期刊
DNA AND CELL BIOLOGY
卷 34, 期 4, 页码 261-273出版社
MARY ANN LIEBERT, INC
DOI: 10.1089/dna.2014.2757
关键词
-
资金
- Fundacao para a Ciencia e a Tecnologia [SFRH/BPD/84163/2012, SFRH/BPD/34712/2007]
- Alzheimer's Association [NIRG-13-282387]
- Fundação para a Ciência e a Tecnologia [SFRH/BPD/34712/2007, SFRH/BPD/84163/2012] Funding Source: FCT
Autophagy is a housekeeping process responsible for the bulk degradation of misfolded protein aggregates and damaged organelles through the lysosomal machinery. Given its key role as a cellular quality control mechanism, autophagy is now a focus of intense scrutiny in Alzheimer's disease (AD). The hallmarks of this devastating neurodegenerative disease are the accumulation of misfolded amyloid-beta (A beta) peptide and hyperphosphorylated tau protein and neuronal loss, which are accompanied by mitochondrial dysfunction and endoplasmic reticulum (ER) stress, suggesting that faulty autophagy is a contributing factor to AD pathology. Indeed, the AD brain is characterized by a massive accumulation of autophagic vacuoles within large swellings along dystrophic neurites and defects at different steps of the autophagic-lysosomal pathway. In this sense, this review provides an overview on the role of autophagy on A beta metabolism, tau processing and clearance, and the contribution of ER-phagy and mitophagy to AD pathology. From a therapeutic perspective, this review also intends to clarify whether, when, and how autophagy can be targeted to efficaciously counteract AD-related symptomatic and neuropathological features.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据