Cellular aging in depression: Permanent imprint or reversible process?: An overview of the current evidence, mechanistic pathways, and targets for interventions

Bioessays. 2014 Oct;36(10):968-78. doi: 10.1002/bies.201400068. Epub 2014 Aug 20.

Abstract

Depression might be associated with accelerated cellular aging. However, does this result in an irreversible state or is the body able to slow down or recover from such a process? Telomeres are DNA-protein complexes that protect the ends of chromosomes and generally shorten with age; and therefore index cellular aging. The majority of studies indicate that persons with depression have shorter leukocyte telomeres than similarly aged non-depressed persons, which may contribute to the observed unfavorable somatic health outcomes in the depressed population. Some small-scale preliminary studies raise the possibility that behavioral or pharmacological interventions may either slow down or else reverse this accelerated telomere shortening, possibly through increasing the activity of the telomere-lengthening enzyme telomerase. This paper covers the current state of evidence in the relationship between depression and the telomere-telomerase system and debates whether depression-related cellular aging should be considered a reversible process or permanent damage.

Keywords: cellular aging; depression; intervention studies; major depressive disorder; telomerase; telomere homeostasis; telomere length.

Publication types

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

MeSH terms

  • Biomedical Research
  • Cellular Senescence*
  • Depression / genetics
  • Depression / pathology*
  • Depression / physiopathology
  • Depression / therapy*
  • Genomic Imprinting*
  • Humans
  • Telomere / genetics
  • Telomere Homeostasis / genetics