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 betaprotein (Abeta) can directly bind to nAChRs. Nicotinic agonists may also protect cells from Abeta toxicity. Drugs which interact with the nAChR or which inhibit Abeta binding to nAChRs may be of value for the treatment of AD.
MeSH terms
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Alcohol Oxidoreductases
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Alzheimer Disease / drug therapy*
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Alzheimer Disease / metabolism*
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Amyloid beta-Peptides / metabolism
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Brain / metabolism*
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Cholinergic Fibers / metabolism*
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DNA-Binding Proteins / metabolism
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Humans
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Long-Term Potentiation
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Neuronal Plasticity / physiology*
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Phosphoproteins / metabolism
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Receptors, N-Methyl-D-Aspartate / metabolism
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Receptors, Neurotransmitter / metabolism*
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Receptors, Nicotinic / drug effects
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Receptors, Nicotinic / metabolism
Substances
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Amyloid beta-Peptides
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DNA-Binding Proteins
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Phosphoproteins
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Receptors, N-Methyl-D-Aspartate
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Receptors, Neurotransmitter
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Receptors, Nicotinic
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Alcohol Oxidoreductases
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C-terminal binding protein