Mechanisms of neurodegeneration in an animal model of tauopathies

将tau转基因小鼠(PrP T44)与Calastatin基因敲除小鼠(CS-KO)杂交，观察calain-calastatin通路对tau基因过表达所致神经退行性变的影响。在PrP T44小鼠中，calastatin的缺失导致行为症状和病理生化改变的加速，表明calain-calastatin通路参与了tau过表达所致的小鼠中枢神经系统的神经退行性变。这项研究结果的潜在机制仍有待进一步调查阐明。

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.