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

Chem Biol Interact. 2005 Dec 15:157-158:211-8. doi: 10.1016/j.cbi.2005.10.032. Epub 2005 Nov 17.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylcholinesterase / chemistry
  • Acetylcholinesterase / metabolism
  • Acetylcholinesterase / pharmacology*
  • Acetylcholinesterase / toxicity*
  • Animals
  • Humans
  • Nerve Degeneration*
  • Neurodegenerative Diseases / metabolism*
  • Neurodegenerative Diseases / pathology
  • Oocytes
  • Peptide Fragments / metabolism
  • Peptide Fragments / pharmacology*
  • Peptide Fragments / toxicity
  • Receptors, Nicotinic / metabolism
  • Signal Transduction / drug effects*
  • Xenopus

Substances

  • Peptide Fragments
  • Receptors, Nicotinic
  • Acetylcholinesterase