期刊
NATURE REVIEWS NEUROSCIENCE
卷 15, 期 6, 页码 394-409出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nrn3680
关键词
-
资金
- Biotechnology and Biological Sciences Research Council (BBSRC)
- Faculty of Medicine and Health Sciences, University of Nottingham, UK, non-clinical senior fellowship
- BBSRC [BBS/E/B/000C0417] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BBS/E/B/000C0417] Funding Source: researchfish
Axon degeneration is a prominent early feature of most neurodegenerative disorders and can also be induced directly by nerve injury in a process known as Wallerian degeneration. The discovery of genetic mutations that delay Wallerian degeneration has provided insight into mechanisms underlying axon degeneration in disease. Rapid Wallerian degeneration requires the pro-degenerative molecules SARM1 and PHR1. Nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2) is essential for axon growth and survival. Its loss from injured axons may activate Wallerian degeneration, whereas NMNAT overexpression rescues axons from degeneration. Here, we discuss the roles of these and other proposed regulators of Wallerian degeneration, new opportunities for understanding disease mechanisms and intriguing links between Wallerian degeneration, innate immunity, synaptic growth and cell death.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据