provided by studies suggesting that the SVZ is a major sAPP binding site, where sAPP regulates proliferation of transit amplifying (type C cells) EGF-responsive cells (Caille et al., 2004; Ohsawa et al., 1999). These cells self-renew in the presence of EGF, and differentiate into neurons and glia upon EGF removal (Morshead et al., 1994). Caille and colleagues show that EGF-induced proliferation of NSC is partly dependent on the EGF-induced release of sAPP into the medium. However, sAPP is necessary but not sufficient, as it does not induce cell division in EGF-free medium (Caille et al., 2004). Taken together with the resemblance between notch and APP processing, it would be tempting to speculate that other metabolites of APP, such as the carboxyl-terminus of APP (APP-CTFs) may play a regulatory role in different aspects of neurogenesis in the adult brain. AICD production has also been linked to AD through the discovery that this transcription factor binds to the neprilysin promoter and induces expression of this Aβ degrading enzyme (Belyaev et al., 2009; Pardossi-Piquard et al., 2005). Recent studies have revealed that Aβ42 enhances the survival and differentiation of progenitor cells (Lopez-Toledano and Shelanski, 2004) or compromise these processes (Haughey et al., 2002a;
