{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Theofilas P"],"funding":["NIA NIH HHS","NINDS NIH HHS","Alzheimer&amp;apos;s Association","National Institute on Aging"],"pagination":["103954"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11866097"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["130"],"pubmed_abstract":["<h4>Background</h4>Tau post-translational modifications (PTMs) result in the gradual build-up of abnormal tau and neuronal degeneration in tauopathies, encompassing variants of frontotemporal lobar degeneration (FTLD) and Alzheimer's disease (AD). Tau proteolytically cleaved by active caspases, including caspase-6, may be neurotoxic and prone to self-aggregation. Also, our recent findings show that caspase-6 truncated tau represents a frequent and understudied aspect of tau pathology in AD in addition to phospho-tau pathology. In AD and Pick's disease, a large percentage of caspase-6 associated cleaved-tau positive neurons lack phospho-tau, suggesting that many vulnerable neurons to tau pathology go undetected when using conventional phospho-tau antibodies and possibly will not respond to "],"journal":["Molecular and cellular neurosciences"],"pubmed_title":["iPSC-induced neurons with the V337M MAPT mutation are selectively vulnerable to caspase-mediated cleavage of tau and apoptotic cell death."],"pmcid":["PMC11866097"],"funding_grant_id":["K24 AG053435","R01 AG054025","R56 AG057528","RF1 AG068125","P30 AG062422","P50 AG023501","P01 AG019724","U54 NS100717","R01 AG075802","K01 AG053433","U54 NS123746"],"pubmed_authors":["Miller BL","Kayed R","Arkin MR","Theofilas P","Wang C","Butler D","Grinberg LT","Petersen C","Ng R","Chin B","Temple S","Karch CM","Gestwicki JE","Gan L","Morales DO","Ambrose A","Yang T","Khan S"],"additional_accession":[]},"is_claimable":false,"name":"iPSC-induced neurons with the V337M MAPT mutation are selectively vulnerable to caspase-mediated cleavage of tau and apoptotic cell death.","description":"<h4>Background</h4>Tau post-translational modifications (PTMs) result in the gradual build-up of abnormal tau and neuronal degeneration in tauopathies, encompassing variants of frontotemporal lobar degeneration (FTLD) and Alzheimer's disease (AD). Tau proteolytically cleaved by active caspases, including caspase-6, may be neurotoxic and prone to self-aggregation. Also, our recent findings show that caspase-6 truncated tau represents a frequent and understudied aspect of tau pathology in AD in addition to phospho-tau pathology. In AD and Pick's disease, a large percentage of caspase-6 associated cleaved-tau positive neurons lack phospho-tau, suggesting that many vulnerable neurons to tau pathology go undetected when using conventional phospho-tau antibodies and possibly will not respond to ","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Sep","modification":"2026-05-28T22:23:25.225Z","creation":"2026-04-08T03:19:22.941Z"},"accession":"S-EPMC11866097","cross_references":{"pubmed":["39032719"],"doi":["10.1016/j.mcn.2024.103954"]}}