Neuronal nicotinic acetylcholine receptors serve as sensitive targets that mediate β-amyloid neurotoxicity

<正> Alzheimer's disease (AD) is the most common form of brain dementia characterizedby the accumulation of β-amyloid peptides (Aβ) and loss of forebrain cholinergicneurons.Aβ accumulation and aggregation are thought to contribute to cholin-ergic neuronal degeneration,in turn causing learning and memory deficits,but thespecific targets that mediate Aβ neurotoxicity remain elusive.Recently,accumu-lating lines of evidence have demonstrated that Aβ directly modulates the func-tion of neuronal nicotinic acetylcholine receptors (nAChRs),which leads to thenew hypothesis that neuronal nAChRs may serve as important targets that medi-ate Aβ neurotoxicity.In this review,we summarize current studies performed inour laboratory and in others to address the question of how Aβ modulates neu-ronal nAChRs,especially nAChR subunit function.