Altered neurogenesis in mouse models of Alzheimer disease.

Neurogenesis (Austin, Tex.) Pub Date : 2017-05-09 eCollection Date: 2017-01-01 DOI:10.1080/23262133.2017.1327002
Oliver Wirths
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引用次数: 37

Abstract

Amyloid-β (Aβ) peptides, as well as a variety of other protein fragments, are derived from proteolytical cleavage of the amyloid precursor protein (APP) and have been demonstrated to play a key role in the pathological changes underlying Alzheimer disease (AD). In AD mouse models, altered neurogenesis has been repeatedly reported to be associated with further AD-typical pathological hallmarks such as extracellular plaque deposition, behavioral deficits or neuroinflammation. While a toxic role of Aβ in neurodegeneration and impaired neuronal progenitor proliferation is likely and well-accepted, recent findings also suggest an important influence of APP-derived proteolitical fragments like the APP intracellular domain (AICD), as well as of APP itself.

Abstract Image

Abstract Image

阿尔茨海默病小鼠模型的神经发生改变。
淀粉样蛋白-β (a β)肽以及各种其他蛋白质片段来源于淀粉样蛋白前体蛋白(APP)的蛋白水解裂解,并已被证明在阿尔茨海默病(AD)的病理变化中发挥关键作用。在阿尔茨海默氏症小鼠模型中,神经发生改变已被反复报道与进一步的阿尔茨海默氏症典型病理特征相关,如细胞外斑块沉积、行为缺陷或神经炎症。虽然a β在神经退行性变和神经元祖细胞增殖受损中的毒性作用可能是公认的,但最近的研究结果也表明,APP衍生的蛋白政治片段(如APP胞内结构域(AICD))以及APP本身也有重要影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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