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Blood transcriptional response to treatment-resistant depression during electroconvulsive therapy

ABSTRACT: This study aimed to elucidate the transcriptional differences in peripheral blood mononuclear cells (PBMC) between individuals with treatment-resistant depression (TRD) and a control group without a psychiatric illness; and between patients with TRD, treated with either standard antidepressant drugs alone, or in combination with electroconvulsive therapy (ECT) or ketamine. Additionally, PBMC transcriptomics were compared between treatment responders, following completion of their treatment protocols. PBMC transcriptomics were compared between treatment responders, following completion of their treatment protocols.

ORGANISM(S): Homo sapiens

PROVIDER: GSE234669 | GEO | 2024/06/30

REPOSITORIES: GEO

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Whole blood transcriptional signatures associated with rapid antidepressant response to ketamine in patients with treatment resistant depression.

Project description:Ketamine has rapid and sustained antidepressant effects in patients with treatment resistant depression (TRD). However, the underlying mechanisms of action are not well understood. There is increasing evidence that TRD is associated with a pro-inflammatory state and that ketamine may inhibit inflammatory cytokine production. We investigated whole blood transcriptional profiles related to TRD and gene expression changes associated with treatment response to ketamine. Whole blood was collected at baseline (21 healthy controls [HC], 26 patients with TRD) and then again in patients with TRD 24 hours following a single intravenous infusion of ketamine (0.5 mg/kg). We performed RNA-sequencing and compared a) baseline transcriptional profiles between patients with TRD and HC, b) responders vs. non-responders before ketamine treatment, and c) gene expression signatures associated with clinical improvement. At baseline, patients with TRD compared to HC were characterized by a gene expression signature indicative of interferon signaling pathway activation. Prior to ketamine administration, the metabotropic glutamate receptor gene GRM2 and the ionotropic glutamate receptor gene GRIN2D were upregulated in responders compared to non-responders. Ketamine response was associated with the downregulation of multiple genes coding for pro-inflammatory cytokines, the predicted inhibition of several interferon signaling associated upstream regulators and the downregulation of Indoleamine 2,3-Dioxygenase 1 (IDO1). The current study indicates that response to ketamine may be associated with up-regulation of glutamate receptors at baseline, and linked to transcriptional changes indicative of an anti-inflammatory response following ketamine. One specific anti-inflammatory mechanism might be the downregulation of IDO1 via inhibition of the interferon pathway.

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Project description:For major depression, the non-drug therapy Electroconvulsive therapy (ECT) treatment is highly effective and fast-acting. Despite a large and long-standing clinical use, the neurobiological mechanisms underlining ECT curative action are still poorly understood. Thanks to a genetic animal model that constitutively exhibit behavioural and biological features relevant to some aspects of major depressive disorder, here we analyse the behavioural and biological consequences of electroconvulsive stimulations (ECS), the animal model of ECT. We found that a classical ECS treatment, with 10 stimulation over 2 weeks period, has a beneficial effect on constitutive behavioural defects. We therefore compared brain and hippocampal majority proteomes from MAP6 KO mice submitted or not to electroconvulsive stimulations.

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Blood transcriptional response to treatment-resistant depression during electroconvulsive therapy

Project description:Blood transcriptional response to treatment-resistant depression during electroconvulsive therapy

| PRJNA982735 | ENA

Electroconvulsive Stimulation modulates Microglia. Transcriptome analysis of Biozzi-ABH mice spinal-cord microglia following electroconvulsive-seizures.

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