neuronal cell death. Furthermore, the method of neurogenic analysis must be comprehensive and consistent (e.g. BrdU regimen, cell markers, age, etc.) Thus, a thorough understanding of the molecular mechanism underlying AD is required for the analysis of neurogenesis in FAD mouse models. This must be done first before a definite conclusion can be made regarding what is implied for the human disease. Interestingly, it becomes increasingly evident that alterations in neurogenesis take place early in life and may be a contributing factor rather than a result of neural dysfunction. A recent study suggests that in APPswe/PS1ΔE9 transgenic mice, impairments in neurogenesis take place long before amyloid deposition (Demars et al., 2009). Impairments in neurogenesis early in life, prior to processes that secondarily affect neurogenesis, such as neuronal loss, Aβ accumulation, and inflammation, may suggest that expression of FAD-linked proteins directly compromises neurogenesis in the adult brain and contribute to the disease. As AD pathology is progressive, it remains to be determined under what conditions impairment in neurogenesis is causative, at least in part, and under what conditions alterations are a downstream effect of AD pathology. Our summary of the molecular links between neurogenic and AD pathways suggest that neurogenesis is
