中国神经再生研究(英文版) ›› 2023, Vol. 18 ›› Issue (3): 547-548.doi: 10.4103/1673-5374.350200

• 观点:神经损伤修复保护与再生 • 上一篇    下一篇

轴突退化:旧剧中的新演员

  

  • 出版日期:2023-03-15 发布日期:2022-08-26

Axon degeneration: new actor in an old play

Marina Herwerth*, Matthias T. Wyss   

  1. Institute of Pharmacology and Toxicology, University of Zurich; Neuroscience Center Zurich, University and ETH Zurich, Zürich, Switzerland (Herwerth M, Wyss MT)
    Former address: Institute of Neuronal Cell Biology; Department of Neurology, Technische Universität München, Munich, Germany (Herwerth M)
  • Online:2023-03-15 Published:2022-08-26
  • Contact: Marina Herwerth, MD, marina.herwerth@pharma.uzh.ch.

摘要: https://orcid.org/0000-0001-5125-4594 (Marina Herwerth)

Abstract: After an insult of white matter tracts, e.g. in the spinal cord or optic nerve, axons react in general by the activation of a tightly regulated self-destruction program. This so-called axon degeneration cascade can be triggered by various causes, including injury, toxins, and genetic defects, and is a shared pathway in many different neurological diseases (Coleman and Hoke, 2020). Axonal degeneration is thought to be responsible for disease progression and accumulation of disability across many neurological conditions. The hallmark of early axonal injury is the appearance of local spheroid formations along the axon, often referred to as a “pearl-on-string” pattern or axonal beading or swelling. Although this striking shape change has been observed after various types of injury, such as mechanical, chemical, or inflammatory stimuli, we know little about its exact mechanism and its immediate impact on axonal functionality. In this perspective, we would like to contrast the classical calcium-dependent form of axonal degeneration with a recently described form of a calcium-independent mechanism underlying axonal beading.