The effect of congenital anemic hypoxia on brain energy metabolism was studied on BERK-Hemi mouse exhibiting poor oxygen delivery secondary to reduced hemoglobin oxygen affinity. Regionally increased CBF in BERK-Hemi mouse was correlated with decreased mean diffusivity and tissue T1. Additionally, BERK-Hemi mouse exhibited elevated concentrations in N-acetylaspartate, glutamate, total choline and glucose in thalamus, but a lower concentration of glutamine. Together, the results suggest BERK-Hemi mice develop a compensatory mechanism which leads to increased glycolysis to combat hypoxia and increased reactive oxygen stress.
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