To maximize the HSV-2 glycoprotein D expression by CJ2-gD2, we replaced both copies of the HSV-2 ICP0 gene with a bi-directional transcription unit that encodes the full-length gD2 gene driven by the tetO-bearing HSV1 ICP4 promoter and the UL9-C535C gene under the control of CMVTO. While CJ2-gD2 expresses little gD2 in tetracycline repressor -expressing cells, it expresses gD2 as efficiently as wild-type HSV-2 infection in non tetR-expressing cells.Dentate gyrus dysfunction such as those seen during normal aging. In the present study, we demonstrate that ginsenoside Rg1 treatment protects hippocampus against abnormalities in a well-characterized aging rat model by D-gal administration. Rg1 treatment improved hippocampus-associated cognition, promoted NSCs/NPCs differentiation into neurons, and delayed cellular senescence in the hippocampus via antioxidant and anti-inflammation ability. D-gal administration model is a mimetic aging model related to free radical and the accumulation of waste substances in metabolism. Similarly, the accumulation of free radicals progressively damages the brain function during natural aging, and D-gal-administrated rodents mimic many characteristics of the normal brain aging process. Therefore, D-gal-induced aging model is regarded as an ideal mimetic aging model to study the mechanism related to the brain aging and screen drugs for brain aging. Furthermore, enhancing endogenous antioxidants is now widely regarded as an attractive therapy for conditions associated with mitochondrial Lapatinib oxidative stress, and ginsenoiside Rg1 is widely reported as having anti-oxidation effect. Therefore, we employed D-gal administration model in this study as we established it previously. In this study, we induced aging by D-gal administration and observed significant reduction in spatial memory, cell proliferation, and neurogenesis in the dentate gyrus. This result was supported by previous studies showing that proliferating progenitor cells were significantly decreased in the seventh week after Dgal administration. In addition, D-gal can induce behavioral impairment in C57BL/6J mice and decrease spatial preference for the target quadrant in the Morris water maze test. We administered ginsenoiside Rg1 to control and D-gal mice and probed spatial memory and learning ability using a water maze test. The administration of ginsenoiside Rg1, a main active component of Panax ginseng, significantly reduced the escape latency in the D-gal group, while Rg1 administration to control mice did not significantly change the escape latency. In addition, the administration of Rg1 to D-gal-induced aging mice significantly improved the deficits in platform crossings in probe trial and spatial preference for the target quadrant. This result was coincided with a previous study that Rg1 has profound neuroprotective effects in an Alzheimer mouse model.