Physical exercise as a possible strategy for brain protection: evidence from mitochondrial-mediated mechanisms

Prog Neurobiol. 2012 Nov;99(2):149-62. doi: 10.1016/j.pneurobio.2012.08.002. Epub 2012 Aug 23.

Abstract

Aging and neurodegenerative conditions such as Alzheimer and Parkinson diseases are characterized by tissue and mitochondrial changes that compromise brain function. Alterations can include increased reactive oxygen species production and impaired antioxidant capacity with a consequent increase in oxidative damage, mitochondrial dysfunction that compromises brain ATP production, and ultimately increased apoptotic signaling and neuronal death. Among several non-pharmacological strategies to prevent brain degeneration, physical exercise is a surprisingly effective strategy, which antagonizes brain tissue and mitochondrial dysfunction. The present review aims to discuss the role of physical exercise in the modulation of the mechanisms involved in neuroprotection including the activation of signaling pathways underlying brain protection.

Publication types

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

MeSH terms

  • Animals
  • Brain / metabolism
  • Brain / physiopathology*
  • Energy Metabolism / physiology
  • Humans
  • Mitochondria / physiology*
  • Neurodegenerative Diseases / physiopathology*
  • Neurodegenerative Diseases / prevention & control
  • Neurodegenerative Diseases / therapy*
  • Oxidative Stress / physiology
  • Physical Conditioning, Animal / physiology*
  • Signal Transduction / physiology