During embryonic development, some of the proliferating neural stem cells enter a quiescent state and is retained till adulthood, thus contributing to adult neurogenesis, a process involving different proteins. From a published microarray of Presenilin-1 knock out embryo, one such protein, VCAM1 was found to be significantly downregulated. In addition, Presenilin-1(PS1) is known to be involved in embryonic neurogenesis as well as in cell cycle regulation. Based on these, we hypothesized PS1 to have a role in neural stem cell quiescence.To address this, we modelled quiescence in vitro by addition of BMP4 to primary embryonic neural stem cells (NSCs). Effect of PS1 overexpression was analysed in primary neural stem cells in vitro and mouse Sub Ventricular Zone in vivo. Localization dynamics of overexpressed PS1 was tracked using live fluorescence imaging.Our results showed that Presenilin-1 is upregulated in quiescent NSCs, unlike other γ- secretase components. Also, γ-secretase activity is found to be absent in quiescent NSCs pointing towards a γ- secretase independent function of PS1. PS1 is found to be more stable in quiescent NSCs possibly owing to its increased nuclear localization in quiescence. A significantly high proportion of phosphorylated PS1 is found in active NSCs compared to quiescent NSCs of which GSK3B seems to be the kinase involved. Interestingly PS1 overexpression tend to affect the NSC proliferation. Thus, when active neural stem cells transit to quiescent state, several attributes of PS1 gets modulated and PS1 might have differential interacting partners in quiescence, about which we are currently investigating.