Microglial autophagy in Alzheimer's disease and Parkinson's disease

被引:20
作者
Wang, Zhifu [1 ]
Wang, Qi [1 ]
Li, Shihua [1 ]
Li, Xiao-Jiang [1 ]
Yang, Weili [1 ]
He, Dajian [1 ]
机构
[1] Jinan Univ, Guangdong Hongkong Macau Inst CNS Regenerat, Guangdong Key Lab Nonhuman Primate Res, Guangzhou, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
neurodegeneration; microglia; autophagy; AD; PD; AMYLOID-BETA PEPTIDE; NLRP3 INFLAMMASOME ACTIVATION; NECROSIS-FACTOR-ALPHA; DOPAMINERGIC NEURODEGENERATION; REACTIVE MICROGLIA; NEURONAL DEATH; TAU PATHOLOGY; GROWTH-FACTOR; CLEARANCE; BRAIN;
D O I
10.3389/fnagi.2022.1065183
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
Alzheimer's disease (AD) and Parkinson's disease (PD) are the most common neurodegenerative diseases, characterized by gradual and selective loss of neurons in the central nervous system. They affect more than 50 million people worldwide, and their incidence increases with age. Although most cases of AD and PD are sporadic, some are caused by genetic mutations that are inherited. Both sporadic and familial cases display complex neuropathology and represent the most perplexing neurological disorders. Because of the undefined pathogenesis and complex clinical manifestations, there is still no effective treatment for both AD and PD. Understanding the pathogenesis of these important neurodegenerative diseases is important for developing successful therapies. Increasing evidence suggests that microglial autophagy is associated with the pathogenesis of AD and PD, and its dysfunction has been implicated in disease progression. In this review, we focus on the autophagy function in microglia and its dysfunction in AD and PD disease models in an attempt to help our understanding of the pathogenesis and identifying new therapeutic targets of AD and PD.
引用
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页数:12
相关论文
共 165 条
[1]  
Abiega O, 2016, PLOS BIOL, V14, DOI [10.1371/journal.pbio.1002508, 10.1371/journal.pbio.1002554, 10.1371/journal.pbio.1002466]
[2]   Andrographolide suppresses NLRP3 inflammasome activation in microglia through induction of parkin-mediated mitophagy in in-vitro and in-vivo models of Parkinson disease [J].
Ahmed, Sahabuddin ;
Kwatra, Mohit ;
Panda, Samir Ranjan ;
Murty, U. S. N. ;
Naidu, V. G. M. .
BRAIN BEHAVIOR AND IMMUNITY, 2021, 91 :142-158
[3]   Immune function of microglia [J].
Aloisi, F .
GLIA, 2001, 36 (02) :165-179
[4]   Hyperphosphorylation of Tau Associates With Changes in Its Function Beyond Microtubule Stability [J].
Alonso, Alejandra D. ;
Cohen, Leah S. ;
Corbo, Christopher ;
Morozova, Viktoriya ;
ElIdrissi, Abdeslem ;
Phillips, Greg ;
Kleiman, Frida E. .
FRONTIERS IN CELLULAR NEUROSCIENCE, 2018, 12
[5]  
Anglade P, 1997, HISTOL HISTOPATHOL, V12, P25
[6]   Depletion of microglia and inhibition of exosome synthesis halt tau propagation [J].
Asai, Hirohide ;
Ikezu, Seiko ;
Tsunoda, Satoshi ;
Medalla, Maria ;
Luebke, Jennifer ;
Haydar, Tank ;
Wolozin, Benjamin ;
Butovsky, Oleg ;
Kuegler, Sebastian ;
Ikezu, Tsuneya .
NATURE NEUROSCIENCE, 2015, 18 (11) :1584-1593
[7]   The Contribution of Microglia to Neuroinflammation in Parkinson's Disease [J].
Badanjak, Katja ;
Fixemer, Sonja ;
Smajic, Semra ;
Skupin, Alexander ;
Gruenewald, Anne .
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 2021, 22 (09)
[8]   Targeting NLRP3-Mediated Neuroinflammation in Alzheimer's Disease Treatment [J].
Barczuk, Julia ;
Siwecka, Natalia ;
Lusa, Weronika ;
Rozpedek-Kaminska, Wioletta ;
Kucharska, Ewa ;
Majsterek, Ireneusz .
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 2022, 23 (16)
[9]   Microglia modulate neurodegeneration in Alzheimer's and Parkinson's diseases [J].
Bartels, Tim ;
De Schepper, Sebastiaan ;
Hong, Soyon .
SCIENCE, 2020, 370 (6512) :66-+
[10]  
Beraud Dawn, 2012, Parkinsonism Relat Disord, V18 Suppl 1, pS17, DOI 10.1016/S1353-8020(11)70008-6