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The articles by Vaishnavi et al. (1) and Vlassenko et al. (2) in PNAS demonstrate regional variation in aerobic glycolysis vs. oxidative phosphorylation in the human brain and then link aerobic glycolysis to amyloid β (Aβ) deposition on the basis of concordant spatial distributions in Alzheimer's disease (AD). As referenced in these articles, the molar ratio of O2 to glucose consumption by the brain is never 6 (the ratio for complete oxidation of glucose to CO2 and H2O). Because the experimentally determined molar ratio is normally ≈5.3, the major portion of glucose flux proceeds through the tricarboxylic acid (TCA) cycle to meet the high ATP demands of the brain, as well as other TCA cycle functions. The term “aerobic glycolysis,” as defined by the authors, refers to flux from glucose to pyruvate without entering the TCA cycle, as well as glucose providing substrates for the pentose phosphate shunt and glycogen synthesis, in conditions whereby oxygen availability is not limiting. Although much less energy efficient than mitochondrial oxidative phosphorylation (36 ATP/glucose), aerobic glycolysis (2 ATP/glucose) can rapidly provide ATP and substrates for biosynthetic pathways. Raichle and colleagues were the first to clearly demonstrate that task-based activation of local regions of the human brain associated with increases in glucose metabolism determined with 2-deoxy-2-[18F]fluoro-d-glucose (FDG) and PET (3) occur with little to no increases in oxygen metabolism, even though local availability of oxygen is sufficient for oxidative phosphorylation (references in ref. 1). These findings indicate that, in execution of these tasks, the involved brain tissue switches to aerobic glycolysis. These “switch points” that alter glucose metabolic flux through various biochemical pathways occur in a number …

Correlation of brain amyloid with “aerobic glycolysis”: A question of assumptions?