Exercise, APOE genotype, and the evolution of the human lifespan

Research output: Contribution to journalArticle

43 Citations (Scopus)

Abstract

Humans have exceptionally long lifespans compared with other mammals. However, our longevity evolved when our ancestors had two copies of the apolipoprotein E (APOE) e{open}4 allele, a genotype that leads to a high risk of Alzheimer's disease (AD), cardiovascular disease, and increased mortality. How did human aging evolve within this genetic constraint? Drawing from neuroscience, anthropology, and brain-imaging research, we propose the hypothesis that the evolution of increased physical activity approximately 2 million years ago served to reduce the amyloid plaque and vascular burden of APOE e{open}4, relaxing genetic constraints on aging. This multidisciplinary approach links human evolution with health and provides a complementary perspective on aging and neurodegenerative disease that may help identify key mechanisms and targets for intervention.

Original languageEnglish (US)
Pages (from-to)247-255
Number of pages9
JournalTrends in Neurosciences
Volume37
Issue number5
DOIs
StatePublished - 2014

Fingerprint

Apolipoproteins E
Genotype
Anthropology
Amyloid Plaques
Neurosciences
Neuroimaging
Neurodegenerative Diseases
Blood Vessels
Mammals
Alzheimer Disease
Cardiovascular Diseases
Alleles
Mortality
Health
Research

Keywords

  • Aerobic fitness
  • Aging
  • Alzheimer's disease
  • Apolipoprotein
  • Dementia
  • Vitamin D

ASJC Scopus subject areas

  • Neuroscience(all)
  • Medicine(all)

Cite this

Exercise, APOE genotype, and the evolution of the human lifespan. / Raichlen, David A; Alexander, Gene E.

In: Trends in Neurosciences, Vol. 37, No. 5, 2014, p. 247-255.

Research output: Contribution to journalArticle

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