전한울
2022년 11월 29일
- - 미토콘드리아의 손상은 신경세포의 에너지 대사를 방해하고 axon의 퇴화를 유도함 (SARM1)
- 파킨슨, 다발성 경화증 등의 질환에서의 axon 손상이 미토콘드리아의 기능 장애와 연관이 있음
- The programmed axon death (Wallerian degeneration) pathway is a druggable and potentially preventable mechanism of axon degeneration. This pathway is involved in axon loss in several preclinical disease models, and emerging evidence supports its relevance to human disease. Mitochondrial dysfunction has long been linked to programmed axon death, with several mechanistic studies indicating roles for mitochondrial dysfunction in the initiation and execution of this axon death pathway.
https://www.cell.com/trends/neurosciences/fulltext/S0166-2236%2821%2900214-9
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.
