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首页> 外文期刊>Neurobiology of disease >Tauroursodeoxycholic acid (TUDCA) supplementation prevents cognitive impairment and amyloid deposition in APP/PS1 mice
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Tauroursodeoxycholic acid (TUDCA) supplementation prevents cognitive impairment and amyloid deposition in APP/PS1 mice

机译：牛磺去氧胆酸（TUDCA）补充可预防APP / PS1小鼠的认知障碍和淀粉样蛋白沉积

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Alzheimer's disease (AD) is a neurodegenerative disease hallmarked by extracellular Aβ1-42 containing plaques, and intracellular neurofibrillary tangles (NFT) containing hyperphosphorylated tau protein. Progressively, memory deficits and cognitive disabilities start to occur as these hallmarks affect hippocampus and frontal cortex, regions highly involved in memory. Connective tissue growth factor (CTGF) expression, which is high in the vicinity of Aβ plaques and NFTs, was found to influence γ-secretase activity, the molecular crux in Aβ1-42 production. Tauroursodeoxycholic acid (TUDCA) is an endogenous bile acid that downregulates CTGF expression in hepatocytes and has been shown to possess therapeutic efficacy in neurodegenerative models. To investigate the possible in vivo therapeutic effects of TUDCA, we provided 0.4% TUDCA-supplemented food to APP/PS1 mice, a well-established AD mouse model. Six months of TUDCA supplementation prevented the spatial, recognition and contextual memory defects observed in APP/PS1 mice at 8months of age. Furthermore, TUDCA-supplemented APP/PS1 mice displayed reduced hippocampal and prefrontal amyloid deposition. These effects of TUDCA supplementation suggest a novel mechanistic route for Alzheimer therapeutics.
机译：阿尔茨海默氏病（AD）是一种神经退行性疾病，其特征在于含有细胞外Aβ1-42的噬菌斑和含有高磷酸化tau蛋白的细胞内神经原纤维缠结（NFT）。随着这些标志影响海马和额叶皮层（高度参与记忆的区域），逐渐出现记忆缺陷和认知障碍。发现结缔组织生长因子（CTGF）表达在Aβ斑块和NFTs附近较高，可影响γ-分泌酶活性，这是Aβ1-42产生的分子关键。牛磺去氧胆酸（TUDCA）是一种内源性胆汁酸，可下调肝细胞中CTGF的表达，在神经退行性模型中已显示出治疗功效。为了研究TUDCA的可能的体内治疗作用，我们向完善的AD小鼠模型APP / PS1小鼠提供了0.4％TUDCA补充的食物。补充六个月的TUDCA可以防止在8个月大时在APP / PS1小鼠中观察到空间，识别和情境记忆缺陷。此外，补充了TUDCA的APP / PS1小鼠显示出减少的海马和前额淀粉样蛋白沉积。 TUDCA补充剂的这些作用提示了阿尔茨海默氏症治疗药物的新机制。

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