Ethanol is a licit drug consumed by a large part of the population, from adolescence to adulthood. High ethanol consumption is a public health problem due to its addictiveness and the risk it produces of developing other diseases, including cardiovascular, hepatic, and mental pathologies. Different patterns of ethanol consumption and its toxic effects in the brain have been reported. Current studies suggest to mitochondria, one of the principal mediators for ethanol neurotoxicity. In this chapter, we will review the effects of ethanol on neurons in different scenarios of ethanol consumption and its relation with mitochondrial function. Finally, we will propose a mechanism of ethanol toxicity in which the mitochondria are the main mediator and in which the mitochondrial alterations correlate with the severity of ethanol consumption. Thus, improving mitochondrial health of brain cells could be considered as a potential therapeutic target to treat ethanol-associated disorders.
Part of the book: Mitochondrial Diseases