IGHE and Alzheimer disease: AD presents with great heterogeneity in terms of severity, clinical features, and course, with a complex underlying pathophysiology [5], which involves an interplay between the dysfunctional skin barrier, immune dysregulation—starting with a core T helper 2 (TH2) response accompanied by IgE sensitization to environmental allergens and progressing with a widening of the adaptive immunity with TH1, TH17, and TH22 responses—and skin microbiome dysbiosis [7,8].