The mechanisms may involve improvement in the brain choline acetyl transferase (ChAT) activity that is decreased in AD rats and induced by Aβ [10], lowering the toxicity of excitatory amino acids [11] and increasing the expression of vascular endothelial growth factor (VEGF) in the brains of rats during chronic cerebral ischemia [11]. The gene discussed is VEGFA; the disease is Alzheimer disease.