The glia-directed activity of PEA was studied by Scuderi and coauthors, who, in a series of papers, demonstrated that PEA or synthetic PPARα agonists, in a PPARα-dependent manner, decreased markers of glial inflammation and improved neuronal viability in animal models of Alzheimer’s disease, as well as in mixed glio-neuronal cell cultures and organotypic neural cultures [157,158,159]. The gene discussed is PPARA; the disease is Alzheimer disease.