of β-CTF, Aβ and sAPPβ, concomitantly with lower levels of sAPPα (Thinakaran et al., 1996; Borchelt et al., 1996). All of these APP metabolites are thought to modulate variable aspects of neurogenesis, and thus the results of these studies suggest that alterations in ratios and amounts of these metabolites caused by the Swedish mutation may not be favorable when it comes to neurogenesis. In addition, infusion of 5μl of 1mM Aβ1-42 or Aβ25-35 into the lateral ventricle decreased cell proliferation in the SVZ over the next five days (Haughey et al., 2002b). While the conformation of the Aβ used in this study was not determined, these results suggest that Aβ levels and/or conformation may affect neurogenesis in vivo. In a different study, oligomeric Aβ42 was shown to enhance neuronal differentiation of embryonic and postnatal NSC in vitro (Lopez-Toledano and Shelanski, 2004). Mirochnic and colleagues examined hippocampal neurogenesis in APP23. They observed an increase in cell proliferation, but ultimately a decrease 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
