colleagues were observed in a separate study using pPDGF-APPSw,Ind (Gan et al., 2008), suggesting an increase in proliferation and differentiation of hippocampal progenitors in these mice at 2 months of age. Interestingly, in contrast to Jin et al. (2004) and Lopez-Toledano et al. (2007), Gan and colleagues observed a decrease in cell proliferation concomitantly with an increase in neuronal differentiation in transgenic mice at 12 months of age (Gan et al., 2008). Examination of BrdU+ cells in Tg9291 mice expressing three FAD linked mutations: APP(695)swe,dutch,Lnd and aged-matched controls revealed amyloid deposition-dependent increase in the number of proliferating cells in the hippocampus (Kolecki et al., 2008). However, the nature of these cells and their cellular lineage is not clear. Ermini and colleagues observed an increase in the number of new neurons in aged but not in adult (pre-onset of amyloid deposition) in APP23 mice expressing KM670/671NL mutated human APPswe under a murine Thy-1 promoter element. However, a decrease in proliferation of hippocampal neural progenitor cells was found in APPKM670/671NL/PS1L166P mice post onset of deposition (Ermini et al., 2008). Several additional studies examined hippocampal neurogenesis in transgenic mice coexpressing FAD-linked APP and PS1 mutant variants. Thus, for example, in APPswe/PS1ΔE9 mice, a
