Banerjee et al. (2000) observed that in the remaining cholinergic neurons there was a higher amount of nAChR, which suggests a possible compensatory mechanism. Many efforts were performed to ameliorate this loss. However, current approved pharmacological agents, such as physostigmine, tacrine, donepezil, rivastigmine and galantamine (Martorana et al., 2010), are targeted to inhibit ACE function increasing the amount of acetylcholine at the synapse cleft and ameliorating the clinical symptoms of AD without halting the progress of the disease. This evidence concerns the gene ACE and Alzheimer disease.