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首页> 外文期刊>Molecular Neurodegeneration >Drosophila melanogaster as a model organism for Alzheimer’s disease
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Drosophila melanogaster as a model organism for Alzheimer’s disease

机译：果蝇（Drosophila melanogaster）是阿尔茨海默氏病的模型生物

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Drosophila melanogaster provides an important resource for in vivo modifier screens of neurodegenerative diseases. To study the underlying pathogenesis of Alzheimer’s disease, fly models that address Tau or amyloid toxicity have been developed. Overexpression of human wild-type or mutant Tau causes age-dependent neurodegeneration, axonal transport defects and early death. Large-scale screens utilizing a neurodegenerative phenotype induced by eye-specific overexpression of human Tau have identified several kinases and phosphatases, apoptotic regulators and cytoskeleton proteins as determinants of Tau toxicity in vivo. The APP ortholog of Drosophila (dAPPl) shares the characteristic domains with vertebrate APP family members, but does not contain the human Aβ42 domain. To circumvent this drawback, researches have developed strategies by either direct secretion of human Aβ42 or triple transgenic flies expressing human APP, β-secretase and Drosophila γ-secretase presenilin (dPsn). Here, we provide a brief overview of how fly models of AD have contributed to our knowledge of the pathomechanisms of disease.
机译：果蝇为神经退行性疾病的体内修饰剂筛选提供了重要资源。为了研究阿尔茨海默氏病的潜在发病机理，已开发出解决Tau或淀粉样蛋白毒性的飞行模型。人类野生型或突变型Tau的过度表达会导致年龄依赖性神经变性，轴突运输缺陷和早期死亡。大规模筛选利用人类Tau的眼睛特异性过表达诱导的神经变性表型，已经确定了几种激酶和磷酸酶，凋亡调节剂和细胞骨架蛋白作为Tau体内毒性的决定因素。果蝇的APP直系同源物（dAPP1）与脊椎动物APP家族成员共享特征结构域，但不包含人Aβ42结构域。为了克服这一缺点，研究人员开发了通过直接分泌人Aβ42或表达人APP，β-分泌酶和果蝇γ-分泌酶早老素（dPsn）的三重转基因果蝇的策略。在此，我们简要概述了AD的飞行模型如何促进我们对疾病发病机理的了解。

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