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. Author manuscript; available in PMC: 2015 Jul 8.
Published in final edited form as: Neurobiol Aging. 2013 Apr 22;34(10):2352–2360. doi: 10.1016/j.neurobiolaging.2013.03.032

Fig. 6.

Fig. 6

No age-related change in APP processing with no evidence for senile plaques. C83 and C99 are the C-terminal fragments that remain after APP processing. The former is a footprint of the non-amyloidogenic pathway, whereas the latter implies an amyloidogenic event. Neither C83 (A) nor C99 (B) changed significantly among young (2 years), older (10–15 years), and the oldest (20+ years) NMRs (ANOVA F = 2.572, p = 0.171; F = 2.149, p = 0.212, respectively). A representative immunoblot of C83 and C99 is shown (C, top) with the corresponding loading control (C, bottom). In all age groups, the ratio between C83 and C99, however, suggests that there are more non-amyloidogenic events than amyloidogenic ones, providing some protection against Aβ production. Immunostaining with 6E10 antibody does not reveal plaques in NMRs. Note that some intraneuronal staining appears; staining with 4G8 antibody revealed the same pattern and is therefore not shown here. No plaques detected in low (D) or high (F) magnification of a 29-year-old NMR. For control purposes, immunohistochemistry was performed in tandem with an 18-month-old 3xTg-AD mouse. Low (E) and high (G) magnification clearly shows Aβ plaques (arrows).