Acetylcholine is a neurotransmitter produced by the cholinergic neurons, which is degraded by Acetylcholinesterase, thus terminating synaptic transmission. Reduced levels of Acetylcholine have been linked with Alzheimer’s disease (AD) symptoms. As such, the standard treatment for patients with AD is the administration of reversible acetylcholinesterase inhibitors (AChEI) to increase Acetylcholine levels. Osteoporosis is often observed in aged patients with Alzheimer’s disease, however the association between these two diseases remains poorly understood. Previous research has shown that low BMD appears to be related to increased risk of AD . It has also been found that patients with AD have increased expression of marker genes for bone turnover. A recent study by Tamimi and colleagues in 2012  reported that treatment of mild to moderate AD with the currently approved AChEI Donepezil and Rivastigmine was associated with lower rates of hip fracture in aged patients; however, no change was observed when these patients were treated with Galantamine. Thus we hypothesized that reversible Acetylcholinesterase inhibitors currently used in Alzheimer’s disease management significantly alter bone homeostasis via direct effect on osteoclasts and osteoblasts. To test this hypothesis we assessed the effects of in vitro treatment with Donepezil, Rivastigmine, and Galantamine on the formation and functional activity of bone resorbing osteoclasts, as well as the formation and functional activity of bone forming osteoblasts. Preliminary results indicate that at equimolar concentrations, Rivastigmine and Donepezil inhibit osteoclastogenesis, whereas Galantamine shows no effect. Interestingly, osteoblast precursors treated with Galantamine for 24 hours show enhanced proliferative capacity. Our study will provide insight into the mechanisms in which the different acetylcholinesterases affect the bone cells. This may influence the future drug choice in elderly patients who are affected by both AD and osteoporosis.