Reduced intracellular accumulation of Aβ and phosphorylated tau levels; decreased acetylcholine-mediated effects and elevated ACh levels; reduced the levels of 2 protein kinases linked with ERK, GSK-3β, and tau phosphorylation; eliminated the glutamate-induced neurotoxic effects; mediated positive outcomes on AD markers; increased levels of N-acetyl aspartate. This evidence concerns the gene GSK3B and Alzheimer disease.