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Immunohistochemical Visualization of Hippocampal Neuron Activity After Spatial Learning in a Mouse Model of Neurodevelopmental Disorders
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Developmental Selective GSK3α Inhibition Rescues Working Memory Deficits in a Mouse Model of Schizophrenia

Johannes Passecker1,2,3, Chloe M Aloimonos1, Aleksandra Dagunts1

  • 1Integrative Neuroscience Section, National Institute of Neurological Disorders and Stroke, Bethesda, MD, USA.

Complex Psychiatry
|December 1, 2025
PubMed
Summary
This summary is machine-generated.

Early postnatal treatment with a selective GSK3α inhibitor improved working memory and exploratory behavior in a mouse model of 22q11.2 deletion syndrome, offering a potential therapeutic strategy for cognitive deficits.

Keywords:
22q11.2 deletion syndromeBRD0705Developmental rescueExplorationGSK3αWorking memory

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Area of Science:

  • Neuroscience
  • Genetics
  • Pharmacology

Background:

  • 22q11.2 deletion syndrome causes cognitive deficits and increases schizophrenia risk.
  • Current treatments lack efficacy and have side effects.
  • GSK3 inhibitors show promise but nonselective ones have toxicity concerns.

Purpose of the Study:

  • To evaluate a novel GSK3α-selective inhibitor for treating cognitive deficits in a 22q11.2 deletion syndrome mouse model.
  • To assess the inhibitor's effects on spatial working memory and behavior.

Main Methods:

  • Utilized the Df(16)A+/- mouse model.
  • Administered a GSK3α-selective inhibitor during early postnatal development (P7-P28).
  • Assessed spatial working memory and approach-avoidance behavior in adult mice.

Main Results:

  • Early GSK3α inhibition restored spatial working memory in Df(16)A+/- mice.
  • Heightened exploratory behavior in Df(16)A+/- mice was normalized by GSK3α inhibition.
  • Effects were observed in a genotype-independent manner.

Conclusions:

  • Paralog-selective GSK3α inhibition is a feasible and effective strategy.
  • This approach shows potential for rescuing cognitive function in neurodevelopmental disorders.
  • Further research into GSK3α inhibitors for 22q11.2 deletion syndrome is warranted.