One of the most prominent features of Alzheimer’s disease (AD) is a significant deficit in cholinergic transmission in certain brain areas.1,2 The concentrations of acetylcholine (ACh) decrease by nearly 90% in patients with AD. Therefore, one main focus of AD treatment is the use of agents that increase the availability of intrinsic ACh by inhibiting the acetylcholinesterase (AChE) enzyme. This may restore the cholinergic function in the brain and significantly reduce the severity of dementia. Another key feature in brain pathology of patients with AD is the progressive deposition of the amyloid β (Aβ) peptide in fibrillar form.3