Studies have shown that ketamine can reduce DNA methylation at specific sites within the BDNF gene, leading to increased expression of this gene and, consequently, more BDNF protein in the brain. This upregulation of BDNF is crucial because it supports the repair and growth of neural circuits often compromised in depression. Additionally, ketamine has been linked to epigenetic changes in genes associated with the serotonergic system, including the serotonin transporter gene (SLC6A4) and serotonin receptors (like 5-HT1A and 5-HT2A). By altering the methylation status of these genes, ketamine may increase serotonin availability and improve the responsiveness of these receptors, further contributing to its antidepressant effects. While the direct impact of ketamine on epigenetic age is still under investigation, its ability to modify key genes associated with neuroplasticity and mood regulation suggests that it may have rejuvenating effects on the brain. By enhancing BDNF signaling and potentially reversing some of the epigenetic markers of stress and aging, ketamine might reduce biological age, particularly in the brain.