Collectively, our results suggest that hippocampal DNMT inhibition can induce cognitive impairments by promoting DNA demethylation, leading to the inactivation of plasticity-related pathways and elevated astrogliosis resembling aging [41], and by abolishing the effects of PrL DBS on serotonergic and dopaminergic systems and cognition. The gene discussed is PRL; the disease is Cognitive impairment.