Elevation of plasma beta-amyloid level by glucose loading in Alzheimer mouse models

Biochem Biophys Res Commun. 2009 Jul 24;385(2):193-7. doi: 10.1016/j.bbrc.2009.05.037. Epub 2009 May 18.

Abstract

With the emergence of a promising approach to treat Alzheimer disease (AD) targeting the beta-amyloid (Abeta) pathway, it is necessary to establish new diagnostic biomarkers that enable the antemortem diagnosis of AD. Although plasma Abeta has been suggested as a non-invasive biomarker, its significance has been inconclusive. Thus, it is important to improve the diagnostic potential of plasma Abeta. One of the potential approaches is to modify plasma Abeta level using various modulators. In this study, we evaluated the influence of glucometabolic status on plasma Abeta level in two lines of AD transgenic mouse. The present study demonstrated that plasma Abeta level rapidly increased after glucose loading. More importantly, the magnitude of the increase in plasma Abeta was significantly larger in AD transgenic mice than in wild-type littermates. These findings might provide a novel diagnostic tool for AD using the elevation of plasma Abeta level after glucose loading.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / blood
  • Alzheimer Disease / diagnosis*
  • Amyloid beta-Peptides / blood*
  • Animals
  • Biomarkers / blood
  • Blood Glucose / analysis
  • Disease Models, Animal
  • Glucose / administration & dosage*
  • Glucose Tolerance Test
  • Male
  • Mice
  • Mice, Transgenic
  • Peptide Fragments / blood

Substances

  • Amyloid beta-Peptides
  • Biomarkers
  • Blood Glucose
  • Peptide Fragments
  • amyloid beta-protein (1-40)
  • amyloid beta-protein (1-42)
  • Glucose