ArticleNPJ Parkinson's disease2025
Lysophosphatidylcholine promoting α-Synuclein aggregation in Parkinson's disease: disrupting GCase glycosylation and lysosomal α-Synuclein degradation.
Article in NPJ Parkinson's disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Parkinson's Disease-Associated Remodeling of SynapticJournal of proteome research · 2026Article
- The Influence of Gut Microbiome on Alpha-Synuclein Aggregation: Implications for Parkinson's Disease Pathogenesis.Molecular neurobiology · 2026Review
- Microglial GPR35 Ameliorates Epileptogenesis and Neuroinflammation via PDGFA Domain 2 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Distinct metabolomic and proteomic signatures in Parkinson's disease patients with REM sleep behavior disorder.Signal transduction and targeted therapy · 2026Article
- Serum Aberrant Expression of miR-431-5p and Their Diagnostic Value in Parkinson's Disease.Neurochemical research · 2026Article
- Multi-Omics Reveals Dysregulation of the Endosome-Lysosome-Autophagy Axis and Immune-Inflammatory Imbalance in Elderly Sepsis.Clinical interventions in aging · 2026Article
- Autophagy-lysosomal pathway in neurodegeneration.Molecular neurodegeneration advances · 2026Review
- Research progress on the α-synuclein-lysosome axis in Parkinson's disease: molecular mechanisms of protein aggregation, autophagy dysfunction, and therapeutic targeting.Frontiers in neuroscience · 2026Review
- Underlying Mechanisms of GBA1 in Parkinson's Disease and Dementia with Lewy Bodies: Narrative Review.Genes · 2025Review
- Abnormal glycosylation changes in brain tissue of kainic acid-induced epileptic rats.Scientific reports · 2025Article
- Multi-omic analysis reveals lipid dysregulation associated with mitochondrial dysfunction in parkinson's disease brain.Nature communications · 2025Article
- p.N370SInternational journal of molecular sciences · 2025Article
- Biosensors for Early Detection of Parkinson's Disease: Principles, Applications, and Future Prospects.Biosensors · 2025Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
In Parkinson's Disease (PD), elevated serum lysophosphatidylcholine (LPC) levels correlate with disease progression. However, the mechanisms by which abnormal LPC elevation contributes to PD-related neurotoxicity remain poorly understood. This study aims to investigate the pathogenic role of LPC in dopaminergic neuronal damage and elucidates its underlying mechanisms. Our results showed LPC induces α-synuclein aggregation, exacerbating cognitive dysfunction. LPC activates Cleaved-Caspase3 via the orphan receptor GPR35-ERK signaling pathway, inhibits GRASP65 expression, and disrupts the polarized structure of the Golgi apparatus. This disruption impairs glycosylation and function of glucocerebrosidase (GCase), preventing its transport to lysosomes and leading to glucosylceramide (GlcCer) accumulation, a scaffold for α-synuclein aggregation. LPC also disrupts the autophagolysosomal pathway and lysosomal acidification, exacerbating toxic α-synuclein accumulation. Restoring GCase glycosylation, limiting GlcCer synthesis, or blocking ERK signaling mitigates these effects. This study highlights LPC's role in promoting α-synuclein aggregation and autophagolysosomal dysfunction, advancing our understanding of PD pathology.
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Registered trials
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