In a new study published in the Journal of Psychiatric Research, researchers led by Angelos Halaris, M.D., Ph.D., a professor of psychiatry and behavioral neurosciences at Loyola University Chicago Stritch School of Medicine, discovered that Escitalopram may reduce neurotoxicity in individuals with Major Depressive Disorder (MDD.)
A pro-inflammatory state and a dysregulation in the tryptophan/kynurenine pathway have been associated with depression. This study set out to examine whether treatment using the popular SSRI, Escitalopram (ESC) could suppress inflammation and beneficially shift metabolites of the kynurenine pathway in patients who suffer from MDD.
Researchers compared blood samples from 30 adults with MDD who were given 20 to 40 mg of Escitalopram daily for 12 weeks with 27 individuals from a control group. They looked closely at plasma levels of inflammatory biomarkers and tryptophan/kynurenine metabolites for both groups and re-measured at 4, 8, and 12 weeks after treatment with Escitalopram. Subjects also took part in clinical assessments throughout using the Hamilton depression (HAM-D), Beck Depression Inventory (BDI), and Clinical Global Impression (CGI) scales.
Researchers found that baseline plasma concentrations were higher in the MDD group compared with the control group, four of which reached statistical significance (hsCRP, TNF-alpha, IL6, and MCP-1). During the ESC treatment, they found that most concentrations of inflammatory biomarkers did not change, except for TNFα which decreased. Metabolites and ratios of the tryptophan/kynurenine pathway showed reductions of neurotoxic metabolites including 3-hydroxykynurenine and quinolinic acid, 3-hydroxykynurenine/kynurenine, quinolinic acid/tryptophan, kynurenic acid/quinolinic acid and quinolinic acid/3-hydroxykynurenine.
Overall, patients showed significant improvements in depression symptoms, but with a high rate of remission. This means the selective-serotonin re-uptake inhibitor (SSRI) Escitalopram may protect against some inflammatory and neurotoxic biomarkers associated with the mood disorder. This also means that ESC may get it’s antidepressant effect in part because of it’s ability to inhibit the synthesis of certain neurotoxic kynurenine metabolites and/or because of it’s ability to reduce the inflammatory response.
The authors of the study noted that, “Although it is not certain at this point whether these biomarker changes are the cause or effect of the clinical improvement achieved at week 8, one clear observation is that, at week 8, escitalopram monotherapy induced reduction of both clinical symptom scores and inflammatory and neurotoxic biomarkers.”
More research needs to be done to fully understand the mechanisms at work here, but this is another great push towards a greater understanding of what factors contribute to the development of depression and how SSRI’s may not play a role in alleviating symptoms.
Dr. Michael Reed is a Nashville based Psychiatrist. Please visit his main website for information about his career.