Because of the age-driven disappearance of NSCs/NPCs via their conversion into mature hippocampal astrocytes. Therefore, we propose that the anti-aging effects produced by Rg1 also Tubulin Acetylation Inducer correlate with increased neurogenesis. Our data in this study supported this hypothesis. Four weeks of Rg1 treatment promoted NSCs/NPCs differentiation to neurons rather than glial cells, because the number of the cells positive for b-tubulin III increased and that of the cells positive for GFAP and Gal-C decreased, compared with the D-gal administration group. b-tubulin III is widely regarded as a neuronal marker in developmental neurobiology and stem cell research. Given the potential significance of new neurons for cognitive function, it has been hypothesized that reduced neurogenesis may contribute to age-related cognitive impairment. The promoted neurogenesis of Rg1 treatment in this study supports the effect of ginsenoside Rg1 in improving cognitive ability and the function of Panax ginseng in preventing memory deterioration. GFAP is highly expressed by astrocytes and is widely used as a marker for differentiated astrocytes, while evidence also indicates that GFAP is expressed by developing NSCs/NPCs. However, in the D-gal administration group of this study, GFAP-positive cells showed morphological characteristics of activated astrocytes. Considering that the activated astrocytes have been identified as a major brain-derived source of inflammatory cytokines, and elevated levels of IL-1b can lead to astrocytes activation in a positive feedback way, we believe that most GFAP positive cells represent astrocytes in this study. In addition, the treatment of Rg1 significantly decreased the GFAP-positvie and Gal-C –positive cells number. Our results suggest Rg1 can counteract the agedriven NSCs/NPCs deletion and excess astrogenesis and promote NSCs/NPCs differentiation into neurons. We further examined whether Rg1 promoted neurogenesis by maintaining the NSCs/NPCs. We employed the wide-spreading NSCs/NPCs markers SOX2 and Nestin. The increase of SOX2 level in the Rg1 treatment plus D-gal administration group indicated that the Rg1 could protect NSCs/NPCs survival against D-gal induced aging. The increase of newly generated cells indicated by BrdU in the Rg1 treatment plus D-gal administration group further revealed the NSCs/NPCs protective effect of Rg1. Moreover, in NSCs/NPCs, telomeres shortened with age and that telomerase-deficient mice exhibited reduced neurogenesis. In this study, the SOX2 expression was well correlated with the changes of lengths of telomeres and the activity of telomerase in each group. These results suggest that ginsenoiside Rg1 effectively protect NSCs/NPCs survival against D-gal induced aging. Interestingly, Nestin expression increased in the D-gal administration group. Nevertheless, this observation was consistent with the bulk of studies suggesting that in pathological conditions adult glial cells are induced to revert to a more primitive glial form, so that earlier stages phenotypic features, including Nestin, were transiently re-expressed. Another study also illustrated that Nestin was re-expressed in the activated astroglial in the damaged brains.