ArticleComplex psychiatry
Developmental Selective GSK3α Inhibition Rescues Working Memory Deficits in a Mouse Model of Schizophrenia Predisposition.
Article in Complex psychiatry. 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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Who cites it
1 citing paper in PubMed.
- Divergent transcriptomic pathways underlie sex-biased cognitive rescue by developmental GSK3B inhibition in a mouse model of 22q11.2 deletion syndrome.Translational psychiatry · 2026Article
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7 authors.
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Abstract
Introduction: The 22q11.2 deletion syndrome is a genetic disorder characterized by pronounced age-dependent emergence of learning and cognitive deficits, including working memory and anxiety-related symptoms. The deletion confers a 20-fold increased risk of a schizophrenia diagnosis, but there are currently no approved pharmacological therapies for this condition. We have previously shown that treatment with a glycogen synthase kinase 3 (GSK3) paralog-nonselective inhibitor during early postnatal development rescues working memory task acquisition in the Methods: Using the Results: We found that early postnatal GSK3α inhibition from postnatal day 7 (P7) to P28 restored spatial working memory performance in adult Conclusion: Overall, we provide evidence supporting the feasibility and effectiveness of paralog-selective GSK3α inhibition-mediated rescue of cognitive function in a model of altered neurodevelopment.
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