Editing Neuron (section)

==Neurological disorders==
{{Main|Neurological disorders}}
{{More citations needed|date=May 2018}}
[[Charcot–Marie–Tooth disease]] (CMT) is a heterogeneous inherited disorder of nerves ([[neuropathy]]) that is characterized by loss of muscle tissue and touch sensation, predominantly in the feet and legs extending to the hands and arms in advanced stages. Presently incurable, this disease is one of the most common inherited [[neurological disorder]]s, affecting 36 in 100,000 people.<ref name=Krajewski>{{cite journal | vauthors = Krajewski KM, Lewis RA, Fuerst DR, Turansky C, Hinderer SR, Garbern J, Kamholz J, Shy ME | title = Neurological dysfunction and axonal degeneration in Charcot-Marie-Tooth disease type 1A | journal = Brain | volume = 123 | issue = 7 | pages = 1516–27 | date = July 2000 | pmid = 10869062 | doi = 10.1093/brain/123.7.1516 | doi-access =  }}</ref>

[[Alzheimer's disease]] (AD), also known simply as ''Alzheimer's'', is a [[neurodegenerative disease]] characterized by progressive [[cognitive]] deterioration, together with declining activities of daily living and [[neuropsychiatric]] symptoms or behavioral changes.<ref name="nihstages">{{cite web|title=About Alzheimer's Disease: Symptoms|url=http://www.nia.nih.gov/alzheimers/topics/symptoms|publisher=National Institute on Aging|access-date=28 December 2011|url-status=live|archive-url=https://web.archive.org/web/20120115201854/http://www.nia.nih.gov/alzheimers/topics/symptoms|archive-date=15 January 2012|df=dmy-all}}</ref> The most striking early symptom is loss of short-term memory ([[amnesia]]), which usually manifests as minor forgetfulness that becomes steadily more pronounced with illness progression, with relative preservation of older memories. As the disorder progresses, cognitive (intellectual) impairment extends to the domains of language ([[aphasia]]), skilled movements ([[apraxia]]), and recognition ([[agnosia]]), and functions such as decision-making and planning become impaired.<ref name="BMJ2009">{{cite journal | vauthors = Burns A, Iliffe S | title = Alzheimer's disease | journal = BMJ | volume = 338 | pages = b158 | date = February 2009 | pmid = 19196745 | doi = 10.1136/bmj.b158 | s2cid = 8570146 }}</ref><ref name=NEJM2010>{{cite journal | vauthors = Querfurth HW, LaFerla FM | title = Alzheimer's disease | journal = The New England Journal of Medicine | volume = 362 | issue = 4 | pages = 329–44 | date = January 2010 | pmid = 20107219 | doi = 10.1056/NEJMra0909142 | s2cid = 205115756 }}</ref>

[[Parkinson's disease]] (PD), also known as ''Parkinson's'', is a degenerative disorder of the central nervous system that often impairs motor skills and speech.<ref name=NIH2016>{{cite web|title=Parkinson's Disease Information Page|url=https://www.ninds.nih.gov/Disorders/All-Disorders/Parkinsons-Disease-Information-Page|website=NINDS|access-date=18 July 2016|date=30 June 2016|url-status=live|archive-url=https://web.archive.org/web/20170104201403/http://www.ninds.nih.gov/Disorders/All-Disorders/Parkinsons-Disease-Information-Page|archive-date=4 January 2017|df=dmy-all}}</ref> Parkinson's disease belongs to a group of conditions called [[movement disorders]].<ref>{{cite web | title = Movement Disorders| url = http://www.neuromodulation.com/movement-disorders | work = The International Neuromodulation Society }}</ref> It is characterized by muscle rigidity, [[tremor]], a slowing of physical movement ([[bradykinesia]]), and in extreme cases, a loss of physical movement ([[akinesia]]). The primary symptoms are the results of decreased stimulation of the [[motor cortex]] by the [[basal ganglia]], normally caused by the insufficient formation and action of dopamine, which is produced in the [[dopaminergic neurons]] of the brain. Secondary symptoms may include high-level [[cognitive dysfunction]] and subtle language problems. PD is both chronic and progressive.

[[Myasthenia gravis]] is a [[neuromuscular disease]] leading to fluctuating [[muscle weakness]] and fatigability during simple activities. Weakness is typically caused by circulating [[antibodies]] that block [[acetylcholine receptors]] at the postsynaptic neuromuscular junction, inhibiting the stimulative effect of the neurotransmitter acetylcholine. Myasthenia is treated with [[immunosuppressants]], [[cholinesterase]] inhibitors and, in selected cases, [[thymectomy]].

===Demyelination===
{{Further|Demyelinating disease}}
[[File:Guillain-barré syndrome - Nerve Damage.gif|thumb|[[Guillain–Barré syndrome]] – demyelination]]
[[Demyelination]] is a process characterized by the gradual loss of the myelin sheath enveloping nerve fibers. When myelin deteriorates, signal conduction along nerves can be significantly impaired or lost, and the nerve eventually withers. Demyelination may affect both central and peripheral nervous systems, contributing to various neurological disorders such as [[multiple sclerosis]], [[Guillain–Barré syndrome|Guillain-Barré syndrome]], and [[chronic inflammatory demyelinating polyneuropathy]]. Although demyelination is often caused by an [[Autoimmunity|autoimmune]] reaction, it may also be caused by viral infections, metabolic disorders, trauma, and some medications.

===Axonal degeneration===
Although most injury responses include a calcium influx signaling to promote resealing of severed parts, axonal injuries initially lead to acute [[axonal degeneration]], which is the rapid separation of the proximal and distal ends, occurring within 30 minutes of injury.<ref name="NM">{{cite journal | vauthors = Kerschensteiner M, Schwab ME, Lichtman JW, Misgeld T | s2cid = 25287010 | title = In vivo imaging of axonal degeneration and regeneration in the injured spinal cord | journal = Nature Medicine | volume = 11 | issue = 5 | pages = 572–7 | date = May 2005 | pmid = 15821747 | doi = 10.1038/nm1229 }}</ref> Degeneration follows with swelling of the [[axolemma]], and eventually leads to bead-like formation. Granular disintegration of the axonal [[cytoskeleton]] and inner [[organelle]]s occurs after axolemma degradation. Early changes include accumulation of [[mitochondria]] in the paranodal regions at the site of injury. The endoplasmic reticulum degrades and mitochondria swell up and eventually disintegrate. The disintegration is dependent on [[ubiquitin]] and [[calpain]] [[proteases]] (caused by the influx of calcium ions), suggesting that axonal degeneration is an active process that produces complete fragmentation. The process takes about roughly 24 hours in the PNS and longer in the CNS. The signaling pathways leading to axolemma degeneration are unknown.