During AD progression, AChE activity decreases to 55–67% of normal values in the hippocampus and temporal cortex, while the activity of BChE gradually increases in the late stage of AD up to 120% of normal levels and accumulates in senile plaques, thus suggesting an extremely critical role for BChE in ACh hydrolysis and disease progression [3,4]. Here, ACHE is linked to Alzheimer disease.