Mechanisms of neurodegeneration in an animal model of tauopathies

将Tau转基因小鼠（PrP T44）与钙蛋白酶抑制蛋白基因敲除小鼠（CS-KO）杂交，以研究钙蛋白酶-钙蛋白酶抑制蛋白通路对与Tau过表达相关的神经变性的影响。在PrP T44小鼠中缺失calpastatin导致行为症状和病理生化变化的加速，表明calpain-calpastatin通路参与tau蛋白过表达诱导的小鼠中枢神经系统神经退行性变。本研究结果的潜在机制仍有待进一步研究阐明。

Tau transgenic mice (PrP T44) were crossbred with calpastatin knock-out mice (CS-KO) to investigate the influence of calpain-calpastatin pathway on neurodegeneration related to tau overexpression. Deletion of calpastatin in PrP T44 mice resulted in acceleration of behavioral symptoms and pathological and biochemical changes, indicating that calpain-calpastatin pathway is involved in the neurodegeneration induced by tau overexpression in the central nervous system in mice. The underlying mechanisms of the findings in this study remain to be elucidated by further investigations.