As described above, the different roles that APP metabolites, PS1 and other critical molecules play in neurogenesis, may account, as least in part, for some of the observed variations in the fate of neurogenesis in the different animal models used in these studies. Importantly, the high responsiveness and sensitivity of neurogenesis to internal and external stimuli may require a careful examination of the data as a function of age, neurodegeneration, extent and onset of amyloidosis, and, other experimental conditions, such as regimen of BrdU injection. Furthermore, differences in behavioral manipulations (e.g. training, and enriched environment) may also account for the observed heterogeneity in observed effects on neurogenesis. For example, notably, two recent studies suggest that induced reduction of amyloidosis enhances neurogenesis. Becker and colleagues show that anti- EFRH immunotherapy (i.e. antibodies raised against the EFRH sequence, encompassing amino acids 3-6 of the 42 residues of the Aβ) reduces amyloid deposition and enhances neurogenesis in PDAPP mice (Becker et al., 2007). Mirochnic and colleagues shows that experience of APP23 in enriched environment enhances neurogenesis, while reducing the ratio of Aβ42/Aβ40 (Mirochnic
