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. Author manuscript; available in PMC: 2016 Oct 1.
Published in final edited form as: Neurobiol Aging. 2015 Jun 21;36(10):2725–2736. doi: 10.1016/j.neurobiolaging.2015.06.021

Fig. 5. Haploinsufficiency of p53/p44 can rescue some of the phenotypic features caused by the overexpression of APP in the mouse.

Fig. 5

(A) Quantitative real-time PCR determination of indicated kinases in the hippocampal formation. Animals (males) were 2.5-month-old when analyzed. All values are mean (n=12) ± sd. *p < 0.05; **p < 0.005. (B) Immunostaining with anti-phospho-tau antibodies shows reduced labeling in APP695/swe;p53+/− mice. Two different antibodies were used: AT8 (against pSer202 and pThr205) and S356 (against pSer356). Mice (males) were ~1-year-old when analyzed. (C) Long-term potentiation (LTP) induction in hippocampal slices. Mice (males) were 2.5-month-old when analyzed. APP695/swe mice display deficits in the late component of LTP. These deficits are rescued by p53/p44 haploinsufficiency. **p < 0.005.