By studying transgenic mice, acceleration of AD pathogenesis in model systems has been achieved by introducing systemic insulin resistance conditions, including dietary manipulation (e.g., high-fat diet [HFD]), leptin knockout (ob/ob), mutant leptin receptor (db/db), and nitrosamine exposure (i.e., administration of streptozotocin [STZ]) [10–13]. The gene discussed is LEPR; the disease is Alzheimer disease.