Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterised by depletion of high-affinity nicotinic acetylcholine receptors (nAChRs), marked loss of cholinergic neurons, occurrence of neurofibrillary tangles and accumulation of senile plaques composed of extracellular deposits of amyloid β (Aβ) protein1–3.Despite disagreements with regard to the precise nature and role of Aβ (the product of proteolytic cleavage of amyloid precursor protein [APP]) in the brain, the therapeutic goal, in general, has been to reduce Aβ levels, especially under pathological conditions4. The gene discussed is APP; the disease is early-onset autosomal dominant Alzheimer disease.