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. 2005 Feb 10;102(8):3046–3051. doi: 10.1073/pnas.0408500102

Fig. 3.

Fig. 3.

APP processing and Aβ deposition are not altered after chronic nicotine administration. (A) Immunoblot shows that APP and C99 levels are not significantly different between treated and untreated 3xTg-AD mice. (B) Quantitative analysis of blots in A after normalizing to β-actin shows that nicotine administration did not significantly alter the steady-state levels of APP or C99. (C and D) Immunohistochemical analysis by using an anti-Aβ42 specific antibody shows that Aβ deposition was not altered after chronic nicotine administration. (E) Densitometric analysis of C and D did not reveal any significant change in the Aβ load in the hippocampus of treated versus untreated 3xTg-AD mice. (F) Sandwich ELISA revealed that Aβ40 and Aβ42 steady-state levels were unaltered after chronic nicotine administration (n = 5 per group). Although there appears to be reduced Aβ40 levels in the treated mice, it did not achieve significance (P = 0.332 and 0.676 for Aβ40 and Aβ42, respectively). (G) The ratio of Aβ42/Aβ40 was also unchanged by the nicotine administration (P = 0.198).