Synaptic protein expression is regulated by a pro-oxidant diet in APPxPS1 mice

J Neural Transm (Vienna). 2012 Apr;119(4):493-6. doi: 10.1007/s00702-011-0727-1. Epub 2011 Nov 5.

Abstract

Dietary factors may play a role in Alzheimer's disease (AD) pathogenesis. In an effort to recapitulate some of the synaptic protein changes observed in the disease, AD transgenic and wild-type mice were fed either a normal or pro-oxidant diet for 3 months from three months of age. Pro-oxidant diet treatment resulted in altered expression of vesicular glutamate transporter-1 and glutamine synthetase, suggesting changes in glutamatergic synaptic function, and increased expression of urokinase plasminogen activator receptor, possibly reflecting oxidative stress.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / diet therapy*
  • Alzheimer Disease / genetics
  • Alzheimer Disease / metabolism
  • Amyloid beta-Protein Precursor / genetics
  • Animals
  • Dietary Supplements
  • Disease Models, Animal
  • Gene Expression Regulation / drug effects*
  • Gene Expression Regulation / genetics
  • Glutamate-Ammonia Ligase / metabolism
  • Humans
  • Mice
  • Mice, Transgenic
  • Mutation / genetics
  • Oxidants / administration & dosage*
  • Presenilin-1 / genetics
  • Receptors, Urokinase Plasminogen Activator / metabolism
  • Synaptophysin / metabolism
  • Vesicular Glutamate Transport Protein 1 / metabolism*

Substances

  • Amyloid beta-Protein Precursor
  • Oxidants
  • PSEN1 protein, human
  • Presenilin-1
  • Receptors, Urokinase Plasminogen Activator
  • SLC17A7 protein, human
  • Synaptophysin
  • Vesicular Glutamate Transport Protein 1
  • Glutamate-Ammonia Ligase