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P1‐238: THE EFFECT OF REPETITIVE MILD TRAUMATIC BRAIN INJURY ON TAU PATHOLOGY
Author(s) -
Edwards George A.,
Dinamarca Nicolas Mendez,
Soto Claudio,
Moreno-Gonzalez Ines
Publication year - 2018
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.2018.06.243
Subject(s) - chronic traumatic encephalopathy , tauopathy , traumatic brain injury , medicine , neuroscience , tau protein , concussion , pathology , psychology , disease , neurodegeneration , alzheimer's disease , psychiatry , poison control , injury prevention , environmental health
than the number of p-Tau+ neurons does (Table 1). The frequencies of PTMs, the percent overlap between PTMs, and significance of difference between early and late Braak stages are depicted in Table 2. Conclusions:Caspase-6 cleavage at Asp401 facilitates the formation of paired helical filaments (PHF). The PTMs that trigger this caspase activity are unclear. These data suggest that acetylation of tau at Lys274 correlates better with cleavage by caspase-6 than phosphorylation of tau at Ser202/Thr205 does. While there is colocalization between p-Tau and c-Tau, the majority of neurons positive for both p-Tau and c-Tau are also positive for a-Tau, suggesting that caspase-mediated cleavage of tau in these neuronsmay be primarily induced by acetylation, rather than phosphorylation. These preliminary data highlight that the acetylation of tau represents a key step in AD pathobiology and warrants further study.