institute on Aging

Publisher

Hindawi Limited

Subject

Health, Toxicology and Mutagenesis,Genetics,Molecular Biology,Molecular Medicine,General Medicine,Biotechnology

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