Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou Medical University, Guangzhou, China.
3 papers in the library · 9 citations · publishing 2024-2025
Abnormal connectivity between a specific amygdala subregion (the left laterobasal amygdala) and the left precuneus in people with major depressive disorder is linked to how well ketamine treatment works. After six doses of ketamine (0.5 mg/kg), differences in connectivity changes between responders and nonresponders appeared in the bilateral centromedial amygdala with the left orbital part of the superior frontal gyrus and in the left laterobasal amygdala with the right middle frontal gyrus. A baseline difference in connectivity between the left laterobasal amygdala and the right superior/middle temporal gyrus predicted the antidepressant effect on Day 13, suggesting that ketamine may improve symptoms by regulating amygdala subregion networks.
Ketamine improves depressive symptoms in major depressive disorder by altering energy metabolism, including changes in adenosine triphosphate, adenosine diphosphate (ADP), and pyruvate. The shift in ADP levels strongly correlated with reductions in depression severity scores. Lower baseline levels of free triiodothyronine (FT3) predicted a better response to ketamine, suggesting FT3 may serve as a biological marker for treatment efficacy. These findings come from a study of 40 patients in a discovery cohort and 24 in a validation cohort, using metabolomic analysis of serum samples.
Plasma proteomic analysis of 30 major depressive disorder patients before and after two weeks of ketamine treatment identified six proteins pivotal to the drug's antidepressive effect. Immune-response pathways were activated in association with symptom relief. Three pre-treatment proteins strongly predicted which patients would respond to ketamine, offering a potential blood test to personalize treatment.