{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ding F"],"funding":["Simon Foundation","Lundbeck Foundations","Novo Nordisk","NCCIH NIH HHS","NIA NIH HHS","Adelson Medical Research Foundation","NHLBI NIH HHS","CNS2, Inc","NINDS NIH HHS","National Institutes of Health","U.S. Army Research Office","NIH HHS"],"pagination":["1726-1739"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11068329"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["147(5)"],"pubmed_abstract":["Progressive neuronal loss is a hallmark feature distinguishing neurodegenerative diseases from normal ageing. However, the underlying mechanisms remain unknown. Extracellular K+ homeostasis is a potential mediator of neuronal injury as K+ elevations increase excitatory activity. The dysregulation of extracellular K+ and potassium channel expressions during neurodegeneration could contribute to this distinction. Here we measured the cortical extracellular K+ concentration ([K+]e) in awake wild-type mice as well as murine models of neurodegeneration using K+-sensitive microelectrodes. Unexpectedly, aged wild-type mice exhibited significantly lower cortical [K+]e than young mice. In contrast, cortical [K+]e was consistently elevated in Alzheimer's disease (APP/PS1), amyotrophic lateral sclero"],"journal":["Brain : a journal of neurology"],"pubmed_title":["Dysregulation of extracellular potassium distinguishes healthy ageing from neurodegeneration."],"pmcid":["PMC11068329"],"funding_grant_id":["R01AT012312","R01 NS110776","R01 AT011439","MURI W911NF1910280","R01AT011439","U19 NS128613","R01 AG072298","R01 AT012312","R01 HL122578","R01HL122578"],"pubmed_authors":["Ding F","Weikop P","Rasmussen RN","Sun Q","Goldman SA","Peng S","Xu Q","Kang N","Nedergaard M","Song W","Long C"],"additional_accession":[]},"is_claimable":false,"name":"Dysregulation of extracellular potassium distinguishes healthy ageing from neurodegeneration.","description":"Progressive neuronal loss is a hallmark feature distinguishing neurodegenerative diseases from normal ageing. However, the underlying mechanisms remain unknown. Extracellular K+ homeostasis is a potential mediator of neuronal injury as K+ elevations increase excitatory activity. The dysregulation of extracellular K+ and potassium channel expressions during neurodegeneration could contribute to this distinction. Here we measured the cortical extracellular K+ concentration ([K+]e) in awake wild-type mice as well as murine models of neurodegeneration using K+-sensitive microelectrodes. Unexpectedly, aged wild-type mice exhibited significantly lower cortical [K+]e than young mice. In contrast, cortical [K+]e was consistently elevated in Alzheimer's disease (APP/PS1), amyotrophic lateral sclero","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 May","modification":"2026-04-30T03:20:06.59Z","creation":"2025-04-05T23:52:10.627Z"},"accession":"S-EPMC11068329","cross_references":{"pubmed":["38462589"],"doi":["10.1093/brain/awae075"]}}