underlie, at least in part, the progressive loss of memory and compromised ability to learn and process new information characterizing the disease. Both olfactory and hippocampal dysfunction might be enhanced by compromised neurogenesis in the SVZ and SGL of the dentate gyrus, respectively. Most strikingly, molecules central to the pathology of FAD play a regulatory role in aspects of neurogenesis in the embryonic and adult brain, suggesting that dysfunction of these proteins may compromise neurogenic signaling. Here we summarize the recent knowledge on neurogenic roles of molecules that, in their mutated forms cause FAD, and on the dysfunction of neurogenic signaling pathways in AD with consequential alterations in neurogenesis in this disorder.
