{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Fancy NN"],"funding":["UK Dementia Research Institute","Medical Research Council","Alzheimer’s Research UK"],"pagination":["78"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11065703"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["147(1)"],"pubmed_abstract":["Aging is associated with cell senescence and is the major risk factor for AD. We characterized premature cell senescence in postmortem brains from non-diseased controls (NDC) and donors with Alzheimer's disease (AD) using imaging mass cytometry (IMC) and single nuclear RNA (snRNA) sequencing (> 200,000 nuclei). We found increases in numbers of glia immunostaining for galactosidase beta (> fourfold) and p16<sup>INK4A</sup> (up to twofold) with AD relative to NDC. Increased glial expression of genes related to senescence was associated with greater β-amyloid load. Prematurely senescent microglia downregulated phagocytic pathways suggesting reduced capacity for β-amyloid clearance. Gene set enrichment and pseudo-time trajectories described extensive DNA double-strand breaks (DSBs), mitochondr"],"journal":["Acta neuropathologica"],"pubmed_title":["Characterisation of premature cell senescence in Alzheimer's disease using single nuclear transcriptomics."],"pmcid":["PMC11065703"],"funding_grant_id":["MR/P024572/1"],"pubmed_authors":["Smith AM","Davey K","Tsartsalis S","Boulger S","Papageorgopoulou M","Jenkyns MH","McGarry A","Adair E","Khozoie C","Chau V","Thomas M","Willumsen N","Gomez-Nicola D","Caramello A","Jackson JS","Fancy NN","Muirhead RCJ","Schneegans E","Matthews PM","Cheung TKD"],"additional_accession":[]},"is_claimable":false,"name":"Characterisation of premature cell senescence in Alzheimer's disease using single nuclear transcriptomics.","description":"Aging is associated with cell senescence and is the major risk factor for AD. We characterized premature cell senescence in postmortem brains from non-diseased controls (NDC) and donors with Alzheimer's disease (AD) using imaging mass cytometry (IMC) and single nuclear RNA (snRNA) sequencing (> 200,000 nuclei). We found increases in numbers of glia immunostaining for galactosidase beta (> fourfold) and p16<sup>INK4A</sup> (up to twofold) with AD relative to NDC. Increased glial expression of genes related to senescence was associated with greater β-amyloid load. Prematurely senescent microglia downregulated phagocytic pathways suggesting reduced capacity for β-amyloid clearance. Gene set enrichment and pseudo-time trajectories described extensive DNA double-strand breaks (DSBs), mitochondr","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 May","modification":"2026-07-15T01:54:37.118Z","creation":"2026-06-27T03:18:38.29Z"},"accession":"S-EPMC11065703","cross_references":{"pubmed":["38695952"],"doi":["10.1007/s00401-024-02727-9"]}}