FLG and Alzheimer disease: Baurecht et al. showed that apart from filaggrin deficiency, S. aureus abundance correlated with ceramide α-Hydroxy fatty acid/sphingosine base activity [105], while Cleary et al. demonstrated that ceramide distribution might structurally inhibit the formation of bacterial biofilms, and proposed that the characteristic pattern of their depletion typical for AD probably served as a conduit for S. aureus growth [106].