ArticleNature communications2025
PTN activity in quiescent neural stem cells mediates Shank3 overexpression-induced manic behavior.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Pleiotrophin regulates presynaptic assembly and function through heparan sulfate-dependent binding to neurexin1.Cell reports · 2026Article
- Deciphering spatial heterogeneity by multimodal spatial transcriptomics modelling with SpatialModal.Bioinformatics (Oxford, England) · 2026Article
- Deciphering the microenvironment of adult neurogenesis: a perspective from neurodegenerative diseases.Translational neurodegeneration · 2026Review
- Single-cell transcriptomic landscape of the mid-secretory eutopic endometrium reveals receptivity defects in adenomyosis.Journal of translational medicine · 2026Article
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Authors and funding
8 authors.
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Abstract
Mania is a complex psychiatric disease characterized by hyperactivity, elevated mood and reduced anxiety. Despite extensive studies on the mechanism of the manic episodes, the molecular targets that control manic pathogenesis remain largely unclear. Here, through single-cell RNA sequencing (scRNA-seq) analysis, we show aberrant adult neurogenesis due to increased numbers of quiescent neural stem cells (qNSC) in a manic mouse model with Shank3 overexpression. Particularly, we found that the excessive Pleiotrophin (PTN), released by dysregulated qNSCs, is a key factor contributing to the manic-like phenotypes in Shank3-overexpressing mouse models. Pharmacological and molecular inhibition of PTN in qNSCs rescued aberrant neurogenesis and effectively alleviated the manic-like social deficits observed in Shank3-overexpressing mice. Taken together, our findings present an approach for modulating PTN activity in qNSCs, proposing it as a promising therapeutic target for manic development.
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