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  • Florey Department of Neuroscience and Mental Health
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    A soluble phosphorylated tau signature links tau, amyloid and the evolution of stages of dominantly inherited Alzheimer's disease

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    26
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    Author
    Barthelemy, NR; Li, Y; Joseph-Mathurin, N; Gordon, BA; Hassenstab, J; Benzinger, TLS; Buckles, V; Fagan, AM; Perrin, RJ; Goate, AM; ...
    Date
    2020-03-01
    Source Title
    Nature Medicine
    Publisher
    NATURE RESEARCH
    University of Melbourne Author/s
    Masters, Colin
    Affiliation
    Florey Department of Neuroscience and Mental Health
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Barthelemy, N. R., Li, Y., Joseph-Mathurin, N., Gordon, B. A., Hassenstab, J., Benzinger, T. L. S., Buckles, V., Fagan, A. M., Perrin, R. J., Goate, A. M., Morris, J. C., Karch, C. M., Xiong, C., Allegri, R., Mendez, P. C., Berman, S. B., Ikeuchi, T., Mori, H., Shimada, H. ,... Xu, X. (2020). A soluble phosphorylated tau signature links tau, amyloid and the evolution of stages of dominantly inherited Alzheimer's disease. NATURE MEDICINE, 26 (3), pp.398-+. https://doi.org/10.1038/s41591-020-0781-z.
    Access Status
    Access this item via the Open Access location
    URI
    http://hdl.handle.net/11343/254044
    DOI
    10.1038/s41591-020-0781-z
    Open Access URL
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7309367
    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.

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