Innate immunity and the etiology of late-onset Alzheimer's disease

Neurodegener Dis. 2012;10(1-4):271-3. doi: 10.1159/000334287. Epub 2012 Jan 17.

Abstract

Background: Neuropathological studies supported by experimental animal studies show that the constituents of the innate immunity are intimately involved in the early steps of the pathological cascade of Alzheimer's disease (AD).

Objectives: To show the evidence that constituents of the innate immunity contribute to the etiology of late-onset AD.

Methods: Evaluation of the relationship between the constituents of the innate immunity and genetic risk factors for late-onset AD.

Results: Complement activation and activated microglia are early neuropathogical events in AD brains. Genome-wide association studies have demonstrated gene loci that are linked to the complement system. The production capacity for inflammatory cytokines is under genetic control and the offspring with a parental history of late-onset AD have a higher production capacity for inflammatory cytokines.

Conclusion: Epidemiological and genetic data suggest that the innate immunity is involved in the etiology of late-onset AD.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Alzheimer Disease / etiology*
  • Alzheimer Disease / immunology*
  • Cytokines / metabolism
  • Humans
  • Immunity, Innate*

Substances

  • Cytokines