The significance of nicotinergic receptors in the pharmacotherapy of Alzheimer's disease

The treatment of dementia and in particular Alzheimer's disease has become easier and more reliable in clinical practice because of new developments in pharmacotherapy. Presently, the pharmacotherapy of Alzheimer's disease is mainly based on the cholinergic hypothesis, i.e. the degeneration of cholinergic neurons in the basal forebrain giving rise to a cholinergic deafferentiation of the entire cortical mantle. New data on the cholinergic changes in Alzheimer's disease have revealed a loss of nicotinergic receptors in the CNS, which contrasts with the known preservation of muscarinergic receptors. The reduction of nicotinergic receptors has functional consequences on the acetylcholine receptors themselves and on the release of several other neurotransmitters. In Alzheimer's disease, a relatively specific treatment option with cholinesterase inhibitors is available. Here, the data on the pathophysiological background of treatment with a new cholinesterase inhibitor, galantamine, is reviewed and the special pharmacological profile of galantamine in the treatment of Alzheimer's disease is discussed, i.e. galantamine being an acetylcholinesterase inhibitor with stimulatory properties on nicotinergic acetylcholine receptors.