While obesity in the presymptomatic stage of the disease had pernicious effects, as manifested by attenuated hippocampal glucose uptake and decreased resting cerebral perfusion; obesity during the symptomatic stage of AD prevented the disease-dependent decrease in hippocampal glucose uptake and cerebrovascular reactivity, despite unabated progression in amyloid and tau pathologies, as seen by our accompanying study in the same animals 46. This evidence concerns the gene MAPT and obesity due to melanocortin 4 receptor deficiency.