Several factors may influence the levels of circulating AAs in AD including both physiological factors such as protein intake and body proteolysis [12,13] and pathological factors such as inflammation [14], in which oral [15] and intestinal [16] dysbioses may play a role, insulin resistance [17], oxidative stress [18], skeletal muscle mitochondrial dysfunction following β-amyloid (Aβ) deposition [19,20,21], and wasting of lean body mass [22]. The gene discussed is INS; the disease is Alzheimer disease.