ArticleMolecular neurobiology2020
Neural Stem Cells from Shank3-ko Mouse Model Autism Spectrum Disorders.
Article in Molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 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
- Autism Spectrum Disorder: From Experimental Models to Probiotic Application with a Special Focus onNutrients · 2025Review
- Structural pathways related to the subventricular zone are decreased in volume with altered microstructure in young adult males with autism spectrum disorder.Cerebral cortex (New York, N.Y. : 1991) · 2025Article
- 3KO-NSCs ameliorate behavioral deficits and modulate gut microbiota in a VPA-induced C57BL/6 mouse model of autism.Frontiers in immunology · 2025Article
- Melatonin AttenuatesInternational journal of molecular sciences · 2024Article
- Mesenchymal Stem Cell-Induced Neuroprotection in Pediatric Neurological Diseases: Recent Update of Underlying Mechanisms and Clinical Utility.Applied biochemistry and biotechnology · 2024Review
- Hepatic Alterations in a BTBR T + Itpr3tf/J Mouse Model of Autism and Improvement Using Melatonin via Mitigation Oxidative Stress, Inflammation and Ferroptosis.International journal of molecular sciences · 2024Article
- TRRAP-mediated acetylation on Sp1 regulates adult neurogenesis.Computational and structural biotechnology journal · 2023Article
- Ablation of Shank3 alleviates cardiac dysfunction in aging mice by promoting CaMKII activation and Parkin-mediated mitophagy.Redox biology · 2022Article
- SHANK family on stem cell fate and development.Cell death & disease · 2022Review
- Dormant state of quiescent neural stem cells links Shank3 mutation to autism development.Molecular psychiatry · 2022Article
- Integration of structural MRI and epigenetic analyses hint at linked cellular defects of the subventricular zone and insular cortex in autism: Findings from a case study.Frontiers in neuroscience · 2022Article
- Expression of Genes Involved in Axon Guidance: How Much Have We Learned?International journal of molecular sciences · 2020Review
- SHANK3 Co-ordinately Regulates Autophagy and Apoptosis in Myocardial Infarction.Frontiers in physiology · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Autism spectrum disorders (ASD) comprise a complex of neurodevelopmental disorders caused by a variety of genetic defects and characterized by alterations in social communication and repetitive behavior. Since the mechanisms leading to early neuronal degeneration remain elusive, we chose to examine the properties of NSCs isolated from an animal model of ASD in order to evaluate whether their neurogenic potential may recapitulate the early phases of neurogenesis in the brain of ASD patients. Mutations of the gene coding for the Shank3 protein play a key role in the impairment of brain development and synaptogenesis in ASD patients. Experiments here reported show that NSCs derived from the subventricular zone (SVZ) of adult Shank3Δ11-/- (Shank3-ko) mice retain self-renewal capacity in vitro, but differentiate earlier than wild-type (wt) cells, displaying an evident endosomal/lysosomal and ubiquitin aggregation in astroglial cells together with mitochondrial impairment and inflammasome activation, suggesting that glial degeneration likely contributes to neuronal damage in ASD. These in vitro observations obtained in our disease model are consistent with data in vivo obtained in ASD patients and suggest that Shank3 deficit could affect the late phases of neurogenesis and/or the survival of mature cells rather than NSC self-renewal. This evidence supports Shank3-ko NSCs as a reliable in vitro disease model and suggests the rescue of glial cells as a therapeutic strategy to prevent neuronal degeneration in ASD.
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