ReviewPathophysiology : the official journal of the International Society for Pathophysiology2025
Thiamine Deficiency and Neuroinflammation Are Important Contributors to Alcohol Use Disorder.
Review in Pathophysiology : the official journal of the International Society for Pathophysiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- Observational
- CIRRHOSIS-ASSOCIATED SARCOPENIA: INTEGRATING IMAGING, FUNCTION, AND METABOLISM FOR CLINICAL DECISION-MAKING.Arquivos de gastroenterologia · 2026Review
- See One, B1, Treat One: Identifying and Managing Thiamine Deficiency in a Patient With Altered Mental Status.Cureus · 2026Article
- Ethanol-Induced Dysbiosis and Systemic Impact: A Meta-Analytical Synthesis of Human and Animal Research.Microorganisms · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite the growing morbidity associated with alcohol use disorder (AUD), current FDA-approved therapeutics fail to adequately address the condition. This is in part due to the complex systemic effects of ethanol (EtOH), which have particularly negative consequences on the gut-liver-brain axis. Importantly, two systemic mechanisms underlying the progression of AUD remain underemphasized in therapeutic development: thiamine deficiency and neuroinflammation. Alcohol-induced thiamine deficiency leads to reduced activity of key metabolic enzymes, thereby resulting in energy deficits, oxidative stress, and severe clinical implications. EtOH also activates TLR4 and NLRP3, both of which play critical roles in the regulation of neuroimmune responses. While research directly investigating the relationship between thiamine deficiency and neuroinflammation is still in its early stages, our review highlights the emerging connections between these two seemingly distinct pathomechanisms. Additionally, potential therapeutic approaches and targets for addressing AUD at a systemic level are discussed.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.