As mitochondrial PDC connects glycolysis to oxidative metabolism (55) and as PDK4 upregulation facilitates FA oxidation, in particular when glucose is scarce during energy deprivation (56), the PDK4 increase observed in LOAD brains correlates with the reduced cerebral glucose utilization found in patients with AD (12), in which early brain peroxisomal and mitochondrial function deficits have been reported (reviewed in refs. 22, 57). This evidence concerns the gene PDC and Alzheimer disease.