Journal of affective disorders
January 15, 2016
Megha M Vasavada, Amber M Leaver, Randall T Espinoza et al.
58 citations
In patients with major depressive disorder, differences in brain white matter structure before ketamine treatment may predict who will respond to the drug 24 hours later. Using diffusion imaging in 10 patients, those who showed more than 50% symptom improvement had greater fractional anisotropy in the cingulum and forceps minor pathways compared to non-responders. Non-responders also had lower fractional anisotropy and higher radial and mean diffusivity in these pathways compared to healthy controls, and they had an earlier age of depression onset and longer current episode. These preliminary findings suggest that the structural integrity of emotion-related brain networks may influence ketamine's antidepressant effect.
Psychological medicine
September 1, 2022
Benjamin S C Wade, Joana Loureiro, Ashish Sahib et al.
18 citations
Before serial ketamine infusion, brain structure, function, and connectivity measures predicted how much depressive symptoms changed afterward. In 60 patients with depression, machine learning models using pretreatment MRI scans explained 19% of variance in core mood and anhedonia symptoms, 27% in a depression subscale, and 1% in rumination reflection. Greater connectivity in the right medial prefrontal cortex, anterior cingulate, and posterior insula, along with lower kurtosis of a white-matter tract, predicted larger symptom reductions. Connectivity of the left posterior cingulate, left insula, and right superior parietal lobule predicted changes in rumination. These findings suggest that anterior default mode network and posterior insula connectivity may serve as biomarkers for antidepressant response.
Journal of neuroscience research
January 1, 2026
Stephanie Njau, Artemis Zavaliangos-Petropulu, Shantanu Joshi et al.
In people with treatment-resistant depression, a single low-dose ketamine infusion increased glutamate levels in the dorsal anterior cingulate cortex only in those who responded to treatment, and lower pre-treatment glutamate levels predicted greater improvement in depression scores. GABA levels did not change after treatment. Other brain metabolites linked to neuronal health and metabolism also increased. These findings suggest that ketamine's antidepressant effect involves sustained enhancement of glutamate-related neurotransmission and that baseline glutamate levels may help predict who will benefit from ketamine.