Alcoholic neurobiology: changes in dependence and recovery
Abstract
This article presents the proceedings of a symposium held at the meeting of the International Society for Biomedical Research on Alcoholism (ISBRA) in Mannheim, Germany, in October, 2004. Chronic alcoholism follows a fluctuating course, which provides a naturalistic experiment in vulnerability, resilience, and recovery of human neural systems in response to presence, absence, and history of the neurotoxic effects of alcoholism. Alcohol dependence is a progressive chronic disease that is associated with changes in neuroanatomy, neurophysiology, neural gene expression, psychology, and behavior. Specifically, alcohol dependence is characterized by a neuropsychological profile of mild to moderate impairment in executive functions, visuospatial abilities, and postural stability, together with relative sparing of declarative memory, language skills, and primary motor and perceptual abilities. Recovery from alcoholism is associated with a partial reversal of CNS deficits that occur in alcoholism. The reversal of deficits during recovery from alcoholism indicates that brain structure is capable of repair and restructuring in response to insult in adulthood. Indirect support of this repair model derives from studies of selective neuropsychological processes, structural and functional neuroimaging studies, and preclinical studies on degeneration and regeneration during the development of alcohol dependence and recovery form dependence. Genetics and brain regional specificity contribute to unique changes in neuropsychology and neuroanatomy in alcoholism and recovery. This symposium includes state-of-the-art presentations on changes that occur during active alcoholism as well as those that may occur during recovery-abstinence from alcohol dependence. Included are human neuroimaging and neuropsychological assessments, changes in human brain gene expression, allelic combinations of genes associated with alcohol dependence and preclinical studies investigating mechanisms of alcohol induced neurotoxicity, and neuroprogenetor cell expansion during recovery from alcohol dependence.
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Drug- and ethanol-induced frontal cortical degeneration and executive function loss contribute to an imbalance between reflective attention-controlled decision-making and a hyperactive limbic system driving impulsive behavior, promoting addiction persistence.
“Drug-and ethanol-induced frontal cortical degeneration and loss of executive function contribute to an imbalance between reflective, attention-controlled decision making, frontal cortical functions, and a hyperactive limbic system that drives impulsive behavior through involuntary signals (Bechara, 2005) (Fig. 1) driving both the progressive and persistent nature of addiction (Crews et al., 2005).”
From Impulsivity, frontal lobes and risk for addiction (2009) · cites this paper as Crews et al., 2005
Diffuse degeneration and loss of neurogenesis in the rat binge model mimic diffuse mild degeneration in human alcohol abusers.
“In general the diffuse degeneration and loss of neurogenesis found in the rat binge model mimics the diffuse mild degeneration reported in human alcohol abusers (Crews et al., 2005).”
From Impulsivity, frontal lobes and risk for addiction (2009) · cites this paper as Crews et al., 2005
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- Authors
- Crews, F. T., Buckley, T., Dodd, P. R., Ende, G., Foley, N., Harper, C., He, J., Innes, D., Loh, E.-W., Pfefferbaum, A., Zou, J., & Sullivan, E. V.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- Corresponding author
- Crews, Fulton T.
- ORCID
- Venue
- Alcoholism: Clinical & Experimental Research
- Publisher
- Wiley
- Published
- 2005-08
- Volume
- 29
- Issue
- 8
- Pages
- 1504-1513
- ISSN
- 0145-6008 (ISSN-L)
- OpenAlex
- W2072741198
- Cited by
- 154
- References
- 72
- Citations by year
- 2026: 1 · 2025: 2 · 2023: 4 · 2022: 5 · 2021: 5 · 2020: 26 · 2019: 10 · 2018: 3 · 2017: 6 · 2016: 9 · 2015: 7 · 2014: 6 · 2013: 11 · 2012: 5
- FWCI
- 6.93
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Alcoholism Clinical and Experimental Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Health and Medical Research Council
- National Medical Research Council
- National Institute on Alcohol Abuse and Alcoholism (AA 12404, AA-05965, AA011605, AA012725-04, R01AA012388, AA17203, AA12388, AA06069, R01AA012404)
- Topics
- Health Sciences › Medicine › Epidemiology › Substance Abuse Treatment and Outcomes
- Health Sciences › Medicine › Neurology › Alcoholism and Thiamine Deficiency
- Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
- Keywords
- alcoholism, chronic alcoholism, alcohol recovery, alcohol neurotoxicity, neuroplasticity, neural repair, neuropsychological deficits, executive function, visuospatial ability, postural stability, brain gene expression, genetic susceptibility, neuroimaging, neural progenitor cells
- MeSH terms
- Adult, Ethanol, Alcoholic Intoxication, Alcoholism, Brain Mapping, DNA Repair, Gene Expression Regulation, Humans, Magnetic Resonance Imaging, Memory, Short-Term, Motivation, Nerve Degeneration, Nerve Regeneration, Neurons, Neuropsychological Tests, Orientation, Receptors, GABA-A, Substance Withdrawal Syndrome
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