Keywords: Biomarkers, Alzheimer's Disease, Deuterium MRS, Brain, Alzheimer's disease, Metabolism, NAD+
Motivation: Glucose hypometabolism due to reduced tri-carboxylic acid (TCA) cycle flux is a characteristic pathology in Alzheimer’s disease (AD). Since, redox balance (NAD+/NADH) plays a crucial role in regulation of TCA cycle, studying NAD+ biosynthetic pathway and its relation to glucose metabolism in AD can provide a therapeutic target.
Goal(s): To monitor glucose metabolism and nicotinamide phosphoribosyltransferase (NAMPT) levels in APPNL-F/NL-F mice.
Approach: Monitoring cerebral 4,4-2H2-Glx labeling from 6,6’-2H2-Glucose using pulse-acquired 2H-MRS and NAMPT immunostaining.
Results: Reduced labeling of 4,4-2H2-Glx in AD mice suggests compromised TCA cycle flux and glucose hypometabolism which could be attributed to reduced NAMPT levels and hence NAD+.
Impact: This preliminary study supports the loss of NAMPT levels as a possible underlying cause of compromised neuroenergetics and metabolism in AD and potential of NAMPT activators in alleviating the symptoms of the disease by upregulating glucose metabolism.
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