The familial form is caused by mutations of amyloid precursor protein (APP) and γ-secretases, presenilin-1 and -2, while alleles of APOE, TREM2, and several other genes, along with risk factors such as aging, diabetes, obesity, and hypertension, increase the risk of developing the more common sporadic late-onset form of the disease [2–5]. This evidence concerns the gene APP and obesity due to melanocortin 4 receptor deficiency.