Content deleted Content added
m Cit. |
Citation bot (talk | contribs) Add: issue, s2cid, doi-access, authors 1-1. Removed proxy/dead URL that duplicated identifier. Removed parameters. Some additions/deletions were parameter name changes. | Use this bot. Report bugs. | Suggested by Headbomb | Linked from Wikipedia:WikiProject_Academic_Journals/Journals_cited_by_Wikipedia/Sandbox2 | #UCB_webform_linked 200/320 |
||
Line 9:
| MeshID = D018721
}}
A '''muscarinic agonist'''<ref>{{Cite journal |
==Clinical significance==
Line 15:
=== M1 ===
M1-type muscarinic [[acetylcholine]] receptors play a role in [[cognition|cognitive]] processing. In [[Alzheimer disease]] (AD), [[amyloid]] formation may decrease the ability of these receptors to transmit signals, leading to decreased cholinergic activity. As these receptors themselves appear relatively unchanged in the disease process, they have become a potential therapeutic target when trying to improve cognitive function in patients with AD.<ref>{{cite journal | vauthors = Fisher A, Brandeis R, Bar-Ner RH, Kliger-Spatz M, Natan N, Sonego H, Marcovitch I, Pittel Z | year = 2002 | title = AF150(S) and AF267B: M1 muscarinic agonists as innovative therapies for Alzheimer's disease | journal = [[J Mol Neurosci]] | volume = 19 | issue = 1–2| pages = 145–53 | pmid = 12212772 | doi = 10.1007/s12031-002-0025-3 | s2cid = 21773972 }}</ref><ref>{{cite journal | vauthors = Fisher A | year = 2000 | title = M1 muscarinic agonists: Their potential in treatment and as disease-modifying agents in Alzheimer's disease | url = http://www3.interscience.wiley.com/cgi-bin/abstract/73504595/ABSTRACT?CRETRY=1&SRETRY=0 | archive-url = https://archive.today/20121210101949/http://www3.interscience.wiley.com/cgi-bin/abstract/73504595/ABSTRACT?CRETRY=1&SRETRY=0 | url-status = dead | archive-date = 2012-12-10 | journal = Drug Development Research | volume = 50 | issue = 3–4 | pages = 291–297 | doi = 10.1002/1098-2299(200007/08)50:3/4<291::aid-ddr12>3.0.co;2-6 | s2cid = 85100519 }}</ref><ref name="pmid18625455">{{cite journal |author=Fisher A |title=Cholinergic treatments with emphasis on m1 muscarinic agonists as potential disease-modifying agents for Alzheimer's disease |journal=[[Neurotherapeutics]] |volume=5 |issue=3 |pages=433–42 |date=July 2008 |pmid=18625455 |doi=10.1016/j.nurt.2008.05.002 |pmc=5084245 }}</ref>
A number of muscarinic agonists have been developed and are under investigation to treat AD. These agents show promise as they are [[neurotrophin|neurotrophic]], decrease amyloid depositions, and improve damage due to [[oxidative stress]]. [[Tau protein|Tau]]-phosphorylation is decreased and cholinergic function enhanced. Notably several agents of the AF series of muscarinic agonists have become the focus of such research:. '''AF102B, AF150(S), AF267B'''. In animal models that are mimicking the damage of AD, these agents appear promising.
The agent [[xanomeline]] has been proposed as a potential treatment for [[schizophrenia]].<ref name="pmid18593778">{{cite journal |vauthors=Shekhar A, Potter WZ, Lightfoot J, etal |title=Selective Muscarinic Receptor Agonist Xanomeline as a Novel Treatment Approach for Schizophrenia |journal=Am J Psychiatry |volume= 165|issue= 8|pages= 1033–9|date=July 2008 |pmid=18593778 |doi=10.1176/appi.ajp.2008.06091591 |s2cid=24308125 }}</ref><ref name="pmid19037177">{{cite journal |vauthors=Sellin AK, Shad M, Tamminga C |title=Muscarinic agonists for the treatment of cognition in schizophrenia |journal=CNS Spectrums |volume=13 |issue=1 |pages=985–96 |date=November 2008 |pmid=19037177 |doi= 10.1017/S1092852900014048|s2cid=12642499 }}</ref>
=== M3 ===
Line 57:
| [[Pilocarpine]] || ++ || - || - || Used in glaucoma.
|-
| [[Oxotremorine]] || ++ ||+<ref>{{Cite journal|title = Activation of muscle nicotinic acetylcholine receptor channels by nicotinic and muscarinic agonists|journal = British Journal of Pharmacology|date = 1999-12-01|issn = 0007-1188|pmc = 1571784|pmid = 10602325|pages = 1467–1476|volume = 128|issue = 7|doi = 10.1038/sj.bjp.0702941|
symptoms of [[Parkinson's disease]].
|}
| |||