Alzheimer disease.

Alzheimer disease.
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DOI:
10.1038/s41572-021-00269-y
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发表时间:
2021-05-13
期刊:
Nature reviews. Disease primers
影响因子:
--
通讯作者:
Jones DT
Jones DT
中科院分区:
其他
文献类型:
--
作者:
Knopman DS;Amieva H;Petersen RC;Chételat G;Holtzman DM;Hyman BT;Nixon RA;Jones DT

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阿尔茨海默病(AD)在生物学上被定义为存在含β-淀粉样蛋白的斑和含tau蛋白的神经元缠结。AD是一种遗传性和散发性神经退行性疾病,在其原型表现中引起遗忘性认知障碍,在其不太常见的变体中引起非遗忘性认知障碍。AD是中年和晚年获得性认知障碍的常见原因,但其临床影响会因其他神经退行性疾病和脑血管疾病而改变。本《引物》认为AD生物学是一种脑部疾病,由高度相关的内体/溶酶体清除途径中突触稳态丧失和功能障碍的复杂相互作用引起,其中Aβ和tau的前体、聚集物质和代谢后修饰产物发挥重要作用。治疗努力仍在努力寻找在此框架内的目标,大大改变AD患者的临床过程。
Alzheimer disease (AD) is biologically defined by the presence of β-amyloid-containing plagues and tau-containing neurofibrillary tangles. AD is a genetic and sporadic neurodegenerative disease that causes an amnestic cognitive impairment in its prototypical presentation and non-amnestic cognitive impairment in its less common variants. AD is a common cause of cognitive impairment acquired in midlife and late-life but its clinical impact is modified by other neurodegenerative and cerebrovascular conditions. This Primer conceives of AD biology as the brain disorder that results from a complex interplay of loss of synaptic homeostasis and dysfunction in the highly interrelated endosomal/lysosomal clearance pathways in which the precursors, aggregated species and post-translationally modified products of Aβ and tau play important roles. Therapeutic endeavours are still struggling to find targets within this framework that substantially change the clinical course in persons with AD.
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