Commentary: Is Alzheimer's disease uniquely human?

Caleb E. Finch, Steven N. Austad

Research output: Contribution to journalArticle

30 Scopus citations

Abstract

That Alzheimer's disease (AD) might be a human-specific disease was hypothesized by Rapoport in 1989. Apes and humans share an identical amyloid beta (Aβ) peptide amino acid sequence and accumulate considerable Aβ deposits after age 40years, an age when amyloid plaques are uncommon in humans. Despite their early Aβ buildup, ape brains have not shown evidence dystrophic neurites near plaques. Aging great ape brains also have few neurofibrillary tangles, with one exception of 1 obese chimpanzee euthanized after a stroke who displayed abundant neurofibrillary tangles, but without the typical AD distribution. We discuss the need for more exacting evaluation of neuron density with age, and note husbandry issues that may allow great apes to live to greater ages. We remain reserved about expectations for fully developed AD-like pathology in the great apes of advanced ages and cautiously support Rapoport's hypothesis.

Original languageEnglish (US)
Pages (from-to)553-555
Number of pages3
JournalNeurobiology of Aging
Volume36
Issue number2
DOIs
StatePublished - Feb 1 2015

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Keywords

  • Aging
  • Alzheimer's disease
  • Chimpanzee
  • Gorilla
  • Life span
  • Obesity

ASJC Scopus subject areas

  • Neuroscience(all)
  • Aging
  • Clinical Neurology
  • Developmental Biology
  • Geriatrics and Gerontology

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