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A peptide derived from acetylcholinesterase is a pivotal signalling molecule in neurodegeneration

Authors
Journal
Chemico-Biological Interactions
0009-2797
Publisher
Elsevier
Publication Date
Identifiers
DOI: 10.1016/j.cbi.2005.10.032
Keywords
  • Acetylcholinesterase
  • Neurodegeneration
  • Alpha-7 Nicotinic Receptor
  • Trophic-Toxic Axis
  • Peptide

Abstract

Abstract 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.

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