Abstract

Adolescence is a critical neurodevelopmental window for maturation of brain structure, neurocircuitry, and glia. This development is sculpted by an individual's unique experiences and genetic background to establish adult level cognitive function and behavioral makeup. Alcohol abuse during adolescence is associated with an increased lifetime risk for developing an alcohol use disorder (AUD). Adolescents participate in heavy, episodic binge drinking that causes persistent changes in neurocircuitry and behavior. These changes may underlie the increased risk for AUD and might also promote cognitive deficits later in life. In this chapter, we have examined research on the persistent effects of adolescent binge-drinking both in humans and in rodent models. These studies implicate roles for neuroimmune signaling as well as epigenetic reprogramming of neurons and glia, which create a vulnerable neuroenvironment. Some of these changes are reversible, giving hope for future treatments to prevent many of the long-term consequences of adolescent alcohol abuse.

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