Figure 5.

In vivo genetic modulation of CDK5 rescues neurogenic deficits in the hippocampus of APP tg mice. Nine-month-old wild-type control mice (non-tg), CDK5 heterozygous deficient (CDK5^+/−), APP tg mice, or crosses (CDK5^+/−/APP) were treated with BrdU. Brain sections were processed for immunohistochemical analysis with antibodies against CDK5, p35/p25, doublecortin (DCX), or BrdU. All images are from the dentate gyrus of the hippocampus. (a–e) Immunohistochemical analysis of the levels of CDK5 immunoreactivity in wild-type, CDK5^+/−, APP tg mice, or CDK5^+/−/APP crosses. (f–j) Immunohistochemical analysis of the levels of p35/p25 immunoreactivity in wild-type, CDK5^+/−, APP tg mice, or CDK5^+/−/APP crosses. (k–o) Immunohistochemical analysis of the numbers of DCX-immunoreactive cells (arrows) in wild-type, CDK5^+/−, APP tg mice, or CDK5^+/−/APP crosses. (p–t) Immunohistochemical analysis of the numbers of BrdU-immunoreactive cells (arrows) in wild-type, CDK5^+/−, APP tg mice, or CDK5^+/−/APP crosses. Scale bar=50 μm. ^*P<0.05 compared with wild-type controls by one-way ANOVA with post hoc Dunnett's test. ^#P<0.05 compared with APP tg mice by one-way ANOVA with post hoc Tukey–Kramer test. N=4 animals per group