Numerous upregulated cytokines in AD lesions, including IL-4, IL-13, IL-31, IL-22, IL-17A, and oncostatin M, are known to alter barrier function through the inhibition of epidermal barrier protein synthesis (corneodesmosin, filaggrin, involucrin, loricrin, keratin-10), tight junctions (desmocollin, ZO-1, claudin-1, and -4), and/or lipids (fatty acid elongases ELOVL3 and ELOVL6, glucocerebrosidase, EO ceramides) (47–58). This evidence concerns the gene IL17A and Alzheimer disease.