Mechanisms of neurodegeneration in an animal model of tauopathies

tau蛋白病动物模型中神经变性的机制

• 批准号: 18590942
• 负责人: ISHIHARA Takeshi
• 金额: $ 2.41万
• 依托单位: Okayama University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2006
• 资助国家: 日本
• 起止时间: 2006 至 2007
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-18590942/
• 关键词: tau; tauopathies; neurodegeneration; calpain-calpastatin pathway; mouse models; Alzheimer's disease; タウ蛋白; 神経変性疾患; 動物モデル; カルパイン; カルパスタチン

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.

将Tau转基因小鼠（PrP T44）与calpastatin敲除小鼠（CS-KO）杂交，研究calpain-calpastatin通路对Tau过表达相关神经退行性变的影响。PrP T44小鼠中calpastatin缺失导致行为症状加速，病理生化变化加快，提示calpain-calpastatin通路参与了小鼠中枢神经系统tau过表达引起的神经退行性变。本研究结果的潜在机制有待进一步研究阐明。