Targeting Aggrephagy for the Treatment of Alzheimer's Disease

Alzheimer's disease (AD) is one of the most common neurodegenerative diseases in older individuals with specific neuropsychiatric symptoms. It is a proteinopathy, pathologically characterized by the presence of misfolded protein (Aβ and Tau) aggregates in the brain, causing progressive dementia...

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Published in:	Cells (Basel, Switzerland) Vol. 9; no. 2; p. 311
Main Authors:	Malampati, Sandeep, Song, Ju-Xian, Chun-Kit Tong, Benjamin, Nalluri, Anusha, Yang, Chuan-Bin, Wang, Ziying, Gopalkrishnashetty Sreenivasmurthy, Sravan, Zhu, Zhou, Liu, Jia, Su, Chengfu, Krishnamoorthi, Senthilkumar, Iyaswamy, Ashok, Cheung, King-Ho, Lu, Jia-Hong, Li, And Min
Format:	Journal Article
Language:	English
Published:	Switzerland MDPI 28-01-2020 MDPI AG
Subjects:	aggregates aggrephagy Alzheimer Disease - pathology Alzheimer Disease - physiopathology Alzheimer Disease - therapy alzheimer’s disease Animals Humans Lysosomes - metabolism Macroautophagy Molecular Targeted Therapy Protein Folding Review selective autophagy TOR Serine-Threonine Kinases - antagonists & inhibitors TOR Serine-Threonine Kinases - metabolism aggregates Alzheimer’s disease aggrephagy selective autophagy
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Summary:	Alzheimer's disease (AD) is one of the most common neurodegenerative diseases in older individuals with specific neuropsychiatric symptoms. It is a proteinopathy, pathologically characterized by the presence of misfolded protein (Aβ and Tau) aggregates in the brain, causing progressive dementia. Increasing studies have provided evidence that the defect in protein-degrading systems, especially the autophagy-lysosome pathway (ALP), plays an important role in the pathogenesis of AD. Recent studies have demonstrated that AD-associated protein aggregates can be selectively recognized by some receptors and then be degraded by ALP, a process termed aggrephagy. In this study, we reviewed the role of aggrephagy in AD development and discussed the strategy of promoting aggrephagy using small molecules for the treatment of AD.
Bibliography:	ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1
ISSN:	2073-4409 2073-4409
DOI:	10.3390/cells9020311