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首页> 外文期刊>Magnetic Resonance Insights >Improvements in a Mouse Model of Alzheimer’s Disease Through SOD2 Overexpression are Due to Functional and Not Structural Alterations
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Improvements in a Mouse Model of Alzheimer’s Disease Through SOD2 Overexpression are Due to Functional and Not Structural Alterations

机译：通过SOD2过表达改善阿尔茨海默氏病小鼠模型的原因是功能性改变而非结构性改变

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Oxidative stress and mitochondrial dysfunction have been implicated in the pathogenesis of Alzheimer’s disease. We and others have shown that over expression of the mitochondrial antioxidant superoxide dismutase 2 (SOD-2) can improve many of the pathologies in the Tg2576 mouse model of Alzheimer’s disease that harbors the Swedish mutation in the amyloid precursor protein. However, it is not clear if these improvements are due to functional improvements or structural/anatomical changes. To answer this question, we used diffusion tensor imaging (DTI) to assess the structural integrity of white matter tracts in the control mice, Tg2576 mouse and Tg2576 mice over expressing SOD-2. We observed minimal differences in diffusion parameters with SOD-2 over expression in this model indicating that the improvements we previously reported are due to functional changes and not any alterations to the white matter tractography.
机译：氧化应激和线粒体功能障碍与阿尔茨海默氏病的发病机理有关。我们和其他人已表明，线粒体抗氧化剂超氧化物歧化酶2（SOD-2）的过度表达可以改善阿尔茨海默氏病Tg2576小鼠模型的许多病理，该模型在淀粉样蛋白前体蛋白中具有瑞典语突变。但是，尚不清楚这些改进是否归因于功能改进或结构/解剖学变化。为了回答这个问题，我们使用扩散张量成像（DTI）来评估过表达SOD-2的对照小鼠，Tg2576小鼠和Tg2576小鼠中白质束的结构完整性。我们观察到该模型中SOD-2过表达的扩散参数差异最小，这表明我们先前报道的改善归因于功能变化，而不是白质束层照相术的任何改变。

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