in the number of newly-differentiated neurons (Mirochnic et al., 2009). Interestingly, examination of neurogenesis in transgenic mice expressing three or more mutations in APP observed enhanced cell proliferation and neuronal differentiation in the hippocampus and/or SVZ. This may suggest that increased fibrillogenic properties or expression level of Aβ to the extent exhibited by triple mutation in APP, and APPswe,Ind in particular, enhances proliferation and neuronal differentiation. Thus, for example, Jin and colleagues (2004) used FAD-linked mutant platelet-derived growth factor- (PDGF)-APPSw,Ind transgenic mice, which express human APP isoforms APP695, APP751, and APP770 with both the Indiana (V717F) and Swedish (K670N M671L) mutations, driven by a PDGF promoter. These mice exhibit increased numbers of newly-proliferating cells in the SGL and SVZ pre- and post-onset of amyloid deposition (Jin et al., 2004b). It should be noted that the APPswe,Ind mice exhibit extracellular amyloid deposits beginning at 6–9 months of age, as well as synaptic loss, astrogliosis and microgliosis, all of which do not occur in the APPswe mice, at least not until very late in life (Borchelt et al., 1996). Caution should be taken as for the interpretation of the observations presented in these studies. Thus for example, some of the studies depend
