ArticleFrontiers in molecular neuroscience2022
Nuclear localization of alpha-synuclein affects the cognitive and motor behavior of mice by inducing DNA damage and abnormal cell cycle of hippocampal neurons.
Article in Frontiers in molecular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 15 citations in OpenAlex.
- Nuclear dysfunction in aging and neurodegeneration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Pathophysiological roles of neural stem cells in neuropsychiatric diseases: from plasticity to pharmacological targeting.Acta pharmacologica Sinica · 2026Review
- Organelle-Targeted Nanotherapeutics for Parkinson's Disease: From Pathogenesis to Preclinical Strategies and Translational Challenges.International journal of nanomedicine · 2026Review
- Retinoic acid alleviates manganese-induced neurotoxicity in SH-SY5Y cells via the Trim28/α-synuclein/H4K91ac epigenetic axis.Frontiers in pharmacology · 2026Article
- Establishment and Characterization of Behavioral Changes in the Nuclear Localization Human α-Synuclein Transgenic Mice.Diseases (Basel, Switzerland) · 2025Article
- Identification of a circRNA-miRNA-mRNA interactome associated with Parkinson's disease progression.Journal of Parkinson's disease · 2025Article
- MJF-14 proximity ligation assay detects early non-inclusion alpha-synuclein pathology with enhanced specificity and sensitivity.NPJ Parkinson's disease · 2024Article
- Special Issue "Neurobiology of Protein Synuclein".International journal of molecular sciences · 2024Article
- Network Analysis Performed on Transcriptomes of Parkinson's Disease Patients Reveals Dysfunction in Protein Translation.International journal of molecular sciences · 2024Article
- DNA Damage-Mediated Neurotoxicity in Parkinson's Disease.International journal of molecular sciences · 2023Review
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8 authors at 1 institution in 1 country.
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Abstract
Nuclear accumulation of alpha-synuclein (α-syn) in neurons can promote neurotoxicity, which is considered the key factor in the pathogenesis of synucleinopathy. The damage to hippocampus neurons driven by α-syn pathology is also the potential cause of memory impairment in Parkinson's disease (PD) patients. In this study, we examined the role of α-syn nuclear translocation in the cognition and motor ability of mice by overexpressing α-syn in cell nuclei in the hippocampus. The results showed that the overexpression of α-syn in nuclei was able to cause significant pathological accumulation of α-syn in the hippocampus, and quickly lead to memory and motor impairments in mice. It might be that nuclear overexpression of α-syn may cause DNA damage of hippocampal neurons, thereby leading to activation and abnormal blocking of cell cycle, and further inducing apoptosis of hippocampal neurons and inflammatory reaction. Meanwhile, the inflammatory reaction further aggravated DNA damage and formed a vicious circle. Therefore, the excessive nuclear translocation of α-syn in hippocampal neurons may be one of the main reasons for cognitive decline in mice.
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