| Literature DB >> 32161412 |
Nicolas R Barthélemy1, Yan Li1,2, Nelly Joseph-Mathurin3, Brian A Gordon3, Jason Hassenstab1, Tammie L S Benzinger3, Virginia Buckles1, Anne M Fagan1, Richard J Perrin4, Alison M Goate5, John C Morris1, Celeste M Karch6, Chengjie Xiong2, Ricardo Allegri7, Patricio Chrem Mendez7, Sarah B Berman8, Takeshi Ikeuchi9, Hiroshi Mori10, Hiroyuki Shimada10, Mikio Shoji11, Kazushi Suzuki12, James Noble13, Martin Farlow14, Jasmeer Chhatwal15, Neill R Graff-Radford16, Stephen Salloway17,18, Peter R Schofield19,20, Colin L Masters21,22, Ralph N Martins23, Antoinette O'Connor24, Nick C Fox24, Johannes Levin25,26,27, Mathias Jucker28,29, Audrey Gabelle30, Sylvain Lehmann30, Chihiro Sato1, Randall J Bateman31, Eric McDade32.
Abstract
Development of tau-based therapies for Alzheimer's disease requires an understanding of the timing of disease-related changes in tau. We quantified the phosphorylation state at multiple sites of the tau protein in cerebrospinal fluid markers across four decades of disease progression in dominantly inherited Alzheimer's disease. We identified a pattern of tau staging where site-specific phosphorylation changes occur at different periods of disease progression and follow distinct trajectories over time. These tau phosphorylation state changes are uniquely associated with structural, metabolic, neurodegenerative and clinical markers of disease, and some (p-tau217 and p-tau181) begin with the initial increases in aggregate amyloid-β as early as two decades before the development of aggregated tau pathology. Others (p-tau205 and t-tau) increase with atrophy and hypometabolism closer to symptom onset. These findings provide insights into the pathways linking tau, amyloid-β and neurodegeneration, and may facilitate clinical trials of tau-based treatments.Entities:
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Year: 2020 PMID: 32161412 PMCID: PMC7309367 DOI: 10.1038/s41591-020-0781-z
Source DB: PubMed Journal: Nat Med ISSN: 1078-8956 Impact factor: 53.440