{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ji C"],"funding":["NIA NIH HHS","Alzheimer's Association Research Fellowships","NINDS NIH HHS","National Institutes of Health","NIH HHS"],"pagination":["7954-7970"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11567809"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["20(11)"],"pubmed_abstract":["<h4>Introduction</h4>It is unclear how early neuronal deficits occur in tauopathies, if these are associated with changes in neuronal network activity, and if they can be alleviated with therapies.<h4>Methods</h4>To address this, we performed in vivo two-photon Ca<sup>2+</sup> imaging in tauopathy mice at 6 versus 12 months, compared to controls, and treated the younger animals with a tau antibody.<h4>Results</h4>Neuronal function was impaired at 6 months but did not deteriorate further at 12 months, presumably because cortical tau burden was comparable at these ages. At 6 months, neurons were mostly hypoactive, with enhanced neuronal synchrony, and had dysregulated responses to stimulus. Ex vivo, electrophysiology revealed altered synaptic transmission and enhanced excitability of motor c"],"journal":["Alzheimer's & dementia : the journal of the Alzheimer's Association"],"pubmed_title":["Neuronal hypofunction and network dysfunction in a mouse model at an early stage of tauopathy."],"pmcid":["PMC11567809"],"funding_grant_id":["R01 AG032611","AARF-22-924783 (Y.J.)","R01 NS077239","R21 AG069475","AARF-22-926735 (C.J.)","RF1 NS120488","R01 NS120488","R01 NS120488 (E.M.S.)","R21 AG059391","AARFD-22-926379 (A.M-A)"],"pubmed_authors":["Yang X","Jiang Y","Ji C","Eleish M","Martin-Avila A","Wu Q","Tetlow AM","Song SC","Sigurdsson EM","Lin Y","Zhou Y","Gan W"],"additional_accession":[]},"is_claimable":false,"name":"Neuronal hypofunction and network dysfunction in a mouse model at an early stage of tauopathy.","description":"<h4>Introduction</h4>It is unclear how early neuronal deficits occur in tauopathies, if these are associated with changes in neuronal network activity, and if they can be alleviated with therapies.<h4>Methods</h4>To address this, we performed in vivo two-photon Ca<sup>2+</sup> imaging in tauopathy mice at 6 versus 12 months, compared to controls, and treated the younger animals with a tau antibody.<h4>Results</h4>Neuronal function was impaired at 6 months but did not deteriorate further at 12 months, presumably because cortical tau burden was comparable at these ages. At 6 months, neurons were mostly hypoactive, with enhanced neuronal synchrony, and had dysregulated responses to stimulus. Ex vivo, electrophysiology revealed altered synaptic transmission and enhanced excitability of motor c","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Nov","modification":"2026-07-16T22:36:40.533Z","creation":"2025-04-07T04:31:05.704Z"},"accession":"S-EPMC11567809","cross_references":{"pubmed":["39368113"],"doi":["10.1002/alz.14273"]}}