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Starvation induces tau hyperphosphorylation in mouse brain: implications for Alzheimer's disease
Author(s) -
Yanagisawa Masahiro,
Planel Emmanuel,
Ishiguro Koichi,
Fujita Shinobu C
Publication year - 1999
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(99)01480-5
Subject(s) - hyperphosphorylation , tauopathy , hippocampus , alzheimer's disease , neuroscience , dephosphorylation , phosphorylation , cerebral cortex , cerebellum , tau protein , pathogenesis , disease , biology , neurodegeneration , medicine , microbiology and biotechnology , phosphatase
Hyperphosphorylated tau is the major component of paired helical filaments in neurofibrillary tangles found in Alzheimer's disease brains, and tau hyperphosphorylation is thought to be a critical event in the pathogenesis of this disease. The objective of this study was to reproduce tau hyperphosphorylation in an animal model by inducing hypoglycemia. Food deprivation of mice for 1 to 3 days progressively enhanced tau hyperphosphorylation in the hippocampus, to a lesser extent in the cerebral cortex, but the effect was least in the cerebellum, in correspondence with the regional selectivity of tauopathy in Alzheimer's disease. This hyperphosphorylation was reversible by refeeding for 1 day. We discuss possible mechanisms of this phenomenon, and propose the starved mouse as a simple model to study in vivo tau phosphorylation and dephosphorylation which are altered in Alzheimer's disease.