A new study published in Nature revealed a shared antidepressant mechanism that connects two rapid depression treatments. This shared antidepressant mechanism highlights how ketamine and electroconvulsive therapy activate the same biological pathway. The finding marks a major advance in global efforts to improve therapies for patients with treatment-resistant depression.
Researchers from leading Chinese institutions collaborated to decode how both treatments trigger fast and sustained clinical effects. The team included scientists from the Beijing Institute for Brain Research and Peking University’s key membrane biology laboratory. Their work also involved chemical biology specialists from the Chinese Academy of Sciences.
The researchers used advanced fluorescent probe technology that allowed real-time visualization of chemical changes in the living brain. Their method revealed that ketamine and electroconvulsive therapy both caused a rapid surge in adenosine levels. The surge occurred in mood-regulating regions that play crucial roles in depression and stress biology.
According to the research team, adenosine release appears to initiate the treatments’ fast therapeutic benefits. They emphasized that this discovery clarifies a central question that challenged neuroscientists for decades. They also explained that the surge in adenosine arises from distinct energy disruptions in the brain.
Ketamine reduces cellular energy production, which pushes cells into stress-response mode. In contrast, electroconvulsive therapy increases energy consumption through intense neural activation. Although the triggers differ, both treatments disrupt energy balance and activate the same shared antidepressant mechanism.
Importantly, the researchers stated that this mechanism operates independently from pathways linked to hallucinations or addiction. This distinction provides new opportunities for designing safer and more selective antidepressant drugs. It also helps explain why ketamine’s side effects do not determine its core therapeutic action.
Based on their findings, the team developed a new ketamine derivative with improved performance. Early animal studies showed that the compound delivered stronger antidepressant results at significantly lower doses. The reduced dosage also correlated with fewer cognitive and behavioral side effects in test models.
The researchers have filed patents for small-molecule drugs and hypoxia-based therapeutic devices. They plan to move rapidly toward clinical translation to expand treatment options for patients. Their next goal involves partnering with medical institutions to begin formal safety evaluations and regulatory preparations.
Mental-health analysts said the study could reshape the future of precision antidepressant therapies. They noted that patients with treatment-resistant depression represent nearly one-third of diagnosed cases worldwide. Consequently, new breakthroughs that rely on a shared antidepressant mechanism may unlock safer and faster approaches.
If clinical development progresses successfully, the new treatment strategy could enter human trials within the coming years. Researchers believe these advances may redefine therapeutic standards and widen access to rapid-acting depression care.
