Editorial Volume 4, Issue 12 pp 854—855

Figure 1. A model whereby mechanisms of aging concurrently contribute to reduced physiologic “fitness” and increased malignant potential of neural stem/progenitor cells. Reduced NSPC “fitness” regulated in part by increased p16 manifests as increased NSPC senescence, reduced proliferation and self-renewal. Conversely, increased NSPC malignant potential or “preconditioning” regulated by decreased p53 function contributes to increased genomic instability, hypoxic tolerance, and possibly mTOR activity. Finally, the rapid cell cycle re-entry [3] and presumed selection advantage of a sub-population of aging NSPCs provides another potential mechanism by which aging NSPCs acquire increased malignant potential.