Nicotinic α7 receptors have been widely implicated in Alzheimer disease and other neurological disorders, but how they participate has been a source of confusion and controversy. This new work from Dineley's group, using a mouse model of Alzheimer disease, suggests an attractive resolution. They show that deletion of the α7 gene exacerbates learning deficits in young animals and alters the pattern of β amyloid peptides that accumulate. The α7 effect, however, may critically depend on animal age because recent work from the Heinemann group examining another mouse model of the disease found a beneficial effect of α7 deletion on learning in older animals (Dziewczapolski et al., 2009). Many lines of evidence point to α7 receptors as an attractive target for therapeutic intervention in Alzheimer disease, but this recent work makes clear the challenge posed by the different effects of the receptor.

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