{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["16(1)"],"submitter":["Wu KJ"],"funding":["National Science and Technology Council, Taiwan"],"pubmed_abstract":["Abnormal accumulation of alpha-synuclein (αSyn) in axons and presynaptic terminals plays a critical role in αSyn-mediated dopaminergic neurodegeneration. A strong correlation between aging and elevated αSyn levels in the substantia nigra has been identified in both humans and non-human primates. Aging is the most prominent risk factor for Parkinson's disease (PD), contributing to nigrostriatal dopamine degeneration and motor impairments. Therefore, reducing intracellular αSyn accumulation in affected neurons may help prevent nigrostriatal degeneration, preserve dopaminergic function, and delay PD onset in aging individuals. Our previous works demonstrated that adeno-associated virus 1 (AAV1)-mediated NAC32 intrabody expression effectively reduced αSyn accumulation and alleviated bradykines"],"journal":["Scientific reports"],"pagination":["4632"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12868895"],"repository":["biostudies-literature"],"pubmed_title":["AAV-mediated intracerebral expression of an α-synuclein-targeting intrabody improves motor functions in aged rats."],"pmcid":["PMC12868895"],"pubmed_authors":["Yu SJ","Hsu SC","Li YC","Peng YC","Chuang YM","Chu CY","Wang YS","Chen CT","Chen YH","Wu KJ","Chiu YS","Wang KL"],"additional_accession":[]},"is_claimable":false,"name":"AAV-mediated intracerebral expression of an α-synuclein-targeting intrabody improves motor functions in aged rats.","description":"Abnormal accumulation of alpha-synuclein (αSyn) in axons and presynaptic terminals plays a critical role in αSyn-mediated dopaminergic neurodegeneration. A strong correlation between aging and elevated αSyn levels in the substantia nigra has been identified in both humans and non-human primates. Aging is the most prominent risk factor for Parkinson's disease (PD), contributing to nigrostriatal dopamine degeneration and motor impairments. Therefore, reducing intracellular αSyn accumulation in affected neurons may help prevent nigrostriatal degeneration, preserve dopaminergic function, and delay PD onset in aging individuals. Our previous works demonstrated that adeno-associated virus 1 (AAV1)-mediated NAC32 intrabody expression effectively reduced αSyn accumulation and alleviated bradykines","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Jan","modification":"2026-07-15T12:03:18.3Z","creation":"2026-07-04T03:12:44.165Z"},"accession":"S-EPMC12868895","cross_references":{"pubmed":["41501394"],"doi":["10.1038/s41598-025-34908-1"]}}