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Alcohol-Related Neurodegeneration and Recovery: Mechanisms From Animal Models
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 dama...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
National Institute on Alcohol Abuse and Alcoholism
2008
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3860462/ https://www.ncbi.nlm.nih.gov/pubmed/23584011 |
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author | Crews, Fulton T. |
author_facet | Crews, Fulton T. |
author_sort | Crews, Fulton T. |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-3860462 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2008 |
publisher | National Institute on Alcohol Abuse and Alcoholism |
record_format | MEDLINE/PubMed |
spelling | pubmed-38604622014-01-13 Alcohol-Related Neurodegeneration and Recovery: Mechanisms From Animal Models Crews, Fulton T. Alcohol Res Health Articles 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. National Institute on Alcohol Abuse and Alcoholism 2008 /pmc/articles/PMC3860462/ /pubmed/23584011 Text en http://creativecommons.org/publicdomain/mark/1.0/ Unless otherwise noted in the text, all material appearing in this journal is in the public domain and may be reproduced without permission. Citation of the source is appreciated. |
spellingShingle | Articles Crews, Fulton T. Alcohol-Related Neurodegeneration and Recovery: Mechanisms From Animal Models |
title | Alcohol-Related Neurodegeneration and Recovery: Mechanisms From Animal Models |
title_full | Alcohol-Related Neurodegeneration and Recovery: Mechanisms From Animal Models |
title_fullStr | Alcohol-Related Neurodegeneration and Recovery: Mechanisms From Animal Models |
title_full_unstemmed | Alcohol-Related Neurodegeneration and Recovery: Mechanisms From Animal Models |
title_short | Alcohol-Related Neurodegeneration and Recovery: Mechanisms From Animal Models |
title_sort | alcohol-related neurodegeneration and recovery: mechanisms from animal models |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3860462/ https://www.ncbi.nlm.nih.gov/pubmed/23584011 |
work_keys_str_mv | AT crewsfultont alcoholrelatedneurodegenerationandrecoverymechanismsfromanimalmodels |