Wirths Oliver
Division of Molecular Psychiatry, Department of Psychiatry and Psychotherapy, University Medical Center (UMG), Georg-August-University, Göttingen, Germany.
Neurogenesis (Austin). 2017 May 9;4(1):e1327002. doi: 10.1080/23262133.2017.1327002. eCollection 2017.
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.
淀粉样β（Aβ）肽以及多种其他蛋白质片段，源自淀粉样前体蛋白（APP）的蛋白水解切割，并且已被证明在阿尔茨海默病（AD）潜在的病理变化中起关键作用。在AD小鼠模型中，神经发生改变已被反复报道与进一步的AD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Aβ在神经退行性变和神经元祖细胞增殖受损中具有毒性作用是可能且被广泛接受的，但最近的研究结果也表明，APP衍生的蛋白水解片段如APP细胞内结构域（AICD）以及APP本身具有重要影响。
