Figure 1 presents schematic diagram showing five of the most important therapeutic targets in Alzheimer’s disease [2]. The treatment of Alzheimer’s disease has as its main aim an increase in the levels of acetylcholine in the synaptic cleft by inhibiting cholinesterase enzymes, which are responsible for the degradation of acetylcholine. The low levels of acetylcholine in patients with Alzheimer’s disease are associated with symptoms to low memory, memory loss and gradual learning decrease [5]. This evidence concerns the gene BCHE and early-onset autosomal dominant Alzheimer disease.