Butyrylcholinesterase-knockout reduces brain deposition of fibrillar β-amyloid in an Alzheimer mouse model

Neuroscience. 2015 Jul 9:298:424-35. doi: 10.1016/j.neuroscience.2015.04.039. Epub 2015 Apr 27.

Abstract

In Alzheimer's disease (AD), numerous β-amyloid (Aβ) plaques are associated with butyrylcholinesterase (BChE) activity, the significance of which is unclear. A mouse model, containing five human familial AD genes (5XFAD), also develops Aβ plaques with BChE activity. Knock-out of BChE in this model showed diminished fibrillar Aβ plaque deposition, more so in males than females. This suggests that lack of BChE reduces deposition of fibrillar Aβ in AD and this effect may be influenced by sex.

Keywords: 5XFAD mouse; Alzheimer’s disease; butyrylcholinesterase; butyrylcholinesterase-knockout; cholinergic system; β-amyloid.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Age Factors
  • Alzheimer Disease / genetics
  • Alzheimer Disease / pathology*
  • Amyloid / metabolism*
  • Amyloid beta-Peptides / metabolism*
  • Amyloid beta-Protein Precursor / genetics
  • Animals
  • Brain / metabolism*
  • Brain / pathology
  • Butyrylcholinesterase / genetics
  • Butyrylcholinesterase / metabolism*
  • Female
  • Gene Expression Regulation / genetics*
  • Humans
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Presenilin-1 / genetics

Substances

  • Amyloid
  • Amyloid beta-Peptides
  • Amyloid beta-Protein Precursor
  • Presenilin-1
  • Butyrylcholinesterase