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Impairment of cholinergic transmission and decreased numbers of nicotinic binding sites are well‐known features accompanying the cognitive dysfunction seen in Alzheimer’s disease (AD). In order to elucidate the underlying cause of this cholinoceptive dysfunction, the expression of two pharmacologically different nicotinic acetylcholine receptor (nAChR) subunits (α4, α7) was studied in the cerebral cortex of Alzheimer patients as compared to controls. Patch‐clamp recordings of 14 dissociated neurons of control cortices showed responses suggesting the existence of α4‐ and α7‐containing functional nAChRs in the human cortex. In cortices of Alzheimer patients and controls, the pattern of distribution and the number of α4 and α7 mRNA‐expressing neurons were similar, whereas at the protein level a decrease in the density of α4‐ and α7‐expressing neurons of ≈ 30% was observed in …