A peptide derived from acetylcholinesterase is a pivotal signalling molecule in neurodegeneration.
It is now widely accepted that acetylcholinesterase (AChE) also displays non-cholinergic functions, completely independent of cholinergic transmission. Indeed, AChE has been implicated in a variety of trophic and toxic actions in a range of different systems. However, it is still uncertain what part of the AChE molecule may be responsible for these actions, and indeed via what receptor. Recent work has identified a peptide towards the C-terminus of the AChE molecule that appears to have very similar effects to non-cholinergic AChE itself. This action is to enhance calcium entry, in acute and chronic preparations across a trophic-toxic spectrum, depending on concentration applied and/or duration of exposure.
Greenfield
Susan
S
University Department of Pharmacology, Mansfield Rd., Oxford OX1 3QT, UK. susan.greenfield@pharm.ox.ac.uk
D000110:Acetylcholinesterase / Q000737:chemistry / Q000378:metabolism / Q000494:pharmacology* / Q000633:toxicity*; D000818:Animals; D006801:Humans; D009410:Nerve Degeneration; D019636:Neurodegenerative Diseases / Q000378:metabolism* / Q000473:pathology; D009865:Oocytes; D010446:Peptide Fragments / Q000378:metabolism / Q000494:pharmacology* / Q000633:toxicity; D011978:Receptors, Nicotinic / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*; D014981:Xenopus
D010446:Peptide Fragments; D011978:Receptors, Nicotinic; D000110:Acetylcholinesterase