Evidence for brain glucose dysregulation in Alzheimer's disease.

Published

Journal Article

INTRODUCTION: It is unclear whether abnormalities in brain glucose homeostasis are associated with Alzheimer's disease (AD) pathogenesis. METHODS: Within the autopsy cohort of the Baltimore Longitudinal Study of Aging, we measured brain glucose concentration and assessed the ratios of the glycolytic amino acids, serine, glycine, and alanine to glucose. We also quantified protein levels of the neuronal (GLUT3) and astrocytic (GLUT1) glucose transporters. Finally, we assessed the relationships between plasma glucose measured before death and brain tissue glucose. RESULTS: Higher brain tissue glucose concentration, reduced glycolytic flux, and lower GLUT3 are related to severity of AD pathology and the expression of AD symptoms. Longitudinal increases in fasting plasma glucose levels are associated with higher brain tissue glucose concentrations. DISCUSSION: Impaired glucose metabolism due to reduced glycolytic flux may be intrinsic to AD pathogenesis. Abnormalities in brain glucose homeostasis may begin several years before the onset of clinical symptoms.

Full Text

Duke Authors

Cited Authors

  • An, Y; Varma, VR; Varma, S; Casanova, R; Dammer, E; Pletnikova, O; Chia, CW; Egan, JM; Ferrucci, L; Troncoso, J; Levey, AI; Lah, J; Seyfried, NT; Legido-Quigley, C; O'Brien, R; Thambisetty, M

Published Date

  • March 2018

Published In

Volume / Issue

  • 14 / 3

Start / End Page

  • 318 - 329

PubMed ID

  • 29055815

Pubmed Central ID

  • 29055815

Electronic International Standard Serial Number (EISSN)

  • 1552-5279

Digital Object Identifier (DOI)

  • 10.1016/j.jalz.2017.09.011

Language

  • eng

Conference Location

  • United States