ArticleBrain, behavior, and immunity2026
Alcohol drinking sex-dependently regulates interleukin-1 pro-inflammatory signaling in the prefrontal cortex of mice and rhesus macaques.
Article in Brain, behavior, and immunity, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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1 citing paper in PubMed.
- The complex link of IL-1RAcP in engendering neuroprotection from alcohol-induced prefrontal cortical dysfunction in rhesus macaques and mice.Brain, behavior, and immunity · 2026Article
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21 authors.
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Abstract
Alcohol use disorder (AUD) causes executive dysfunction, leading to reduced treatment adherence, worse clinical outcomes, and relapse. Current medications do not address these symptoms. Targeting the neuroimmune interleukin-1 (IL-1) system has potential, but its mechanistic role in prefrontal cortex (PFC) dysfunction is unclear. Here we investigated how chronic alcohol consumption shifts IL-1 regulation of the rodent and non-human primate PFC. We found that alcohol drinking decreased reference memory and shifted the search strategy in mice of both sexes, and this deficit correlated with altered IL-1 receptor accessory protein (IL-1RAcP) mRNA levels in the medial PFC (mPFC) of male mice. Notably, the IL-1 system triggers either neuroprotective or proinflammatory cascades depending on the IL-1RAcP isoform recruited to the IL-1 receptor 1 complex. Alcohol drinking sex-dependently shifted mPFC IL-1RAcP gene expression (increased neuroprotective IL-1RAcP mRNA in female mice) and IL-1 regulation of mPFC synapses (increased GABA transmission that was specifically prevented by pharmacological blockade of the proinflammatory IL-1RAcP pathway in male mice) to support resilience in females vs. susceptibility in males. Notably, female alcohol-drinking rhesus macaques showed a similar increase in dorsolateral PFC (dlPFC) neuroprotective IL-1RAcP mRNA, with no change in males. Therefore, IL-1RAcP is a key AUD neural substrate that may sex-dependently switch the dl/mPFC from engaging in neuroprotective to proinflammatory synaptic mechanisms. This type of signaling bias is a recent focus of rational drug development and supports development of novel AUD pharmacotherapeutics based on biased IL-1 signaling, particularly for men.
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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 Socratic graph.