Whereas in the early-onset AD, the underlying cause can be pinpointed to increased Aβ production due to gene mutations in its precursor, amyloid precursor protein (APP), or APP-cleaving presenilin 1 or 2 (PSEN1, PSEN2) [1–3], the pathogenesis of the sporadic disease form appears to be a multifactorial cascade involving genetic, health and environmental factors, such as heart disease, obesity and associated diseases, inflammatory responses and reactive oxygen species [1–3]. Here, APP is linked to obesity due to melanocortin 4 receptor deficiency.