Recent progress in the role of autophagy in neurological diseases

Authors:

Tian Meng1,#, Shiyin Lin1,#, Haixia Zhuang1, Haofeng Huang2, Zhengjie He1, Yongquan Hu1, Qing Gong3 and Du Feng1

Affiliations:

1 State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University; Affiliated Cancer Hospital of Guangzhou Medical University, Guangzhou 511436, China.

2 Institute of Neurology, Guangdong Key Laboratory of Age-Related Cardiac-Cerebral Vascular Disease, Affiliated Hospital of Guangdong Medical College, Zhanjiang, Guangdong, China.

3 Department of Biochemistry and Molecular Biology, GMU-GIBH Joint School of Life Sciences, Guangzhou Medical University, Guangzhou 511436, People’s Republic of China.

# These authors contributed equally to this work.

Keywords: 

autophagy, neuro-degenerative diseases, mTOR, Parkinson’s disease, Alzheimer’s disease, Huntington’s disease, Amyotrophic lateral sclerosis.

Abbreviatons:

Aβ – amyloid beta,

AD – Alzheimer’s disease,

ALS – amyotrophic lateral sclerosis,

AMPK – AMP-activated protein kinase,

APP – amyloid precursor protein,

ATG – autophagy related,

AV – autophagic vacuole,

C9ORF72 – Chromosome 9 open reading frame 72,

CMA – chaperone-mediated autophagy,

CTF – C-terminal fragment,

ESCRT – endosomal sorting complexes required for transport,

FTD – frontotemporal dementia,

HD – Huntington’s disease,

HTT – huntingtin,

mHTT – mutant HTT,

mTOR – mammalian target of rapamycin,

MVB – multi-vesicular body,

PD – Parkinson’s disease,

PI3K – phosphatidyl inositol 3-kinase, polyQ – poly-glutamine,

VCP – valosin-containing protein.

Corresponding Author(s):

Dr. Du Feng, State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University; Affiliated Cancer Hospital of Guangzhou Medical University, Guangzhou 511436, China feng_du@foxmail.com

Conflict of interest statement:

The authors declare that they have no conflict of inter-ests.

Please cite this article as:

Tian Meng, Shiyin Lin, Haixia Zhuang, Haofeng Huang, Zhengjie He, Yongquan Hu, Qing Gong and Du Feng (2019). Re-cent progress in the role of autophagy in neurological diseases. Cell Stress 3(5): 141-161. doi: 10.15698/cst2019.05.186

© 2019 Meng et al. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduc-tion in any medium, provided the original author and source are acknowledged.

Abstract:

Autophagy (here refers to macroautophagy) is a catabolic pathway by which large protein aggregates and damaged organelles are first sequestered into a double-membraned structure called autophagosome and then delivered to lysosome for destruction. Recently, tremendous progress has been made to elucidate the molecular mechanism and functions of this essential cellular metabolic process. In addition to being either a rubbish clearing system or a cellular surviving program in response to different stresses, autophagy plays important roles in a large number of pathophysiological conditions, such as cancer, diabetes, and especially neurodegenerative disorders. Here we review recent progress in the role of autophagy in neurological diseases and discuss how dysregulation of autophagy initiation, autophagosome formation, maturation, and/or autophagosome-lysosomal fusion step contributes to the pathogenesis of these disorders in the nervous system.