This coat is important for moisturizing the skin. The remaining Ceramide will be hydrolyzed to Sphingosine and Free Fatty Acids. In the case of xerosis senilis, the Ceramide will become more active with increasing age, so there will be less Ceramide, and the skin will dry up. AD, however, does not effect the activity of Ceramidase, Sphingomyelinase, and βglucocerebrosidase.

AD patients, on the other hand, suffer from high Glucosylsphingosine levels induced from high Glucosylceramide deacylase activity. In addition, since the Glucosylceramide deacylase is so active, the βglucocerebrosidase will have to compete with it, which decreases Acylglucosylceramides, a key ingredient in the skin’s barrier. The skin will also produce more Sphingosylphosphorylcholine than Ceramide since the activity of Sphingomyelindeacylas is unnaturally high, which makes it compete with Glucosylceramide deacylase as well. As a result, the combination of reactions (a) and (b) will yield less Ceramide (If you’ve actually read everything to this point, give yourself a pat on the back!! Don’t, worry; you do not need to understand all the medical terms). Simply put, for all the reasons stated above, AD patients have less Ceramides which makes the skin’s moisturizing abilities abysmal.