Neurogenesis in Alzheimer’s Disease

The potential of hippocampal neurogenesis, the innate capacity of “self” stem cells in the hippocampus to generate new neurons throughout our lifespan, is rapidly gaining importance not only as a potential therapeutic avenue (i.e., replacement of damaged neurons) but also as a potential pathogenic mechanism for disease (i.e., inability to generate new neurons) for various disease processes, most notably neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease. In this review, we focus on the role of neurogenesis in AD in which it is notable that conditions that improve cognitive output and increase neurogenesis are associated with a decreased incidence of AD, whereas, conversely, conditions that lead to declines in behavioral output and neurogenesis are associated with increases in incidence. These parallels suggest that changes in hippocampal neurogenesis may play a significant role in the development of AD and that modulating this process may provide a mechanistic and therapeutic inroad to the disease. However, contradictions within the neurogenesis literature itself and across studies examining this process in animal models of AD have led to a confusing state of affairs regarding the role of neurogenesis in AD. Herein, we critically examine these contradicting reports and provide additional/alternate insight into the function of hippocampal neurogenesis in AD.