Axons are essential for nervous system function and axonal pathology is a common hallmark of many neurodegenerative diseases. Over a century and a half after the original description of Wallerian axon degeneration, advances over the past five years have heralded the emergence of a comprehensive, mechanistic model of an endogenous axon degenerative process that can be activated by both injury and disease. Axonal integrity is maintained by the opposing actions of the survival factors NMNAT2 and STMN2 and pro-degenerative molecules DLK and SARM1. The balance between axon survival and self-destruction is intimately tied to axonal NAD+ metabolism. These mechanistic insights may enable axon-protective therapies for a variety of human neurodegenerative diseases including peripheral neuropathy, traumatic brain injury and potentially ALS and Parkinson's.

中文翻译：

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SARM1 轴突退化途径：NAD+ 代谢组的控制调节轴突在健康和疾病中的存活。

轴突对神经系统功能至关重要，轴突病理学是许多神经退行性疾病的共同标志。在最初描述沃勒轴突退化一个半世纪后，过去五年的进展预示着一种内源性轴突退化过程的全面机械模型的出现，该过程可以被损伤和疾病激活。轴突完整性由存活因子 NMNAT2 和 STMN2 以及促退行性分子 DLK 和 SARM1 的相反作用来维持。轴突存活和自我毁灭之间的平衡与轴突 NAD+ 代谢密切相关。这些机制见解可能使轴突保护疗法能够治疗多种人类神经退行性疾病，包括周围神经病变、创伤性脑损伤以及潜在的 ALS 和帕金森氏症。