Role of microglia in regulation of ethanol neurotoxic action

Int Rev Neurobiol. 2014:118:81-103. doi: 10.1016/B978-0-12-801284-0.00004-X.

Abstract

Exposure to alcohol, during development or adulthood, may result in damage to the nervous system, which underlies neurological and cognitive disruptions observed in patients with alcohol-related disorders, including fetal alcohol spectrum disorders (FASDs) and alcohol-use disorders (AUDs). Both clinical and preclinical evidence suggest microglia, the immune cells of the central nervous system, play a key role in modulating alcohol-induced neurotoxicity. Particularly, microglia are implicated in alcohol-induced neuroinflammation and in alcohol-induced increases in oxidative stress, which can lead to neuronal apoptosis. Recent studies also suggest a regenerative role for microglia in reestablishing homeostasis after alcohol exposure. These studies are summarized and reviewed in this chapter with emphasis on relevance to FASD and AUD.

Keywords: Alcohol; Alcohol-use disorder; Apoptosis; Fetal alcohol spectrum disorder; Inflammation; Microglia; Neurotoxicity; Reactive oxygen species.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Alcohol-Related Disorders* / complications
  • Alcohol-Related Disorders* / etiology
  • Alcohol-Related Disorders* / pathology
  • Animals
  • Apoptosis / drug effects
  • Central Nervous System / pathology*
  • Encephalitis / complications*
  • Ethanol / toxicity*
  • Humans
  • Microglia / metabolism
  • Microglia / pathology*
  • Neurons / pathology
  • Oxidative Stress / drug effects
  • Reactive Oxygen Species / metabolism

Substances

  • Reactive Oxygen Species
  • Ethanol