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

Elizabeth H Corder1, John F Ervin, Evelyn Lockhart

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

Journal of Biomedicine & Biotechnology
|July 28, 2005
PubMed

Insights

Autopsy studies reveal limited links between atherosclerosis and Alzheimer disease (AD), despite both conditions sharing the APOE epsilon 4 gene. Myocardial and valve damage were more common in AD patients.

Area of Science:

  • Neuropathology
  • Cardiovascular Pathology
  • Genetics

Background:

  • Alzheimer disease (AD) is a neurodegenerative disorder with complex pathophysiology.
  • Cardiovascular health is increasingly recognized as a factor influencing brain health.
  • The role of vascular damage in AD pathogenesis requires further elucidation.

Purpose of the Study:

  • To investigate cardiovascular damage in pathologically confirmed Alzheimer disease (AD) patients.
  • To identify patterns of vascular damage associated with different AD subtypes and controls.
  • To explore the relationship between atherosclerosis, AD, and the APOE epsilon 4 allele.

Main Methods:

  • Autopsy data from 84 AD patients and 60 non-AD controls were analyzed.
  • A grade-of-membership model was applied to 51 items describing vascular damage.
  • Latent class analysis identified five distinct patient groups based on pathology.

Main Results:

  • Five latent groups emerged: early-onset AD, controls with cancer, controls with extensive atherosclerosis, late-onset AD (male), and late-onset AD (female).
  • Groups with late-onset AD showed elevated APOE epsilon 4 frequency.
  • Unexpectedly, limited atherosclerosis but frequent myocardial, valve, and ventricular damage were observed in AD patients.

Conclusions:

  • A strong direct relationship between atherosclerosis and AD was not supported, though both are linked to APOE epsilon 4.
  • Extensive atherosclerosis was associated with possible AD and premature death, not definite AD.
  • Findings suggest brain hypoperfusion may contribute to AD pathogenesis, and APOE epsilon 4 might directly impact heart tissue.

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