The different autophagy degradation pathways and neurodegeneration.
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Authors
Bourdenx, Mathieu
Fujimaki, Motoki
Karabiyik, Cansu
Krause, Gregory J
Lopez, Ana
Martín-Segura, Adrián
Puri, Claudia
Scrivo, Aurora
Son, Sung Min
Stamatakou, Eleanna
Wrobel, Lidia
Zhu, Ye
Cuervo, Ana Maria
Rubinsztein, David C
Publication Date
2022-03-16Journal Title
Neuron
ISSN
0896-6273
Publisher
Elsevier BV
Type
Article
This Version
AM
Metadata
Show full item recordCitation
Fleming, A., Bourdenx, M., Fujimaki, M., Karabiyik, C., Krause, G. J., Lopez, A., Martín-Segura, A., et al. (2022). The different autophagy degradation pathways and neurodegeneration.. Neuron https://doi.org/10.1016/j.neuron.2022.01.017
Abstract
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 autophagic 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.
Sponsorship
This work was supported by UK Dementia Research Institute (funded by the MRC, Alzheimer's Research UK and the Alzheimer's Society), Alzheimer's Research UK (ARUK-2022DDI-CAM, ARUK-TC2020-1 and ARUK-PG2018C-001), The Tau Consortium, Cambridge Centre for Parkinson-Plus, the National Institutes of Health grants AG054108, AG031782, AG021904, NS100717 and the generous support of the Rainwater Charitable Foundation, The JPB Foundation, The Backus Foundation, The Glenn Foundation and R&R Belfer and the NIHR Cambridge Biomedical Research Centre (BRC-1215-20014). The views expressed are those of the authors and not necessarily those of the NIHR or the Department of Health and Social Care'. AMS is supported by a Ramon Areces postdoctoral fellowship and GJK by a T32 GM007491 and a T32 GM007288. MB is supported by an ‘Allocation Jeune Chercheur’ from Fondation Alzheimer (France).
Funder references
Cambridge University Hospitals NHS Foundation Trust (CUH) (RG50822)
Alzheimer's Research UK (ARUK-PG2018C-001)
Alzheimer's Research UK (ARUK-2021DDI-CAM)
National Institute for Health Research (IS-BRC-1215-20014)
Embargo Lift Date
2023-03-16
Identifiers
External DOI: https://doi.org/10.1016/j.neuron.2022.01.017
This record's URL: https://www.repository.cam.ac.uk/handle/1810/335336
Rights
Attribution-NonCommercial-NoDerivatives 4.0 International
Licence URL: https://creativecommons.org/licenses/by-nc-nd/4.0/
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