ArticleFrontiers in immunology2025
Chronic ethanol administration exacerbates memory loss by altering N6-methyladenosine-mediated epigenetic signaling.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Chronic alcohol use disorder (AUD) is recognized as one of the most critical risk factors for the progression of Alzheimer's disease (AD). Epigenetic and neuroimmune alterations are closely associated with the development of memory impairment related to AUD and AD. Methods: Adult APP/PS1 transgenic mice received intermittently intraperitoneal injections of ethanol (EtOH, 2.5 g/kg, i.p.) or vehicle with two "drug" treatment days, and one and two "drug-free" days every 7 days for 10 weeks. The novel object recognition (NOR) and Y-maze tests were performed to determine whether chronic ethanol treatment exacerbated memory impairment in these mice. The brain tissues were collected for pathological changes through MeRIP/RNA-sequence analyses and molecular biological assays. Results: The results suggested that chronic intermittent ethanol (CIE) treatment for 10 weeks exacerbated sporadic and spatial memory deficits in NOR and Y-maze tests in the APP/PS1 mice. The pathological assays revealed that CIE procedure increased Aβ plaque burden in the brain of the AD mice, which were consistent with memory behavioral deficits. The subsequent MeRIP/RNA sequence analyses showed that two genes, e.g. Rbm15b and Hnrnpa2b1, were related to N6-methyladenosine (m Conclusions: The conclusion is drawn that m
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