Neural Regeneration Research ›› 2015, Vol. 10 ›› Issue (8): 1237-1238.doi: 10.4103/1673-5374.162753

Previous Articles     Next Articles

Aminoacyl tRNA synthetases and their relationships with peripheral nerve degeneration and regeneration

Junyang Jung   

  1. Department of Anatomy and Neurobiology, School of Medicine,
    Biomedical Science Institution, Kyung Hee University, Seoul, Republic of Korea
  • Received:2015-07-14 Online:2015-08-24 Published:2015-08-24
  • Contact: Junyang Jung, M.D., Ph.D., jjung@khu.ac.kr.
  • Supported by:

    This work was supported by a grant from the Kyung Hee University in 2013 (KHU20130548).

Abstract:

Following damage resulting from mechanical injury, viral infection, or autoimmunity, peripheral nerves degenerate and a variety of complications, including sensory loss, muscular paralysis, skin thinning, and a loss of tendon reflexes, can manifest. If these complications persist, they can cause a number of debilitating personal and/or social problems. For example, Guillain-Barre syndrome is induced by the degradation of myelin sheaths, and if the symptoms are not controlled the disease can be life-threatening due to the demyelination of respiratory muscle nerves. To date, effective treatment strategies that can inhibit the demyelination of peripheral nerves in the early stages of disease have yet to be developed. Thus, as with severe cases of Guillain-Barre syndrome, devices that alleviate the symptoms of respiratory muscular paralysis, including breathing machines, must be utilized until a cure can be developed.