Translational Psychiatry
May 9, 2023
Jared M. Kopelman, T. Keller, Benjamin Panny et al.
57 citations
A single intravenous infusion of ketamine (0.5 mg/kg) in 98 adults with unipolar depression who had not responded to at least one antidepressant was associated with rapid changes in gray matter microstructure measured by diffusion tensor imaging (DTI) 24 hours later. Greater decreases in DTI mean diffusivity, a marker of neuroplasticity enhancement, in several brain regions (left and right BA10, left amygdala) correlated with larger improvements in depression scores, particularly in the ketamine group. In the hippocampus, the relationship was reversed for one depression scale. The findings suggest that ketamine's acute antidepressant effects may involve rapid neuroplastic changes detectable with brain imaging.
Biological psychiatry global open science
July 1, 2024
Julia Aepfelbacher, Benjamin Panny, Rebecca B. Price
13 citations
Ketamine infusion strongly induced feelings of awe in people with depression, and these awe experiences consistently predicted and mediated improvements in depression scores over 1 to 30 days, unlike general dissociative effects, which did not mediate outcomes. In a study of 116 participants with depression, 77 received a ketamine infusion and 39 received saline placebo. Awe was measured 40 minutes after infusion, and depression severity was assessed at five time points afterward. Awe scores were significantly higher in the ketamine group and statistically mediated the relationship between ketamine and depression improvement at all time points, suggesting that the awe-inspiring properties of ketamine may contribute to its antidepressant effects.
Brain, behavior, and immunity
April 4, 2025
Manivel Rengasamy, Benjamin Panny, Zakary Hutchinson et al.
3 citations
In adults with treatment-resistant depression, a single ketamine infusion did not produce detectable changes in blood markers of neurotrophic and inflammatory factors compared with a saline placebo, nor were those markers linked to depression improvement over five days. Among 133 participants, only one subgroup—those with a body-mass index below 25—showed an association: rising levels of interleukin-1 receptor antagonist in the first day after ketamine correlated with less reduction in depression symptoms. The results do not support the idea that peripheral neurotrophic or inflammatory factors mediate ketamine's rapid antidepressant effects, though central nervous system activity may still be involved.
Journal of psychopathology and clinical science
April 1, 2025
Shabnam Hossein, Mary L Woody, Benjamin Panny et al.
3 citations
Ketamine rapidly improves symptoms of treatment-resistant depression (TRD), but because TRD varies widely among patients, markers are needed to personalize treatment. This study measured brain functional connectivity during positive mood processing in 152 adults with TRD before they received either ketamine or a saline placebo. Two connectivity-based subgroups emerged: Subgroup A (110 patients) and Subgroup B (42 patients). Ketamine improved depression uniformly across both subgroups. However, among patients given saline, those in Subgroup B were more likely to show a placebo response 24 hours later than those in Subgroup A. Thus, brain connectivity patterns predicted placebo response but not ketamine response.
Molecular psychiatry
November 1, 2024
H Nur Eken, Crystal Spotts, Benjamin Panny et al.
1 citation
A combination of ketamine infusion and a digital training program called automated self-association training (ASAT) produced more positive implicit self-associations immediately after treatment in adults with treatment-resistant depression, compared to control groups that received only one active component. These changes in implicit self-worth tracked with concurrent depression symptom improvement across all groups and specifically predicted longer-term depression relief at 30 days for the combined treatment group. The findings indicate that shifting implicit self-esteem during a post-ketamine 'plasticity window' is a key mechanism behind the combined treatment's antidepressant effect, confirming the intended cognitive target.