Stress and Alzheimer's disease: A senescence link?

Neurosci Biobehav Rev. 2020 Aug;115:285-298. doi: 10.1016/j.neubiorev.2020.05.010. Epub 2020 May 24.

Abstract

Chronic stress has been shown to promote numerous aging-related diseases, and to accelerate the aging process itself. Of particular interest is the impact of stress on Alzheimer's disease (AD), the most prevalent form of dementia. The vast majority of AD cases have no known genetic cause, making it vital to identify the environmental factors involved in the onset and progression of the disease. Age is the greatest risk factor for AD, and measures of biological aging such as shorter telomere length, significantly increase likelihood for developing AD. Stress is also considered a crucial contributor to AD, as indicated by a formidable body of research, although the mechanisms underlying this association remain unclear. Here we review human and animal literature on the impact of stress on AD and discuss the mechanisms implicated in the interaction. In particular we will focus on the burgeoning body of research demonstrating that senescent cells, which accumulate with age and actively drive a number of aging-related diseases, may be a key mechanism through which stress drives AD.

Keywords: APP; Amyloid β; Corticosterone; Corticotropin releasing hormone; Cortisol; Neurodegeneration; Neuroinflammation; Tau; Telomere.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Aging
  • Alzheimer Disease* / genetics
  • Animals
  • Humans