Editing Inositol trisphosphate (section)

=== Alzheimer's disease===
[[Alzheimer's disease]] involves the progressive degeneration of the brain, severely impacting mental faculties.<ref>Alzheimer's Society of Canada. (2009). Alzheimer's Disease:What is Alzheimer's? Retrieved from: http://www.alzheimer.ca/english/disease/whatisit-intro.htm {{Webarchive|url=https://web.archive.org/web/20111205113228/http://www.alzheimer.ca/english/disease/whatisit-intro.htm |date=2011-12-05 }}</ref> Since the Ca<sup>2+</sup> hypothesis of Alzheimer's was proposed in 1994, several studies have shown that disruptions in Ca<sup>2+</sup> signaling are the primary cause of Alzheimer's disease. [[Early onset Alzheimer's|Familial Alzheimer's disease]] has been strongly linked to mutations in the [[presenilin 1]] (PS1), [[presenilin 2]] (PS2), and [[amyloid precursor protein]] (APP) [[genes]]. All of the mutated forms of these genes observed to date have been found to cause abnormal Ca<sup>2+</sup> signaling in the ER. Mutations in PS1 have been shown to increase IP<sub>3</sub>-mediated Ca<sup>2+</sup> release from the ER in several animal models. [[Calcium channel blockers]] have been used to treat Alzheimer's disease with some success, and the use of [[Lithium_(medication) | lithium]] to decrease IP<sub>3</sub> turnover has also been suggested as a possible method of treatment.<ref>{{cite journal | last1 = Stutzmann | first1 = G. E. | year = 2005 | title = Calcium Dysregulation, IP3 Signaling, and Alzheimer's Disease | journal = Neuroscientist | volume = 11 | issue = 2| pages = 110–115 | doi = 10.1177/1073858404270899 | pmid = 15746379| s2cid = 20512555 }}</ref><ref>{{cite journal | last1 = Berridge | first1 = M. J. | year = 2016 | title = The Inositol Trisphosphate/Calcium Signaling Pathway in Health and Disease | journal = Physiological Reviews | volume = 96 | issue = 4| pages = 1261–1296 | doi=10.1152/physrev.00006.2016 | pmid = 27512009| doi-access = free }}</ref>