Evidence map›Paper›PMID 41321713›Full record

ArticleComplex psychiatry

Developmental Selective GSK3α Inhibition Rescues Working Memory Deficits in a Mouse Model of Schizophrenia Predisposition.

Johannes Passecker, Chloe M Aloimonos, Aleksandra Dagunts, Florence F Wagner, David A Kupferschmidt, Joseph Gogos, Joshua A Gordon

Abstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Johannes PasseckerIntegrative Neuroscience Section, National Institute of Neurological Disorders and Stroke, Bethesda, MD, USA.
Chloe M AloimonosIntegrative Neuroscience Section, National Institute of Neurological Disorders and Stroke, Bethesda, MD, USA.
Aleksandra DaguntsIntegrative Neuroscience Section, National Institute of Neurological Disorders and Stroke, Bethesda, MD, USA.
Florence F WagnerThe Broad Institute of MIT and Harvard Center for the Development of Therapeutics Cambridge MA, Cambridge, MA, USA.
David A KupferschmidtIntegrative Neuroscience Section, National Institute of Neurological Disorders and Stroke, Bethesda, MD, USA.
Joseph GogosMortimer B. Zuckerman Mind Brain and Behavior Institute, Columbia University, New York, NY, USA.
Joshua A GordonDepartment of Neuroscience, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

22q11.2 deletion syndromeBRD0705Developmental rescueExplorationGSK3αWorking memory

Identifiers

PMID41321713
PMCPMC12659633

What OpenQuestion holds

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Registered trials

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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 OpenQuestion graph.