自噬
老年斑
τ蛋白
发病机制
细胞内
β淀粉样蛋白
疾病
蛋白质聚集
机制(生物学)
医学
痴呆
淀粉样蛋白(真菌学)
细胞生物学
神经科学
阿尔茨海默病
生物
病理
生物化学
细胞凋亡
哲学
认识论
作者
Yuan Zhao,Yidan Zhang,Jian Zhang,Xiangjian Zhang,Guofeng Yang
标识
DOI:10.2174/1570159x18666200114163636
摘要
: Alzheimer’s disease (AD) is a neurodegenerative disorder of progressive dementia that is characterized by the accumulation of beta-amyloid (Aβ)-containing neuritic plaques and intracellular Tau protein tangles. This distinctive pathology indicates that the protein quality control is compromised in AD. Autophagy functions as a “neuronal housekeeper” that eliminates aberrant protein aggregates by wrapping then into autophagosomes and delivering them to lysosomes for degradation. Several studies have suggested that autophagy deficits in autophagy participate in the accumulation and propagation of misfolded proteins (including Aβ and Tau). In this review, we summarize current knowledge of autophagy in the pathogenesis of AD, as well as some pathways targeting the restoration of autophagy. Moreover, we discuss how these aspects can contribute to the development of disease-modifying therapies in AD.
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