{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ramakrishnan A"],"funding":["NIA NIH HHS","NINDS NIH HHS"],"pagination":["1235-1248.e5"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11031321"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["112(8)"],"pubmed_abstract":["The peripheral immune system in Alzheimer's disease (AD) has not been thoroughly studied with modern sequencing methods. To investigate epigenetic and transcriptional alterations to the AD peripheral immune system, we used single-cell sequencing strategies, including assay for transposase-accessible chromatin and RNA sequencing. We reveal a striking amount of open chromatin in peripheral immune cells in AD. In CD8 T cells, we uncover a cis-regulatory DNA element co-accessible with the CXC motif chemokine receptor 3 gene promoter. In monocytes, we identify a novel AD-specific RELA transcription factor binding site adjacent to an open chromatin region in the nuclear factor kappa B subunit 2 gene. We also demonstrate apolipoprotein E genotype-dependent epigenetic changes in monocytes. Surprisingly, we also identify differentially accessible chromatin regions in genes associated with sporadic AD risk. Our findings provide novel insights into the complex relationship between epigenetics and genetic risk factors in AD peripheral immunity."],"journal":["Neuron"],"pubmed_title":["Epigenetic dysregulation in Alzheimer's disease peripheral immunity."],"pmcid":["PMC11031321"],"funding_grant_id":["P30 AG072977","K99 NS112458","P30 AG066515","R00 NS112458","R01 AG078713"],"pubmed_authors":["van Olst L","Piehl N","Zhang Z","Ramakrishnan A","Gate D","Parikh M","Simonton B","Teregulova V"],"additional_accession":[]},"is_claimable":false,"name":"Epigenetic dysregulation in Alzheimer's disease peripheral immunity.","description":"The peripheral immune system in Alzheimer's disease (AD) has not been thoroughly studied with modern sequencing methods. To investigate epigenetic and transcriptional alterations to the AD peripheral immune system, we used single-cell sequencing strategies, including assay for transposase-accessible chromatin and RNA sequencing. We reveal a striking amount of open chromatin in peripheral immune cells in AD. In CD8 T cells, we uncover a cis-regulatory DNA element co-accessible with the CXC motif chemokine receptor 3 gene promoter. In monocytes, we identify a novel AD-specific RELA transcription factor binding site adjacent to an open chromatin region in the nuclear factor kappa B subunit 2 gene. We also demonstrate apolipoprotein E genotype-dependent epigenetic changes in monocytes. Surprisingly, we also identify differentially accessible chromatin regions in genes associated with sporadic AD risk. Our findings provide novel insights into the complex relationship between epigenetics and genetic risk factors in AD peripheral immunity.","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Apr","modification":"2026-06-01T17:48:35.734Z","creation":"2025-06-26T03:06:20.613Z"},"accession":"S-EPMC11031321","cross_references":{"pubmed":["38340719"],"doi":["10.1016/j.neuron.2024.01.013"]}}