Role of glial cells in neurotoxicological effects of alcohol

Abstract

Alcohol (ethanol), presumably consumed as wine as far back as 7000 BC, is most likely the first addictive substance known to man. In modern days, its abuse leading to neurotoxicity and a myriad of organ damages, is of considerable social and medical concern. In the United States alone, approximately 180,000 people die yearly because of alcohol-related accidents and diseases. Given its ubiquitous nature, alcohol may interact with many cellular components. In this chapter, we specifically concentrate on its neurotoxic mechanisms involving glial cells and their role in neuroinflammation. Moreover, exploitation of this knowledge for potential novel interventions in alcohol-induced neurotoxicity are touched upon.

Fig. 1

Schematic diagram depicting the consequences of heavy alcohol use either as binge or chronic on motor, nonmotor and cognitive functions. The neurotoxic effects are underscored by inflammation and are influenced by sex and age at every stage. WKS = Wernicke-Korsakoff Syndrome.

Fig. 2

Schematic diagram depicting the role of various glial cells on alcohol-induced neurotoxicity. Specific effects of alcohol on each glial cell type are highlighted. Not shown are the extensive interactions between the glial cells. AUD = alcohol use disorder, BBB = blood-brain barrier, EAE = experimental autoimmune encephalomyelitis, WKS = Wernicke-Korsakoff Syndrome.