ArticleMolecular psychiatry2026
Aberrant neural stem cell quiescence is the gateway to autism development linked to Arid1b.
Article in Molecular psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autism spectrum disorder is a neurodevelopmental disorder with social communication deficits, repetitive behaviors, and restricted interests. While previous studies have demonstrated a close link between aberrant neurogenesis and the development of autism, a fundamental question remains unresolved: Does the anomalous neurogenesis observed in autism serve as a causative factor, and if so, could restoring aberrant neurogenesis alleviate autistic behaviors? In this study, we demonstrate that the manifestation of autistic behaviors can be caused by the aberrant activity of quiescent neural stem cells (qNSCs), resulting from the conditional deletion of Arid1b in adult brain NSCs. Particularly, increased H3K27me3 levels in qNSCs due to conditional Arid1b deficiency precipitated autism-related phenotypes, but rescuing this through H3K27me3 inhibition effectively reversed autistic-like phenotypes. Importantly, we also found quiescent like NSCs in humans carrying the ARID1B mutation, as well as in NSCs of sporadic autism patients. These results highlight the significant role of aberrant qNSCs associated with adult neurogenesis for autism development in adult brain, offering a novel avenue for potentially controlling qNSC activity as a therapeutic strategy for autism.
Indexed as
Identifiers
40885843What 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.