Plasma brain derived neurotrophic factor (BDNF) and response to ketamine in treatment-resistant depression
Colin N. Haile, James W. Murrough, Dan V. Iosifescu, Lee C. Chang, Rayan K. Al Jurdi, Alexandra L. Foulkes, Sidra Iqbal, James J. Mahoney, Richard de la Garza, Dennis S. Charney, Thomas F. Newton, Sanjay J. Mathew
The International Journal of Neuropsychopharmacology October 8, 2013 DOI: 10.1017/s1461145713001119 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Randomized controlled trial Peer reviewed |
|---|---|
| Sample size | 22 |
| Population | Patients with treatment-resistant depression |
| Interventions | Ketamine Midazolam |
| Duration | 240 min post-infusion, with follow-up at 24, 48, and 72 hours |
| Topics | Depression Ketamine Esketamine |
| Keywords | Brain-derived neurotrophic factor Neurotrophic factors Depression economics Antidepressant Biomarker Midazolam Oncology Anesthesia Hippocampus Pharmacology Receptor |
| Citations | 251 |
| Key findings | Ketamine significantly increased plasma BDNF levels in responders compared to non-responders, and BDNF levels were negatively correlated with depression scores. |
Abstract
Ketamine produces rapid antidepressant effects in treatment-resistant depression (TRD), but the magnitude of response varies considerably between individual patients. Brain-derived neurotrophic factor (BDNF) has been investigated as a biomarker of treatment response in depression and has been implicated in the mechanism of action of ketamine. We evaluated plasma BDNF and associations with symptoms in 22 patients with TRD enrolled in a randomized controlled trial of ketamine compared to an anaesthetic control (midazolam). Ketamine significantly increased plasma BDNF levels in responders compared to non-responders 240 min post-infusion, and Montgomery-Åsberg Depression Rating Scale (MADRS) scores were negatively correlated with BDNF (r=-0.701, p = 0.008). Plasma BDNF levels at 240 min post-infusion were highly negatively associated with MADRS scores at 240 min (r = -0.897, p=.002), 24 h (r = -0.791, p = 0.038), 48 h (r = -0.944, p = 0.001) and 72 h (r = -0.977, p = 0.010). No associations with BDNF were found for patients receiving midazolam. These data support plasma BDNF as a peripheral biomarker relevant to ketamine antidepressant response.
Comparable studies
Other randomized controlled trials on ketamine for depression, most cited first.
Citations in the library
Cited by 94
- Better Biomarkers, Faster Drugs, Stronger Models: Progress Towards Precision Psychiatry. Missouri medicine 2023
- Ketamine and Rapid-Acting Antidepressants: A Window into a New Neurobiology for Mood Disorder Therapeutics Annual Review of Medicine October 23, 2014
- Neuroplasticity as a convergent mechanism of ketamine and classical psychedelics TIPS - Trends in Pharmacological Sciences September 24, 2021
- Distinct acute effects of LSD, MDMA, and d-amphetamine in healthy subjects Neuropsychopharmacology November 16, 2019
- Acute dose-dependent effects of lysergic acid diethylamide in a double-blind placebo-controlled study in healthy subjects Neuropsychopharmacology October 15, 2020
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Cites 8
- A Randomized Trial of an N-methyl-D-aspartate Antagonist in Treatment-Resistant Major Depression Archives of General Psychiatry August 1, 2006
- mTOR-Dependent Synapse Formation Underlies the Rapid Antidepressant Effects of NMDA Antagonists Science August 19, 2010
- Antidepressant Efficacy of Ketamine in Treatment-Resistant Major Depression: A Two-Site Randomized Controlled Trial American Journal of Psychiatry August 28, 2013
- Concomitant BDNF and sleep slow wave changes indicate ketamine-induced plasticity in major depressive disorder The International Journal of Neuropsychopharmacology June 7, 2012
- Brain-Derived Neurotrophic Factor and Initial Antidepressant Response to anN-Methyl-D-Aspartate Antagonist The Journal of Clinical Psychiatry September 8, 2009
and 3 more in the library