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P4‐002: AN INDUCIBLE MURINE MODEL OF TAU PHOSPHORYLATION
Author(s) -
Havas Daniel,
Mitrovic Martina,
Schweinzer Cornelia,
HutterPaier Birgit
Publication year - 2014
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.2014.05.1516
Subject(s) - phosphorylation , dephosphorylation , pentobarbital , serine , threonine , kinase , tau protein , chemistry , microbiology and biotechnology , neuroscience , pharmacology , biochemistry , phosphatase , biology , medicine , alzheimer's disease , disease
Daniel Havas, Martina Mitrovic, Cornelia Schweinzer, Birgit Hutter-Paier QPS Austria, Parkring 12, 8074 Grambach, Austria Background Aggregates of hyperphosphorylated Tau protein are characteristics of tauopathies and many other neurodegenerative diseases (ND). The physiological role of Tau in the central nervous systems (CNS) is the assembly and stability of microtubuli, a process that requires a homeostatic balance between kinase phosphorylation and phosphatase dephosphorylation. Hyperphosphorylated Tau has been shown to dissociate from microtubuli, resulting in the breakdown of the axonal flow, impaired neuronal viability and function. Since Tau presents a promising target for e.g. kinase inhibitors, an inducible model of Tau phosphorylation would be a useful tool for studying CNS drug effects.