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. Author manuscript; available in PMC: 2013 Aug 1.
Published in final edited form as: Neurobiol Aging. 2011 Jul 30;33(8):1493–1506. doi: 10.1016/j.neurobiolaging.2011.06.008

Figure 3. APα reversed the learning and neurogenic deficits in 9-month-old 3xTgAD mice.

Figure 3

(A) Learning curve of 9-month-old nonTg mice: NonTg mice showed low level of learning similar to 6-month-old nonTg mice. Treatment with APα did not affect their learning. (B) Learning curve of 9-month-old 3xTgAD mice: Compared to the nonTg group, 3xTgAD mice showed a significant deficit in their maximum level of learning (P < 0.05). APα significantly increased learning compared to the vehicle-treated group (P < 0.05). 3xTgAD treated with APα exhibited a significant increase in associative learning at day 1, which was sustained at asymptote throughout the learning trial period compared to vehicle-treated 3xTgAD mice and restored learning to a level comparable to vehicle-treated nonTg performance at day 5 (P > 0.05). (C) Memory test in 9-month-old mice: 3xTgAD mice exhibited memory deficit as compared to nonTg mice (P < 0.001). APα significantly enhanced the memory performance of 3xTgAD mice to a level comparable to that of age-matched nonTg group. No effect of APα was observed in nonTg mice. (D) Cell survival analyses: 3xTgAD mice had a significantly reduced cell survival as compared to nonTg mice (P < 0.001). APα treatment increased the number of BrdU+ cells in 3xTgAD mice significantly, but showed no effect on cell survival in the nonTg group. * P < 0.05, as compared to 3xTgAD + vehicle group; † P < 0.001 as compared to nonTg + vehicle group. Data are presented as average ± SEM (n ≥ 9).