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The ordered assembly of tau is the gain‐of‐toxic function that causes human tauopathies
Author(s) -
Goedert Michel
Publication year - 2016
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2016.09.001
Subject(s) - neurodegeneration , fibril , function (biology) , gain of function , tau protein , neuroscience , tauopathy , tau pathology , disease , chemistry , biology , biophysics , microbiology and biotechnology , alzheimer's disease , biochemistry , medicine , pathology , phenotype , gene
A pathological pathway leading from soluble to insoluble and filamentous tau underlies human tauopathies. This ordered assembly causes disease and is the gain‐of‐toxic function. It involves the transition from an intrinsically disordered monomer to a highly structured filament. Based on recent findings, one can divide the ordered assembly into propagation of pathology and neurodegeneration. Short tau fibrils constitute the major species of seed‐competent tau in the brains of mice transgenic for human P301S tau. The molecular species of aggregated tau that are essential for neurodegeneration remain to be identified.