{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE348nnn/GSE348131/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE348131"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"A deep cellular atlas of the human ventral substantia nigra in Parkinson's identifies a genetic and molecular overlap with insulin resistance [ipsc-DaNs]","description":"Parkinson’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.","dates":{"publication":"2026/09/24"},"accession":"GSE348131","cross_references":{"GSM":["GSM10066952","GSM10066953","GSM10066950","GSM10066951","GSM10066954","GSM10066955"],"GPL":["24676"],"GSE":["348131"],"taxon":["Homo sapiens"]}}