ArticleMolecular psychiatry2022
Dormant state of quiescent neural stem cells links Shank3 mutation to autism development.
Article in Molecular psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- "SHANK3 deficiency alters early progenitor dynamics and reveals shared pathways with neurodegeneration".Molecular psychiatry · 2026Article
- Pathophysiological roles of neural stem cells in neuropsychiatric diseases: from plasticity to pharmacological targeting.Acta pharmacologica Sinica · 2026Review
- Aberrant neural stem cell quiescence is the gateway to autism development linked to Arid1b.Molecular psychiatry · 2026Article
- Review
- Developmental Disturbances in Animal Models of Autism Spectrum Disorder.Developmental neurobiology · 2025Review
- Parkinson's Disease Modeling Using Directly Converted 3D Induced Dopaminergic Neuron Organoids and Assembloids.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- PTN activity in quiescent neural stem cells mediates Shank3 overexpression-induced manic behavior.Nature communications · 2025Article
- Epigenetic Dynamics in Reprogramming to Dopaminergic Neurons for Parkinson's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Pharmacological modulation of developmental and synaptic phenotypes in human SHANK3 deficient stem cell-derived neuronal models.Translational psychiatry · 2024Article
- Disrupted extracellular matrix and cell cycle genes in autism-associated Shank3 deficiency are targeted by lithium.Molecular psychiatry · 2024Article
- Altered hippocampal neurogenesis in a mouse model of autism revealed by genetic polymorphisms and by atypical development of newborn neurons.Scientific reports · 2024Article
- TheThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Efficient generation of brain organoids using magnetized gold nanoparticles.Scientific reports · 2023Article
- Single-nucleus transcriptomic mapping uncovers targets for traumatic brain injury.Genome research · 2023Article
- Single-cell RNA-sequencing identifies disease-associated oligodendrocytes in male APP NL-G-F and 5XFAD mice.Nature communications · 2023Article
- SHANK family on stem cell fate and development.Cell death & disease · 2022Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autism spectrum disorders (ASDs) are common neurodevelopmental disorders characterized by deficits in social interactions and communication, restricted interests, and repetitive behaviors. Despite extensive study, the molecular targets that control ASD development remain largely unclear. Here, we report that the dormancy of quiescent neural stem cells (qNSCs) is a therapeutic target for controlling the development of ASD phenotypes driven by Shank3 deficiency. Using single-cell RNA sequencing (scRNA-seq) and transposase accessible chromatin profiling (ATAC-seq), we find that abnormal epigenetic features including H3K4me3 accumulation due to up-regulation of Kmt2a levels lead to increased dormancy of qNSCs in the absence of Shank3. This result in decreased active neurogenesis in the Shank3 deficient mouse brain. Remarkably, pharmacological and molecular inhibition of qNSC dormancy restored adult neurogenesis and ameliorated the social deficits observed in Shank3-deficient mice. Moreover, we confirmed restored human qNSC activity rescues abnormal neurogenesis and autism-like phenotypes in SHANK3-targeted human NSCs. Taken together, our results offer a novel strategy to control qNSC activity as a potential therapeutic target for the development of autism.
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