Research Paper Volume 7, Issue 6 pp 435—449

Premature aging of the hippocampal neurogenic niche in adult Bmal1‐ deficient mice


Figure 9. Schematic illustration summarizing the observed differences in neurogenesis in DG between Bmal1‐/‐ and Bmal1+/+. In young (5 weeks old) Bmal1‐/‐ mice there was an enhanced proliferation of hippocampal NPCs probably due to dysregulated cell cycle [17]. In young adult (8 weeks old) Bmal1‐/‐ mice, no difference in proliferating hippocampal NPCs was found [15], indicating that the promoting effect of Bmal1‐deficiency on NPC mitotic activity is transient and age‐dependent. In our study, adult Bmal1‐/‐ (10‐15 weeks old) mice showed a significant decrease in the pool of hippocampal NPCs indicating a dramatic down‐regulation in proliferation activity of NPCs presumably due to ROS‐induced accelerated aging/senescence. Moreover, NPCs of adult Bmal1‐/‐ mice showed a shifted differentiation towards the astroglial lineage at the expense of neurons, presumably as a consequence of Sirt1 activation.