GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE329nnn/GSE329625/suppl/GSE329625_processed_gene_matrix.txt.gzftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE329nnn/GSE329625/suppl/GSE329625_full_metadata.csv.gzftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE329nnn/GSE329625/primaryOK200TranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE329625GEOGSEfalseA deep cellular atlas of the human ventral substantia nigra in Parkinson's identifies a genetic and molecular overlap with insulin resistanceParkinson’s disease (PD) is a complex neurodegenerative disorder characterised by selective neuronal loss. We integrate deep full-length single-nuclei sequencing of the human substantia nigra with novel genome-wide association studies (GWAS) identifying genetic and cellular drivers of PD. Genetic risk converges on AGTR1+ dopaminergic neurons and perineuronal oligodendrocytes (pODCs), both reduced in PD, as well as oligodendrocyte precursor cells, enriched among disease-disrupted intercellular interactions. AGTR1+ neurons represent a metabolically stressed state, characterised by renin-angiotensin system (RAS) and MAPK activation, oxidative stress, and mitochondrial dysfunction, rather than a distinct subtype. AGTR1+ neurons and pODCs link PD risk to metabolic traits; in pODCs, this association reflects insulin resistance with downregulated PI3K–AKT signalling.2026/05/10GSE329625GSM9707824GSM9707813GSM9707825GSM9707814GSM9707815GSM9707826GSM9707816GSM9707820GSM9707821GSM9707810GSM9707811GSM9707822GSM9707812GSM9707823GSM9707817GSM9707818GSM9707807GSM9707819GSM9707808GSM970780924676329625Homo sapiens