Cerebral effects of inducing diabetes or insulin resistance in normal rodents (i.e., non-AD rodent models) and in rodents genetically modified to accumulate Aβ in the brain (i.e., AD rodent models). Common interventions to induce diabetic conditions in rodents included recessive mutations in the obesity gene (ob, also known as Lep), defects in the leptin receptor (Ob-R), diet, and administration of streptozotocin. Rodents with pancreatic overexpression of human amylin spontaneously develop both type-2 diabetes and dementia-like pathology.