期刊
NEURON
卷 110, 期 6, 页码 935-966出版社
CELL PRESS
DOI: 10.1016/j.neuron.2022.01.017
关键词
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资金
- UK Dementia Research Institute (MRC)
- UK Dementia Research Institute (Alzheimer's Research UK)
- UK Dementia Research Institute (Alzheimer's Society)
- Alz-heimer's Research UK [ARUK-2022DDI-CAM, ARUK-TC2020-1, ARUK-PG2018C-001]
- Tau Consortium, Cambridge Centre for Parkin-son-Plus
- National Institutes of Health [AG054108, AG031782, AG021904, NS100717]
- Rainwater Charitable Foundation
- JPB Foundation
- Backus Foundation
- Glenn Foundation
- RR Belfer
- NIHR Cambridge Biomedical Research Centre [BRC-1215-20014]
- Ramon Areces postdoc-toral fellowship
- Allocation Jeune Chercheurfrom Fondation Alz-heimer (France)
- [T32 GM007491]
- [T32 GM007288]
Autophagy is crucial for maintaining cellular homeostasis by degrading proteins and organelles. The nervous system is particularly dependent on these pathways, which may become less effective with age. Autophagy pathways play a protective role in neurodegenerative diseases and are also linked to different types of programmed cell death.
The term autophagy encompasses different pathways that route cytoplasmic material to lysosomes for degradation and includes macroautophagy, chaperone-mediated autophagy, and microautophagy. Since these pathways are crucial for degradation of aggregate-prone proteins and dysfunctional organelles such as mitochondria, they help to maintain cellular homeostasis. As post-mitotic neurons cannot dilute unwanted protein and organelle accumulation by cell division, the nervous system is particularly dependent on auto-phagic pathways. This dependence may be a vulnerability as people age and these processes become less effective in the brain. Here, we will review how the different autophagic pathways may protect against neurodegeneration, giving examples of both polygenic and monogenic diseases. We have considered how autophagy may have roles in normal CNS functions and the relationships between these degradative pathways and different types of programmed cell death. Finally, we will provide an overview of recently described strategies for upregulating autophagic pathways for therapeutic purposes.
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