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Human brain ageing is associated with reductions in a variety of nicotinic receptors subtypes, whereas changes in age-related disorders including Alzheimer's disease or Parkinson's disease are more selective. In Alzheimer's disease, in the cortex there is a selective loss of the α4 (but not α3 or 7) subunit immunoreactivity and of nicotine or epibatidine binding but not α-bungarotoxin binding. Epibatidine binding is inversely correlated with clinical dementia ratings and with the level of Aβ1–42, but not related to plaque or tangle densities. In contrast, α-bungarotoxin binding is positively correlated with plaque densities in the entorhinal cortex. In human temporal cortex loss of acetylcholinesterase catalytic activity is positively correlated with decreased epibatidine binding and in a transgenic mouse model over expressing acetylcholinesterase, epibatidine binding is elevated. In Parkinson's disease, loss of striatal nicotine …