In the progression of Alzheimer's disease, oxidative stress is one of the initial events before the formation of AD plaques; to counteract this effect with interrelated factors is to raise the conation of ACH through the inhibition of AChE (acetylcholinesterase) and BChE (butyrylcholinesterase), which are responsible for the breakdown of acetylcholine in the synaptic clefts [26]. This evidence concerns the gene ACHE and early-onset autosomal dominant Alzheimer disease.