Stress and Alzheimer's disease: A senescence link?

Carey E. Lyons, Alessandro Bartolomucci

Research output: Contribution to journalReview articlepeer-review

23 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)285-298
Number of pages14
JournalNeuroscience and Biobehavioral Reviews
StatePublished - Aug 2020

Bibliographical note

Funding Information:
Supported by Minnesota Partnership for Biotechnology and Medical Genomics #18.04 and National Institutes of Health (NIH) National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) R01DK117504 to A.B. C.L. received support from NIH/Ntional Institute of Aging (NIA) T32AG029796.

Publisher Copyright:
© 2020 Elsevier Ltd


  • APP
  • Amyloid β
  • Corticosterone
  • Corticotropin releasing hormone
  • Cortisol
  • Neurodegeneration
  • Neuroinflammation
  • Tau
  • Telomere

PubMed: MeSH publication types

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


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