Abstract
There is increasing evidence for disturbances in nicotinic acetylcholine receptor (nAChR) function in Alzheimer's disease (AD). nAChRs are involved in the regulation of many processes, including synaptic plasticity and memory. Levels of nAChRs are altered in the Alzheimer brain and there is evidence that the amyloid βprotein (Aβ) can directly bind to nAChRs. Nicotinic agonists may also protect cells from Aβ toxicity. Drugs which interact with the nAChR or which inhibit Aβ binding to nAChRs may be of value for the treatment of AD.
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