Alterations in brain glucose and energy metabolism is observed in Huntington’s Disease (HD) and HD animal models. 1H-[13C]-MRS can be readily adapted to measure metabolic pathway flux by use of 13C-labeled substrates. In this study we assessed whether activation of the astroglial Nrf2-ARE pathway in the R6/2 mouse model of HD, which has shown therapeutic potential in HD animal models, can reverse the reduction in 13C labeling seen previously in R6/2 mice. In cortex and striatum, astroglial Nrf2 activation led to increased amino acid 13C labeling, suggesting a degree of improvement in mitochondrial and neurotransmitter fluxes in the R6/2 mice.
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