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Mitochondrial dysfunction as a trigger of programmed axon death.

Accepted version
Peer-reviewed

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Type

Article

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Authors

Merlini, Elisa 
Coleman, Michael P 

Abstract

Mitochondrial failure has long been associated with programmed axon death (Wallerian degeneration, WD), a widespread and potentially preventable mechanism of axon degeneration. While early findings in axotomised axons indicated that mitochondria are involved during the execution steps of this pathway, recent studies suggest that in addition, mitochondrial dysfunction can initiate programmed axon death without physical injury. As mitochondrial dysfunction is associated with disorders involving early axon loss, including Parkinson's disease, peripheral neuropathies, and multiple sclerosis, the findings that programmed axon death is activated by mitochondrial impairment could indicate the involvement of druggable mechanisms whose disruption may protect axons in such diseases. Here, we review the latest developments linking mitochondrial dysfunction to programmed axon death and discuss their implications for injury and disease.

Description

Keywords

Parkinson’s disease, SARM1, Wallerian degeneration, axon degeneration, mitochondrial dysfunction, programmed axon death, Armadillo Domain Proteins, Axons, Cytoskeletal Proteins, Humans, Mitochondria, Peripheral Nervous System Diseases, Wallerian Degeneration

Journal Title

Trends Neurosci

Conference Name

Journal ISSN

0166-2236
1878-108X

Volume Title

Publisher

Elsevier BV
Sponsorship
Wellcome Trust (210904/Z/18/Z)
Biotechnology and Biological Sciences Research Council (BB/S009582/1)