Editing Axon (section)

==Clinical significance==
{{Main|Nerve injury |Peripheral neuropathy |Demyelinating disease}}
In order of degree of severity, injury to a nerve in the peripheral nervous system can be described as [[neurapraxia]], [[axonotmesis]], or [[neurotmesis]].
[[Concussion]] is considered a mild form of [[diffuse axonal injury]].<ref>{{cite web |url=https://emedicine.medscape.com/article/326510-overview |title=Traumatic Brain Injury (TBI) - Definition, Epidemiology, Pathophysiology | first = Segun Toyin | last = Dawodu | name-list-style = vanc |date=16 August 2017 |website=Medscape |access-date=14 July 2018 |url-status=live |archive-url=https://web.archive.org/web/20180612184940/https://emedicine.medscape.com/article/326510-overview |archive-date=12 June 2018}}</ref> Axonal injury can also cause [[central chromatolysis]]. The dysfunction of axons in the nervous system is one of the major causes of many inherited and acquired [[neurological disorder]]s that affect both peripheral and central neurons.<ref name="Debanne"/>

When an axon is crushed, an active process of [[Wallerian degeneration#Axonal degeneration|axonal degeneration]] takes place at the part of the axon furthest from the cell body. This degeneration takes place quickly following the injury, with the part of the axon being sealed off at the membranes and broken down by macrophages. This is known as [[Wallerian degeneration]].<ref name="UCSF">[http://missinglink.ucsf.edu/lm/ids_104_cns_injury/Response%20_to_Injury/WallerianDegeneration.htm Trauma and Wallerian Degeneration] {{Webarchive|url=https://web.archive.org/web/20060502020349/http://missinglink.ucsf.edu/lm/ids_104_cns_injury/Response%20_to_Injury/WallerianDegeneration.htm |date=2 May 2006 }}, [[University of California, San Francisco]]</ref> Dying back of an axon can also take place in many [[neurodegenerative disease]]s, particularly when axonal transport is impaired, this is known as Wallerian-like degeneration.<ref name="pmid20345246">{{cite journal | vauthors = Coleman MP, Freeman MR | title = Wallerian degeneration, wld(s), and nmnat | journal = Annual Review of Neuroscience | volume = 33 | issue = 1 | pages = 245–67 | date = 1 June 2010 | pmid = 20345246 | pmc = 5223592 | doi = 10.1146/annurev-neuro-060909-153248 }}</ref> Studies suggest that the degeneration happens as
a result of the axonal protein [[NMNAT2]], being prevented from reaching all of the axon.<ref name="Gilley">{{cite journal | vauthors = Gilley J, Coleman MP | title = Endogenous Nmnat2 is an essential survival factor for maintenance of healthy axons | journal = PLOS Biology | volume = 8 | issue = 1 | pages = e1000300 | date = January 2010 | pmid = 20126265 | pmc = 2811159 | doi = 10.1371/journal.pbio.1000300 | doi-access = free }}</ref>

[[Demyelinating disease|Demyelination of axons]] causes the multitude of neurological symptoms found in the disease [[multiple sclerosis]].

[[Myelin#Dysmyelination|Dysmyelination]] is the abnormal formation of the myelin sheath. This is implicated in several [[leukodystrophy|leukodystrophies]], and also in [[schizophrenia]].<ref>{{cite journal | vauthors = Krämer-Albers EM, Gehrig-Burger K, Thiele C, Trotter J, Nave KA | title = Perturbed interactions of mutant proteolipid protein/DM20 with cholesterol and lipid rafts in oligodendroglia: implications for dysmyelination in spastic paraplegia | journal = The Journal of Neuroscience | volume = 26 | issue = 45 | pages = 11743–52 | date = November 2006 | pmid = 17093095 | pmc = 6674790 | doi = 10.1523/JNEUROSCI.3581-06.2006 }}</ref><ref>{{Cite book|vauthors=Matalon R, Michals-Matalon K, Surendran S, Tyring SK |chapter=Canavan Disease: Studies on the Knockout Mouse |title=N-Acetylaspartate |s2cid=44405442 |volume=576 |pages=77–93; discussion 361–3 |year=2006 |pmid=16802706 |doi=10.1007/0-387-30172-0_6 |series=Advances in Experimental Medicine and Biology |isbn=978-0-387-30171-6}}</ref><ref>{{cite journal | vauthors = Tkachev D, Mimmack ML, Huffaker SJ, Ryan M, Bahn S | title = Further evidence for altered myelin biosynthesis and glutamatergic dysfunction in schizophrenia | journal = The International Journal of Neuropsychopharmacology | volume = 10 | issue = 4 | pages = 557–63 | date = August 2007 | pmid = 17291371 | doi = 10.1017/S1461145706007334 | doi-access = free }}</ref>

A severe [[traumatic brain injury]] can result in widespread lesions to nerve tracts damaging the axons in a condition known as [[diffuse axonal injury]]. This can lead to a [[persistent vegetative state]].<ref name="Healthcare">{{cite web|url=http://www.medcyclopaedia.com/library/topics/volume_vi_1/b/BRAIN_INJURY_TRAUMATIC.aspx|archive-url=https://archive.today/20110526162429/http://www.medcyclopaedia.com/library/topics/volume_vi_1/b/BRAIN_INJURY_TRAUMATIC.aspx|url-status=dead|archive-date=26 May 2011|title=Brain Injury, Traumatic|publisher=[[General Electric|GE]]|website=Medcyclopaedia|access-date=20 June 2018}}</ref> It has been shown in studies on the [[rat]] that axonal damage from a single mild traumatic brain injury, can leave a susceptibility to further damage, after repeated mild traumatic brain injuries.<ref>{{cite journal | vauthors = Wright DK, Brady RD, Kamnaksh A, Trezise J, Sun M, McDonald SJ, Mychasiuk R, Kolbe SC, Law M, Johnston LA, O'Brien TJ, Agoston DV, Shultz SR | display-authors = 6 | title = Repeated mild traumatic brain injuries induce persistent changes in plasma protein and magnetic resonance imaging biomarkers in the rat | journal = Scientific Reports | volume = 9 | issue = 1 | pages = 14626 | date = October 2019 | pmid = 31602002 | pmc = 6787341 | doi = 10.1038/s41598-019-51267-w | bibcode = 2019NatSR...914626W }}</ref>

A [[nerve guidance conduit]] is an artificial means of guiding axon growth to enable [[neuroregeneration]], and is one of the many treatments used for different kinds of [[nerve injury]].