期刊
CELLS
卷 11, 期 8, 页码 -出版社
MDPI
DOI: 10.3390/cells11081358
关键词
axon regeneration; chemotherapy-induced peripheral neuropathies; dying back; microtubules; Parkinson's disease; ubiquitin proteasome system
类别
资金
- Fondazione Cariplo [2019-1482, 2017ZFJCS3]
Axonal degeneration is a key feature of many neurological disorders. This article focuses on the similarities in the mechanisms and molecular players driving the early phase of axon degeneration in Parkinson's disease and chemotherapy-induced peripheral neuropathies. It also reviews key molecules that can modulate these targets, potentially improving patients' quality of life by blocking axonal degeneration and promoting neuronal regeneration.
Axonal degeneration is an active process that differs from neuronal death, and it is the hallmark of many disorders affecting the central and peripheral nervous system. Starting from the analyses of Wallerian degeneration, the simplest experimental model, here we describe how the long projecting neuronal populations affected in Parkinson's disease and chemotherapy-induced peripheral neuropathies share commonalities in the mechanisms and molecular players driving the earliest phase of axon degeneration. Indeed, both dopaminergic and sensory neurons are particularly susceptible to alterations of microtubules and axonal transport as well as to dysfunctions of the ubiquitin proteasome system and protein quality control. Finally, we report an updated review on current knowledge of key molecules able to modulate these targets, blocking the on-going axonal degeneration and inducing neuronal regeneration. These molecules might represent good candidates for disease-modifying treatment, which might expand the window of intervention improving patients' quality of life.
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