Ai-Ling Lin1, Peter T. Fox1, Holly Van Remmen2, Andrew Bresnen1, Anuradha Soundararajan1, Eric Muir1, Arlan G. Richardson2, Timothy Q. Duong1
1Research Imaging Institute, University of Texas Health Science Center at San Anotnio, San Antonio, TX, United States; 2Barshop Institute for Logevity and Aging Studies, University of Texas Health Science Center at San Anotnio, San Antonio, TX, United States
Reduced mitochondrial function has been recently found to be associated with increased lifespan in various organisms. Herein we measured the effects on metabolism in mouse brain of decreased mitochondrial function induced by a genetic manipulation (Surf1 knock out) which reduced levels of cytochrome c oxidase (COX). Using non-invasive, in vivo neuroimaging, we quantified metabolic function in Surf1 KO mice and WT controls. Significant increases in glucose uptake and lactate concentration (an index of glycolysis) were found in both young (6-7 months old) and aged (17-18 months old) adult Surf1 KO mice compared to age-matched WT controls. Concentrations of essential neuronal metabolites (e.g., NAA and glutamate/glutamine) and energy substrates (i.e., ATP) remained unchanged in Surf1 KO mice during aging but decreased significantly in WT controls. Our results suggest that decreased mitochondrial function can mitigate age-related declines in brain physiology and may provide an explanation for the extended lifespan of Surf1 KO mice.