ArticleMolecular therapy : the journal of the American Society of Gene Therapy2022
Synapsin III gene silencing redeems alpha-synuclein transgenic mice from Parkinson's disease-like phenotype.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 23 citations in OpenAlex.
- Charting the human-specific properties of gene expression networks in the infant prefrontal cortex.Science advances · 2026Article
- The Influence of Gut Microbiome on Alpha-Synuclein Aggregation: Implications for Parkinson's Disease Pathogenesis.Molecular neurobiology · 2026Review
- Syn III participated in rTMS-modulated emotional rescue in the prefrontal cortex under simulated space composite environment.Molecular psychiatry · 2026Article
- Sex-related differences in phenotype and nigro-striatal degeneration of c-relBiology of sex differences · 2025Article
- Contrasting Behavioural and Biochemical Characteristics of Normal and Spontaneously α-Synuclein-Deficient Mice Treated With MPTP.Journal of neurochemistry · 2025Article
- Lewy pathology formation in patient-derived GBA1 Parkinson's disease midbrain organoids.Brain : a journal of neurology · 2025Article
- Contrastive machine learning reveals Parkinson's disease specific features associated with disease severity and progression.Communications biology · 2024Article
- PLCγ1 in dopamine neurons critically regulates striatal dopamine release via VMAT2 and synapsin III.Experimental & molecular medicine · 2023Article
- Altered Distribution of SNARE Proteins in Primary Neurons Exposed to Different Alpha-Synuclein Proteoforms.Cellular and molecular neurobiology · 2023Article
- Parkinson's disease relevant pathological features are manifested in male Pink1/Parkin deficient rats.Brain, behavior, & immunity - health · 2023Article
- Methylphenidate Analogues as a New Class of Potential Disease-Modifying Agents for Parkinson's Disease: Evidence from Cell Models and Alpha-Synuclein Transgenic Mice.Pharmaceutics · 2022Article
- SNCA-AS1 in aging and Parkinson's disease.Aging · 2022Article
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Authors and funding
15 authors at 5 institutions in 3 countries.
Funding
Abstract
Fibrillary aggregated α-synuclein (α-syn) deposition in Lewy bodies (LB) characterizes Parkinson's disease (PD) and is believed to trigger dopaminergic synaptic failure and a retrograde terminal-to-cell body neuronal degeneration. We described that the neuronal phosphoprotein synapsin III (Syn III) cooperates with α-syn to regulate dopamine (DA) release and can be found in the insoluble α-syn fibrils composing LB. Moreover, we showed that α-syn aggregates deposition, and the associated onset of synaptic deficits and neuronal degeneration occurring following adeno-associated viral vectors-mediated overexpression of human α-syn in the nigrostriatal system are hindered in Syn III knock out mice. This supports that Syn III facilitates α-syn aggregation. Here, in an interventional experimental design, we found that by inducing the gene silencing of Syn III in human α-syn transgenic mice at PD-like stage with advanced α-syn aggregation and overt striatal synaptic failure, we could lower α-syn aggregates and striatal fibers loss. In parallel, we observed recovery from synaptic vesicles clumping, DA release failure, and motor functions impairment. This supports that Syn III consolidates α-syn aggregates, while its downregulation enables their reduction and redeems the PD-like phenotype. Strategies targeting Syn III could thus constitute a therapeutic option for PD.
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