ArticleNPJ Parkinson's disease2022
Cofilin 1 promotes the pathogenicity and transmission of pathological α-synuclein in mouse models of Parkinson's disease.
Article in NPJ Parkinson's disease, 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, 77 citations in OpenAlex.
- SYNGR3 Accelerates α-Synuclein Aggregation and Neurodegeneration in Parkinson's Disease.CNS neuroscience & therapeutics · 2026Article
- Identification of genes associated with smell dysfunction in Parkinson's disease.Clinical parkinsonism & related disorders · 2026Article
- Beyond Organ Boundaries: Molecular Mechanisms of Hepatic Encephalopathy and Parkinson's Disease from the Perspective of the Gut-Liver-Brain Axis.Research (Washington, D.C.) · 2026Review
- Brain-derived extracellular vesicle proteomics reveals neuroprotection induced by the ARB candesartan in Parkinson's disease patients.NPJ Parkinson's disease · 2025Article
- ACE2 Alleviates Microglia Neuroinflammation by RANK-RANKL-OPG Axis in Parkinson's Disease.Inflammation · 2025Article
- Neuropathological stages of neuronal, astrocytic and oligodendrocytic alpha-synuclein pathology in Parkinson's disease.Acta neuropathologica communications · 2025Article
- Inhibition of iron-induced cofilin activation and inflammation in microglia by a novel cofilin inhibitor.Journal of neurochemistry · 2025Article
- Microglia Process α-Synuclein Fibrils and Enhance their Pathogenicity in a TREM2-Dependent Manner.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Systematic identification of structure-specific protein-protein interactions.Molecular systems biology · 2024Article
- α-Synuclein triggers cofilin pathology and dendritic spine impairment via a PrPCell death & disease · 2024Article
- Pathological and physiological functional cross-talks of α-synuclein and tau in the central nervous system.Neural regeneration research · 2024Review
- Review
- α-Synuclein-mediated mitochondrial translocation of cofilin-1 leads to oxidative stress and cell apoptosis in PD.Frontiers in neuroscience · 2024Article
- Article
- Pathological characterization of a novel mouse model expressing the PD-linked CHCHD2-T61I mutation.Human molecular genetics · 2022Article
- The circadian clock protein Rev-erbα provides neuroprotection and attenuates neuroinflammation against Parkinson's disease via the microglial NLRP3 inflammasome.Journal of neuroinflammation · 2022Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
The pathological hallmark of Parkinson's disease (PD) is the presence of Lewy bodies (LBs) with aggregated α-synuclein being the major component. The abnormal α-synuclein aggregates transfer between cells, recruit endogenous α-synuclein into toxic LBs, and finally trigger neuronal injury. However, the molecular mechanisms mediating the aggregation and transmission of pathological α-synuclein remain unknown. Previously we found that cofilin 1, a member of the actin-binding protein, promotes the aggregation and pathogenicity of α-synuclein in vitro. Here we further investigated the effect of cofilin 1 in mouse models of PD. We found that the mixed fibrils composed of cofilin 1 and α-synuclein are more pathogenic to mice and more prone to propagation than pure α-synuclein fibrils. Overexpression of cofilin 1 enhances the seeding and spreading of α-synuclein aggregates, and induces PD-like behavioral impairments in mice. Together, these results illustrate the important role of cofilin 1 in the pathogenicity and transmission of α-synuclein during the onset and progression of PD.
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