The pathogenesis of AD is typically defined by increases in T helper (Th) 2-mediated inflammatory responses, including the release of immunoglobulin E (IgE); recruitment of eosinophils; production of interleukin (IL)-4, IL-5, and IL-13; and Th1-dominant skin inflammation in the chronic phase [2,3,4,5]. This evidence concerns the gene IGHE and Alzheimer disease.