In LPS, Aβ1-42 and triple-transgenic-induced AD mice, luteolin ameliorates behavior impairment, inhibits overproduction of pro-inflammatory mediators (26, 29–31), as well as restrains GFAP, p38 protein expression and the phosphorylation of JNK and p65 (26, 31). This evidence concerns the gene GFAP and Alzheimer disease.