Higher temperatures reported in more severe AD patients possibly suggest greater vascularization and degree of inflammation [44], which is further supported by several biomarkers such as T helper 2-skewed markers (IL-13, CCL17, CCL22, IL-5), markers of innate activation (IL-18, IL-1α, IL1β, CXCL8), and angiogenesis (Flt-1, vascular endothelial growth factor) [45]. This evidence concerns the gene IL18 and Alzheimer disease.