Evidence for Brain Glucose Dysregulation in Alzheimer’s Disease
Yang An, Vijay R. Varma, Sudhir Varma, Ramon Casanova, Eric Dammer et al.
Laboratory of Behavioral Neuroscience,
National Institute on Aging (NIA),
National Institutes of Health (NIH),
Baltimore, MD, USA.
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.
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