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Specifically, three-repeat tau and four-repeat tau in Alzheimer\u2019s disease, three-repeat tau in Pick\u2019s disease (PiD) and four-repeat tau in progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) form amyloid-like fibrous structures that accumulate in neurons and\/or glial cells. Amplification and cell-to-cell transmission of abnormal tau based on the prion hypothesis are believed to explain the onset and progression of tauopathies. Recent studies support not only the self-propagation of abnormal tau, but also the presence of conformationally distinct tau aggregates, namely tau strains. Cryogenic electron microscopy analyses of patient-derived tau filaments have revealed disease-specific ordered tau structures. However, it remains unclear whether the ultrastructural and biochemical properties of tau strains are inherited during the amplification of abnormal tau in the brain. In this study, we investigated template-dependent amplification of tau aggregates using a cellular model of seeded aggregation. Tau strains extracted from human tauopathies caused strain-dependent accumulation of insoluble filamentous tau in SH-SY5Y cells. The seeding activity towards full-length four-repeat tau substrate was highest in CBD-tau seeds, followed by PSP-tau and Alzheimer\u2019s disease (AD)-tau seeds, while AD-tau seeds showed higher seeding activity than PiD-tau seeds towards three-repeat tau substrate. Abnormal tau amplified in cells inherited the ultrastructural and biochemical properties of the original seeds. These results strongly suggest that the structural differences of patient-derived tau strains underlie the diversity of tauopathies, and that seeded aggregation and filament formation mimicking the pathogenesis of sporadic tauopathy can be reproduced in cultured cells. Our results indicate that the disease-specific conformation of tau aggregates determines the tau isoform substrate that is recruited for templated amplification, and also influences the prion-like seeding activity.<\/jats:p>","DOI":"10.1093\/brain\/awab091","type":"journal-article","created":{"date-parts":[[2021,3,6]],"date-time":"2021-03-06T12:10:24Z","timestamp":1615032624000},"page":"2333-2348","source":"Crossref","is-referenced-by-count":42,"title":["Human tauopathy-derived tau strains determine the substrates recruited for templated amplification"],"prefix":"10.1093","volume":"144","author":[{"given":"Airi","family":"Tarutani","sequence":"first","affiliation":[{"name":"Department of Brain and Neurosciences, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan"},{"name":"Laboratory of Neuropathology and Neuroscience, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo 113-0033, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Haruka","family":"Miyata","sequence":"additional","affiliation":[{"name":"Department of Brain and Neurosciences, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0830-9403","authenticated-orcid":false,"given":"Takashi","family":"Nonaka","sequence":"additional","affiliation":[{"name":"Department of Brain and Neurosciences, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kazuko","family":"Hasegawa","sequence":"additional","affiliation":[{"name":"Division of Neurology, Sagamihara National Hospital, Kanagawa 252-0392, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mari","family":"Yoshida","sequence":"additional","affiliation":[{"name":"Department of Neuropathology, Institute for Medical Science of Aging, Aichi Medical University, Aichi 480-1195, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuko","family":"Saito","sequence":"additional","affiliation":[{"name":"Department of Neuropathology, Tokyo Metropolitan Institute of Gerontology, Tokyo 173-0015, Japan"},{"name":"Department of Pathology and Laboratory Medicine, National Center Hospital, National Center of Neurology and Psychiatry, Tokyo 187-8551, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shigeo","family":"Murayama","sequence":"additional","affiliation":[{"name":"Department of Neuropathology, Tokyo Metropolitan Institute of Gerontology, Tokyo 173-0015, Japan"},{"name":"Brain Bank for Neurodevelopmental, Neurological and Psychiatric Disorders, United Graduate School of Child Development, Osaka University, Osaka 565-0871, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew C","family":"Robinson","sequence":"additional","affiliation":[{"name":"Faculty of Biology, Medicine and Health, School of Biological Sciences, Division of Neuroscience and Experimental Psychology, The University of Manchester, Salford Royal Hospital, Salford M6 8HD, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David M A","family":"Mann","sequence":"additional","affiliation":[{"name":"Faculty of Biology, Medicine and Health, School of Biological Sciences, Division of Neuroscience and Experimental Psychology, The University of Manchester, Salford Royal Hospital, Salford M6 8HD, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0075-5943","authenticated-orcid":false,"given":"Taisuke","family":"Tomita","sequence":"additional","affiliation":[{"name":"Laboratory of Neuropathology and Neuroscience, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo 113-0033, 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