The effect of monoamines in AD might extend beyond a contribution to neuropsychiatric symptoms; for example, the cleavage of the Amyloid Protein Precursor (APP: which yields the toxic β-amyloid (Aβ) peptide in AD) is sensitive to 5-HT via activation of the 5-HT2a, 5-HT2c, and 5-HT4 receptors (Nitsch et al., 1996; Cochet et al., 2013). This evidence concerns the gene HTR2C and Alzheimer disease.