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Blood Markers May Help Match Patients to Best Depression Treatment

Biomarkers of inflammation predict treatment response (Sept. 20)

Researchers at King’s College London’s Institute of Psychiatry (IoP) have identified new biomarkers for antidepressant treatment response — an important step towards developing personalized treatments for depression. The study, announced by IoP on September 20 and published in Neuropsychopharmacology, is the first to identify blood biomarkers for antidepressant response in a clinical controlled study.

“The study confirms previous evidence that increased inflammation is part of the mechanism leading to depression, especially to particular forms of depression that are less responsive to antidepressants,” said lead author Professor Carmine Pariante. “The study shows that we could use a blood-based test to personalize the treatment of depression. If a patient had high levels of inflammation, they could immediately begin with a more intensive treatment program, such as combining antidepressants or stepping up the doses.”

The researchers aimed to identify two types of biomarkers: ones that could predict future responses to antidepressant treatment (predictors), and others that are targeted by antidepressants and change over the course of treatment (targets).

Within human cells, information from genes is transcribed into messenger ribonucleic acid (mRNA) before the effect is visible as a physical or biochemical characteristic. Previous research has shown that depression interferes with three key biological systems: the glucocorticoid receptor complex, inflammation levels, and neuroplasticity. The researchers therefore monitored how mRNA was produced for 15 specific genes linked to these three systems.

The study involved 74 depressed patients. Their levels of mRNA expression were tested before and after 8 weeks of treatment with either escitalopram (n = 38) or nortriptyline (n = 36). Escitalopram, a serotonin reuptake inhibitor, and nortriptyline, a tricyclic antidepressant, are commonly prescribed first-line antidepressant treatments in the U.K.

Individuals who did not respond well to treatment showed significantly higher levels of three inflammation markers before treatment (interleukin-1beta [IL-1beta] +33%; tumor necrosis factor-alpha [TNF-alpha] +39%; and macrophage migration inhibitory factor [MIF] +48%), suggesting that these three biomarkers could be used to identify individuals who are least likely to respond to antidepressant treatment.

“Additionally, these findings provide novel mechanistic insight into mRNA gene expression changes associated with antidepressant response, which is likely to generate new ideas for novel and more effective antidepressants,” Professor Pariante said.

For more information, visit the King’s College London Web site.

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