Human alcohol-related neuropathology
Open accessAbstract
Alcohol-related diseases of the nervous system are caused by excessive exposures to alcohol, with or without co-existing nutritional or vitamin deficiencies. Toxic and metabolic effects of alcohol (ethanol) vary with brain region, age/developmental stage, dose, and duration of exposures. In the mature brain, heavy chronic or binge alcohol exposures can cause severe debilitating diseases of the central and peripheral nervous systems, and skeletal muscle. Most commonly, long-standing heavy alcohol abuse leads to disproportionate loss of cerebral white matter and impairments in executive function. The cerebellum (especially the vermis), cortical-limbic circuits, skeletal muscle, and peripheral nerves are also important targets of chronic alcohol-related metabolic injury and degeneration. Although all cell types within the nervous system are vulnerable to the toxic, metabolic, and degenerative effects of alcohol, astrocytes, oligodendrocytes, and synaptic terminals are major targets, accounting for the white matter atrophy, neural inflammation and toxicity, and impairments in synaptogenesis. Besides chronic degenerative neuropathology, alcoholics are predisposed to develop severe potentially life-threatening acute or subacute symmetrical hemorrhagic injury in the diencephalon and brainstem due to thiamine deficiency, which exerts toxic/metabolic effects on glia, myelin, and the microvasculature. Alcohol also has devastating neurotoxic and teratogenic effects on the developing brain in association with fetal alcohol spectrum disorder/fetal alcohol syndrome. Alcohol impairs function of neurons and glia, disrupting a broad array of functions including neuronal survival, cell migration, and glial cell (astrocytes and oligodendrocytes) differentiation. Further progress is needed to better understand the pathophysiology of this exposure-related constellation of nervous system diseases and better correlate the underlying pathology with in vivo imaging and biochemical lesions.
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Chronic drug use, especially chronic alcohol use, causes cortical atrophy.
“chronic drug use (specifically chronic alcohol use) leads to cortical atrophy [36]”
The brain generally lacks defensive or protective enzymes/proteins compared to peripheral tissues such as the liver and kidney.
“However, it generally lacks defensive or protective enzymes/proteins compared to peripheral tissues such as the liver and kidney102.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [102]
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- Authors
- de la Monte, S. M., & Kril, J. J.
- Affiliations
- The University of Sydney (AU)
- ORCID
- Kril, Jillian J.
- Venue
- Acta Neuropathologica
- Published
- 2013-12-27
- Volume
- 127
- Issue
- 1
- Pages
- 71-90
- ISSN
- 0001-6322 (ISSN-L)
- 1432-0533
- PMC
- PMC4532397
- OpenAlex
- W2121884198
- Cited by
- 416
- References
- 178
- Citations by year
- 2026: 16 · 2025: 37 · 2024: 39 · 2023: 43 · 2022: 47 · 2021: 44 · 2020: 37 · 2019: 37 · 2018: 28 · 2017: 27 · 2016: 23 · 2015: 22 · 2014: 15 · 2012: 1
- FWCI
- 2.61
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Acta Neuropathologica (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (5r01aa011431-26)
- National Institute on Alcohol Abuse and Alcoholism (R01-AA011431, AA12725, AA-12908, AA11431, R01AA012725, R24AA012725, R56AA011431, R01AA012908, R37AA011431, R28AA012725)
- Topics
- Health Sciences › Medicine › Neurology › Alcoholism and Thiamine Deficiency
- Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Prenatal Substance Exposure Effects
- Keywords
- ethanol neurotoxicity, chronic alcohol abuse, binge drinking, white matter atrophy, cerebellar vermis, peripheral neuropathy, skeletal muscle degeneration, thiamine deficiency, Wernicke's encephalopathy, fetal alcohol spectrum disorders, fetal alcohol syndrome, astrocytes, oligodendrocytes, synaptogenesis, neuroinflammation, myelin, brainstem hemorrhage, executive dysfunction
- MeSH terms
- Ethanol, Alcoholism, Brain, Brain Diseases, Humans, Alcohol-Induced Disorders, Nervous System
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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