Previous studies have reported that Aβ deposition in AD transgenic mice and acute i.c.v. administration of Aβ25-35 peptides in rats were able to activate the hypothalamic-pituitary-adrenal (HPA) axis since soluble Aβ has been shown to activate the CRH neurons located in the paraventricular region of the hypothalamus [56–58]. The gene discussed is CRH; the disease is Alzheimer disease.