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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Overexpression of SOD-2 reduces hippocampal superoxide and prevents memory deficits in a mouse model of Alzheimer's disease
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Overexpression of SOD-2 reduces hippocampal superoxide and prevents memory deficits in a mouse model of Alzheimer's disease

机译：SOD-2的过度表达可降低海默症模型的海马结构并预防记忆缺陷

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Alzheimer's disease (AD) is a neurodegenerative disease characterized by impaired cognitive function and the deposition of extracellular amyloid plaques and intracellular tangles. Although the proximal cause of AD is not well understood, it is clear that amyloid-β (Aβ) plays a critical role in AD pathology. Recent studies also implicate mitochondrial abnormalities in AD. We investigated this idea by crossing mice that overexpress mitochondrial super-oxide dismutase (SOD-2) with the Tg2576 mouse model of AD that overexpresses the humn amyloid precursor protein carrying the Swedish mutation (K670N:M671L). We found that overexpression of SOD-2 decreased hippocampal superoxide, prevented AD-re-lated learning and memory deficits, and reduced Aβ plaques. Interestingly, SOD-2 overexpression did not affect the absolute levels of Aβ_(1-40) and Aβ_(1-42), but did significantly reduce the Aβ_(1-42) to Aβ_(1-40) ratio, thereby shifting the balance toward a less amy-loidogenic Aβ composition. These findings directly link mitochondrial superoxide to AD pathology and demonstrate the beneficial effects of a mitochondrial anti-oxidant enzyme, hence offering significant therapeutic implications for AD.
机译：阿尔茨海默氏病（AD）是一种神经退行性疾病，其特征在于认知功能受损以及细胞外淀粉样斑块和细胞内缠结的沉积。尽管尚不清楚AD的近端原因，但很明显，淀粉样β（Aβ）在AD病理中起着关键作用。最近的研究还暗示了AD中的线粒体异常。我们通过过表达线粒体超氧化物歧化酶（SOD-2）的小鼠与过表达携带瑞典突变（K670N：M671L）的腐殖淀粉样前体蛋白的AD Tg2576小鼠模型杂交来研究这一想法。我们发现SOD-2的过度表达减少了海马超氧化物歧化酶，防止了AD相关的学习和记忆缺陷，并减少了Aβ斑块。有趣的是，SOD-2的过表达不会影响Aβ_（1-40）和Aβ_（1-42）的绝对水平，但会显着降低Aβ_（1-42）与Aβ_（1-40）的比率，从而改变平衡，以减少淀粉样蛋白生成的Aβ组成。这些发现直接将线粒体超氧化物与AD病理联系起来，并证明了线粒体抗氧化酶的有益作用，因此对AD具有重要的治疗意义。

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