Accelerated aging and aging process in the brain

Rev Neurosci. 2018 Mar 28;29(3):233-240. doi: 10.1515/revneuro-2017-0051.

Abstract

One of the approaches to the research of the problem of aging is the study of genetic pathologies leading to accelerated aging, such as the Hutchinson-Gilford progeria syndrome, Werner syndrome, and Down syndrome. Probably, this approach can be used in an attempt to understand the neuronal mechanisms underlying normal and pathological brain aging. The analysis of the current state of scientific knowledge about these pathologies shows that in the Hutchinson-Gilford progeria and Werner syndrome, the rate of brain aging is significantly lower than the rate of whole body aging, whereas in Down syndrome, the brain ages faster than other organs due to amyloid-beta accumulation and chronic oxidative stress in the brain tissue. The main point of a previously proposed hypothesis is that the aging of higher animals and humans is associated with an increased level of reactive oxygen species in mitochondria with age, which activates apoptosis, thus reducing the number of functioning cells.

Keywords: Alzheimer’s disease; Down syndrome; Hutchinson-Gilford progeria syndrome; Werner syndrome; mitochondria; reactive oxygen species.

Publication types

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

MeSH terms

  • Aging / pathology*
  • Aging / physiology
  • Animals
  • Apoptosis / physiology
  • Brain / pathology*
  • Brain / physiopathology*
  • Humans
  • Mitochondria / metabolism
  • Mitochondria / pathology
  • Progeria / genetics
  • Progeria / pathology
  • Reactive Oxygen Species / metabolism
  • Werner Syndrome / genetics
  • Werner Syndrome / pathology

Substances

  • Reactive Oxygen Species