Synaptic loss in alcohol use disorder: clinical and mechanistic insights from a PET imaging study.
editorial · Level V
Where this comes from
- Record sourced from PubMed, PMID 41919494.
- Also identified by DOI 10.1172/JCI204460 and PMC identifier 13038198.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
Alcohol use disorder (AUD) is linked with changes in brain structure and function, with robust evidence for neurodegenerative changes, including synaptic loss in preclinical models. Developing therapeutic strategies to target synaptic loss will require human studies that clarify their clinical relevance of these changes. In the current issue, Zakiniaeiz et al. demonstrate that AUD and alcohol consumption are associated with lower synaptic vesicle glycoprotein 2a (SV2A) expression, indexed by regional [11C]UCB-J PET. This is, to our knowledge, the first in vivo evidence of relationships between synaptic density and alcohol use, and, as such, it represents an important step toward understanding how AUD influences brain structure and function. Here, we describe two longstanding clinical issues in the AUD population - relapse and dementia risk - and how the results of the present study may guide future investigations of these issues.
Medical subject headings
- Positron-Emission Tomography
- Alcoholism
- Synapses
- Brain