Psychedelics and non-hallucinogenic analogs work through the same receptor, up to a point
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Updates every hour. Last Updated: 11-Sep-2025 13:11 ET (11-Sep-2025 17:11 GMT/UTC)
In a discovery that could guide the development of next-generation antidepressants and antipsychotic medications, researchers at the Icahn School of Medicine at Mount Sinai have developed new insights into how a critical brain receptor works at the molecular level and why that matters for mental health treatments. The study, published in the August 1 online issue of Science Advances, focuses on the 5-HT1A serotonin receptor, a major player in regulating mood and a common target of both traditional antidepressants and newer therapies such as psychedelics. Despite its clinical importance, this receptor has remained poorly understood, with many of its molecular and pharmacological properties largely understudied—until now.
An analysis published today in The Journal of Clinical Investigation explains how leptin affects the brain and how it might be used in future therapeutics.
DKA happens when the body is unable to make insulin and begins to break down fat for fuel. This can lead to a life-threatening buildup of sugar (glucose) and ketoacids in the blood. Doctors have typically administered insulin to address the complication, authors noted.
But evidence now shows that, when insulin is insufficient, the brain plays a key role in driving DKA, according to the new analysis, based in literature and research that includes studies conducted at UW Medicine since 2011.
Novel imaging research indicates that young adults with a higher genetic risk for depression showed less brain activity in several areas when responding to rewards and punishments. The study also uncovered notable differences between men and women. The findings from this new study in Biological Psychiatry: Cognitive Neuroscience and Neuroimaging, published by Elsevier, highlight potential early indicators for depression before clinical symptoms fully manifest.