Nicotine reduces Aβ in the brain and cerebral vessels of APPsw mice

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Abstract
Ten days treatment with nicotine reduced insoluble amyloid Aβ1–40 and Αβ1–42 peptides by 80% in the cortex of 9‐month‐old APPsw mice, which is more than that observed in 14.5‐month‐old mice following nicotine treatment for 5.5 months. A reduction in Aβ associated with cerebral vessels was observed in addition to that deposited as parenchymal plaques after 5.5 months treatment. The diminution in Aβ peptides observed was not accompanied by changes in brain α, β or γ secretase‐like activities, NGF or BDNF protein expression measured in brain homogenates. A significant increase in sAPP was observed after nicotine treatment of SH‐SY5Yneuroblastoma cells that could be blocked by the nicotinic antagonist mecamylamine. Attenuation of elevated [125I]‐αbungarotoxin binding (α7) in APPsw mice was observed after 5.5 months nicotine treatment. Both these observations suggest that the reduction in insoluble Aβ by nicotine might be in part mediated via the α7 nicotinic receptor. Further studies are required to identify potential mechanisms of the nicotine's amyloid‐reducing effect.