ArticleCell death and differentiation2024
The PM20D1-NADA pathway protects against Parkinson's disease.
Article in Cell death and differentiation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Immune cell-specific genetic architecture of Alzheimer's disease revealed by multi-omics analysis for therapeutic target discovery and prioritization.Translational psychiatry · 2026Article
- Charting the human-specific properties of gene expression networks in the infant prefrontal cortex.Science advances · 2026Article
- The PM20D1-OLE pathway induces microglia rewiring to ameliorate Alzheimer disease.Cell death & disease · 2026Article
- Modulation of PM20D1 expression by rosiglitazone confers neuroprotection in tramadol-induced Parkinsonian rats.Toxicology reports · 2025Article
- Integrated transcriptomics and proteomics reveal ferroptosis induced by B[a]P and BPDE in mouse hippocampal neurons.Scientific reports · 2025Article
- Early-stage administration of hydroxytyrosol extends lifespan and delays aging in C. elegans.Biology direct · 2025Article
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Authors and funding
17 authors.
Funding
Abstract
Parkinson's disease (PD) is characterized by the selective loss of dopaminergic neurons in the substantia nigra and the accumulation of α-synuclein (α-Syn) aggregates. However, the molecular mechanisms regulating α-Syn aggregation and neuronal degeneration remain poorly understood. The peptidase M20 domain containing 1 (PM20D1) gene lies within the PARK16 locus genetically linked to PD. Single nucleotide polymorphisms regulating PM20D1 expression are associated with changed risk of PD. Dopamine (DA) metabolism and DA metabolites have been reported to regulate α-Syn pathology. Here we report that PM20D1 catalyzes the conversion of DA to N-arachidonoyl dopamine (NADA), which interacts with α-Syn and inhibits its aggregation. Simultaneously, NADA competes with α-Syn fibrils to regulate TRPV4-mediated calcium influx and downstream phosphatases, thus alleviating α-Syn phosphorylation. The expression of PM20D1 decreases during aging. Overexpression of PM20D1 or the administration of NADA in a mouse model of synucleinopathy alleviated α-Syn pathology, dopaminergic neurodegeneration, and motor impairments. These observations support the protective effect of the PM20D1-NADA pathway against the progression of α-Syn pathology in PD.
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