title: Alcohol-related neurodegeneration and recovery: mechanisms from animal models.
abstract: Human studies have found alcoholics to have a smaller brain size than moderate drinkers; however, these studies are complicated by many uncontrollable factors, including timing and amount of alcohol use. Animal experiments, which can control many factors, have established that alcohol can cause damage to brain cells (i.e., neurons), which results in their loss of structure or function (i.e., neurodegeneration) in multiple brain regions, similar to the damage found in human alcoholics. In addition, animal studies indicate that inhibition of the creation of neurons (i.e., neurogenesis) and other brain-cell genesis contributes to alcoholic neurodegeneration. Animal studies also suggest that neurodegeneration changes cognition, contributing to alcohol use disorders. Risk factors such as adolescent age and genetic predisposition toward alcohol consumption worsen neurodegeneration. Mild impairment of executive functions similar to that found in humans occurs in animals following binge alcohol treatment. Thus, animal studies suggest that heavy alcohol use contributes to neurodegeneration and the progressive loss of control over drinking. Despite the negative consequences of heavy drinking, there is hope of recovery with abstinence, which in animal models can result in neural stem-cell proliferation and the formation of new neurons and other brain cells, indicative of brain growth.
authors.affiliation: Bowles Center for Alcohol Studies, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
authors.forename: Fulton T
authors.initials: FT
authors.lastname: Crews
mesh_terms: D000428:Alcohol Drinking / Q000009:adverse effects* / Q000473:pathology*; D000437:Alcoholism / Q000209:etiology / Q000473:pathology*; D000818:Animals; D063425:Binge Drinking / Q000150:complications / Q000473:pathology; D001921:Brain / Q000187:drug effects / Q000473:pathology; D006801:Humans; D023421:Models, Animal; D019636:Neurodegenerative Diseases / Q000209:etiology / Q000473:pathology*; D009474:Neurons / Q000473:pathology; D020127:Recovery of Function / Q000502:physiology*