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Ye Ju, Toru Asahi and Naoya Sawamura Arctic mutant Aβ40 aggregates on α7 nicotinic acetylcholine receptors and inhibits their functions Journal of Neurochemistry 131

Version of Record online: 14 AUG 2014 | DOI: 10.1111/jnc.12837

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Amyloid β protein (Aβ) plays a central role in the pathogenesis of Alzheimer's disease (AD). The ‘Arctic’ mutation within the Aβ sequence has a purely cognitive phenotype typical of AD. Here, we show that Arctic Aβ40 aggregation was enhanced by the addition of neuronal acetylcholine receptor subunit alpha-7 (CHRNA7), which destabilized CHRNA7 functions via inhibition of the Ca2+ response and activation of ERK1/2. These findings may reflect the mechanism underlying familial AD caused by the Arctic Aβ mutation.

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