（原文中“of”后面缺少具体内容，无法准确完整翻译，仅按字面翻译为）在阿尔茨海默病中的作用。
The role of in Alzheimer's disease.
作者信息
Li Quan, Wang Bai-Ling, Sun Fu-Rong, Li Jie-Qiong, Cao Xi-Peng, Tan Lan
机构信息
Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao 266071, China.
Department of Geriatrics, Qingdao Mental Health Center, Qingdao 266034, China.
出版信息
Ann Transl Med. 2018 May;6(10):178. doi: 10.21037/atm.2018.04.43.
Alzheimer's disease (AD) is a chronic progressive neurodegenerative disease in adults characterized by the deposition of extracellular plaques of β-amyloid protein (Aβ), intracellular neurofibrillary tangles (NFTs), synaptic loss and neuronal apoptosis. AD has a strong and complex genetic component that involving into multiple genes. With recent advances in whole-exome sequencing (WES) and whole-genome sequencing (WGS) technology, was identified to have association with AD. Emerging studies on cell and animal models identified that aberrant may contribute to AD by activating death-associated protein kinase 1 (DAPK1) which is a new component involved in AD pathogenesis with an extensive involvement in aberrant tau, Aβ and neuronal apoptosis/autophagy. In this review, we briefly summarize the biochemical properties, genetics, epigenetics, and the speculative role of in AD. We hope our review would bring comprehensive understandings of AD pathogenesis and provide new therapeutic targets for AD.
阿尔茨海默病（AD）是一种成人慢性进行性神经退行性疾病，其特征在于细胞外β-淀粉样蛋白（Aβ）斑块沉积、细胞内神经原纤维缠结（NFTs）、突触丧失和神经元凋亡。AD具有强大而复杂的遗传成分，涉及多个基因。随着全外显子组测序（WES）和全基因组测序（WGS）技术的最新进展，已确定其与AD有关联。关于细胞和动物模型的新兴研究表明，异常的[此处原文缺失具体内容]可能通过激活死亡相关蛋白激酶1（DAPK1）而导致AD，DAPK1是AD发病机制中的一个新成分，广泛参与异常的tau、Aβ和神经元凋亡/自噬。在本综述中，我们简要总结了[此处原文缺失具体内容]的生化特性、遗传学、表观遗传学以及在AD中的推测作用。我们希望我们的综述能带来对AD发病机制的全面理解，并为AD提供新的治疗靶点。
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