In AD patients, changes in the skin barrier (SB) lead to increased transepidermal water loss (TEWL), defects in the metabolism of pro-filaggrin,13 and lower expression of filaggrin and claudin 1 (protein located in tight junctions ‒ TJ).14, 15 In addition, there is a decrease in ceramide levels,13, 16 cholesterol sulfate and accumulation of sphingosylphosphorylcholine, due to increased expression of the enzyme sphingomyelin deacylase.17, 18 Other contributors include decreased antimicrobial peptides (AMPs), increased serine protease (SP), reduced SP inhibitors and disrupted TJs.19 This evidence concerns the gene CLDN1 and Alzheimer disease.