ArticleNeuropharmacology2026
Emerging role of N6-methyladenosine (m6A) epitranscriptomic changes in adult anxiety after adolescent alcohol exposure.
Article in Neuropharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Super-resolved, three-dimensional spatial transcriptomics reveals cell-type and brain-region-specific modulation of key epitranscriptomic switches following adolescent alcohol exposure.bioRxiv : the preprint server for biology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Adolescent intermittent ethanol (AIE) exposure affects multiple brain regions by producing long-lasting effects on epigenetic mechanisms and behavioral phenotypes later in life. Recently, it has been shown that epigenetic switches can control epitranscriptomics, or RNA modifications. Specifically, the most abundant RNA modification, known as N6-methyladenosine (m6A), has been the subject of intense investigation in brain plasticity; however, little is known about its role in adult psychopathology after AIE. Herein, we investigated whether changes in m6A modifiers (writers, erasers, and readers) after AIE regulate phenotypes of anxiety in adulthood using an animal model. We characterized m6A regulators in the amygdala, hippocampus, medial prefrontal cortex, and the nucleus accumbens of rats after AIE in adolescence and adulthood. AIE induces differential gene expression of m6A modifiers, with some brain regions being more affected during adolescence, while other limbic brain regions show long-lasting changes in adulthood. We observed that Mettl3 mRNA levels were significantly increased in the amygdala and medial prefrontal cortex in adulthood after AIE, as measured by real-time polymerase chain reaction. We further evaluated changes in METTL3 expression and global m6A methylation in amygdala nuclei using a histochemical procedure. Indeed, protein and mRNA levels of METTL3, as well as m6A levels, were upregulated in the central and medial nucleus of the amygdala after AIE in adulthood. We pharmacologically inhibited METTL3 activity using STM2457, which significantly attenuated AIE-induced anxiety-like behaviors in adulthood. These results suggest that m6A epitranscriptomics can serve as a novel avenue in the exploration of therapeutics for AIE-induced adult psychopathology.
Indexed as
Identifiers
What OpenQuestion holds
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.