There is also evidence that suggests that luteolin can directly influence the formation of Aβ plaques by selectively inhibiting the activity of N-acetyl-α-galactosaminyltransferase (ppGalNAc-T) isoforms [71] and in in vivo models of AD by selectively binding to Aβ fibrils, inactivating the glycogen synthase kinase-3 alpha (GSK-3α) isoform, suppressing Aβ and promoting tau disaggregation [27, 48, 63, 72, 73]. Here, GSK3A is linked to Alzheimer disease.