中国神经再生研究(英文版) ›› 2021, Vol. 16 ›› Issue (5): 980-981.doi: 10.4103/1673-5374.297070

• 观点:脑损伤修复保护与再生 • 上一篇    下一篇

Wallerian变性的出现是继发性脑损伤的机制

  

  • 出版日期:2021-05-15 发布日期:2020-12-29

Emergence of the Wallerian degeneration pathway as a mechanism of secondary brain injury

Ciaran Scott Hill*, Andrea Loreto   

  1. National Hospital for Neurology and Neurosurgery, University College London Hospitals; UCL Cancer Institute, University College London, London, UK (Hill CS)
    Jon Van Geest Centre for Brain Repair, University of Cambridge, Cambridge, UK (Loreto A)
  • Online:2021-05-15 Published:2020-12-29
  • Contact: Ciaran Scott Hill, MRCP, FRCS(SN), PhD, ciaran.hill@ucl.ac.uk.
  • Supported by:
    We apologize for omissions in citing relevant publications due to the reference limit.

    CSH was supported by a National Institute for Health Research (NIHR) Academic Clinical Lectureship.

摘要: https://orcid.org/0000-0002-4488-4034 (Ciaran Scott Hill) 

Abstract: Augustus Volney Waller was a renowned British neurophysiologist who birthed the axon degeneration field in 1850 by describing curdling and fragmentation of the glossopharyngeal and hypoglossal cranial nerves of a frog following a transection injury. The degeneration of axons after a transection injury is now known as Wallerian degeneration (WD). Waller’s work was expanded by Santiago Ramón y Cajal who described in detail the morphological stages of WD from monitory fragmentation of the axon and the granular disintegration of the neurofibrils to the final resorption of the axon. Interest in this field burgeoned in the early 1990’s with the fortuitous discovery of a mutant mouse, known as the Wallerian degeneration Slow (WldS) mouse. Although overtly normal, its remarkable phenotype was discovered when the animals were subjected to a physical nerve injury and a profoundly slowed rate of axonal degeneration was revealed. This slow axon breakdown is intrinsic to neurons, present in central and peripheral nervous system axons, and associated with structural preservation and retention of the ability to conduct axon potentials for up to 2 weeks (a 10-fold delay).