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Published on: June 23, 2023
Beyond Neurons: Oligodendrocyte Dysfunction and Myelin Pathophysiology in Alcohol Use Disorder
Hazen Westover1, Esther Melamed2, Jennifer T Wolstenholme3
1Department of Molecular Pharmacology and Neuroscience, Loyola University Chicago, Maywood, IL, USA.
Physiology & Behavior
|August 13, 2026
Summary
Alcohol Use Disorder (AUD) disrupts brain white matter by damaging oligodendrocytes (OLs), crucial for myelin. This leads to cognitive and emotional deficits, highlighting OLs as key targets for AUD treatment.
Area of Science:
- Neuroscience
- Cell Biology
- Addiction Research
Background:
- Alcohol Use Disorder (AUD) is a major cause of neurological damage.
- Neuronal adaptations to alcohol are well-studied, but glial cell roles are emerging.
- Oligodendrocytes (OLs) and their progenitors (OPCs) are implicated in AUD pathology.
Purpose of the Study:
- To review the role of OLs and OPCs in alcohol-induced white matter (WM) alterations.
- To explore mechanisms underlying alcohol's impact on OLs and myelination.
- To highlight OLs as potential therapeutic targets for AUD.
Main Methods:
- Review of human neuroimaging and postmortem brain studies.
- Analysis of preclinical models investigating alcohol's effects on OLs.
- Examination of molecular pathways involved in alcohol-induced OL dysregulation.
Main Results:
- Human studies show reduced WM integrity and impaired myelin in AUD.
- Preclinical models demonstrate alcohol-induced OL dysregulation at multiple levels.
- Key mechanisms include oxidative stress, neuroinflammation, and lipid dysregulation.
- Prenatal and adolescent alcohol exposure cause lasting OL and myelination deficits.
Conclusions:
- Alcohol-induced OL dysregulation contributes significantly to AUD pathology and associated deficits.
- OLs and OPCs are critical for maintaining WM integrity and neural function.
- Targeting OLs offers potential for novel AUD diagnostics and therapeutics.
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