Bioprofiling of platelets in medicated patients with depression

Hüfner, Katharina; Kandler, Christina; Koudouovoh-Tripp, Pia; Egeter, Jonas; Hochstrasser, Tanja; Stemer, Bettina; Malík, Peter; Giesinger, Johannes; Humpel, Christian; Sperner‐Unterweger, Barbara

doi:10.1016/j.jad.2014.09.029

Cited by 17 publications

(18 citation statements)

References 52 publications

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“…Consistently with the majority of previous studies about peripheral serotonin levels (blood, platelet, serum, or plasma), we observed a dramatic decrease in fasting serotonin plasma levels in MDE patients as compared to HC. Interestingly, serotonin levels were 20‐fold lower in AD‐free MDE patients than in HC, which rules out the role of previous AD drug treatment to account for this observation.…”

Section: Discussionsupporting

confidence: 92%

Peripheral tryptophan, serotonin, kynurenine, and their metabolites in major depression: A case–control study

Colle

Masson

Verstuyft

et al. 2019

Psychiatry Clin Neurosci

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Aim Tryptophan is the sole precursor of both peripherally and centrally produced serotonin and kynurenine. In depressed patients, tryptophan, serotonin, kynurenine, and their metabolite levels remain unclear. Therefore, peripheral tryptophan and metabolites of serotonin and kynurenine were investigated extensively in 173 patients suffering from a current major depressive episode (MDE) and compared to 214 healthy controls (HC). Methods Fasting plasma levels of 11 peripheral metabolites were quantified: tryptophan, serotonin pathway (serotonin, its precursor 5‐hydroxytryptophan and its metabolite 5‐hydroxyindoleacetic acid), and kynurenine pathway (kynurenine and six of its metabolites: anthranilic acid, kynurenic acid, nicotinamide, picolinic acid, xanthurenic acid, and 3‐hydroxyanthranilic acid). Results Sixty (34.7%) patients were antidepressant‐drug free. Tryptophan levels did not differ between MDE patients and HC. Serotonin and its precursor (5‐hydroxytryptophan) levels were lower in MDE patients than in HC, whereas, its metabolite (5‐hydroxyindoleacetic acid) levels were within the standard range. Kynurenine and four of its metabolites (kynurenic acid, nicotinamide, picolinic acid, and xanthurenic acid) were lower in MDE patients. Conclusion Whilst the results of this study demonstrate an association between the metabolites studied and depression, conclusions about causality cannot be made. This study uses the largest ever sample of MDE patients, with an extensive assessment of peripheral tryptophan metabolism in plasma. These findings provide new insights into the peripheral signature of MDE. The reasons for these changes should be further investigated. These results might suggest new antidepressant therapeutic strategies.

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Section: Discussionsupporting

confidence: 92%

Peripheral tryptophan, serotonin, kynurenine, and their metabolites in major depression: A case–control study

Colle

Masson

Verstuyft

et al. 2019

Psychiatry Clin Neurosci

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show abstract

“…The latter finding was confirmed by an independent study that found higher baseline mRNA levels of IL-1b (þ33%) in non-responders (Cattaneo et al 2013). Platelet content of IL-1b was also associated with MDD (Hufner et al 2014).…”

Section: Peripheral Biomarkersmentioning

confidence: 58%

Consensus paper of the WFSBP Task Force on Genetics: Genetics, epigenetics and gene expression markers of major depressive disorder and antidepressant response

Fabbri

Hosák

Mößner

et al. 2016

The World Journal of Biological Psychiatry

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Major depressive disorder (MDD) is a heritable disease with a heavy personal and socio-economic burden. Antidepressants of different classes are prescribed to treat MDD, but reliable and reproducible markers of efficacy are not available for clinical use. Further complicating treatment, the diagnosis of MDD is not guided by objective criteria, resulting in the risk of under-or overtreatment. A number of markers of MDD and antidepressant response have been investigated at the genetic, epigenetic, gene expression and protein levels. Polymorphisms in genes involved in anti-depressant metabolism (cytochrome P450 isoenzymes), antidepressant transport (ABCB1), glucocorticoid signalling (FKBP5) and serotonin neurotransmission (SLC6A4 and HTR2A) were among those included in the first pharmacogenetic assays that have been tested for clinical applicability. The results of these investigations were encouraging when examining patient-outcome improvement. Furthermore, a nine-serum biomarker panel (including BDNF, cortisol and soluble TNF-a receptor type II) showed good sensitivity and specificity in differentiating between MDD and healthy controls. These first diagnostic and response-predictive tests for MDD provided a source of optimism for future clinical applications. However, such findings should be considered very carefully because their benefit/cost ratio and clinical indications were not clearly demonstrated. Future tests may include combinations of different types of biomarkers and be specific for MDD subtypes or pathological dimensions.

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“…Platelet ICAM-1 levels have been successfully evaluated in psychiatric patients with different diseases [56]. Platelet PECAM-1 expression can be reduced by treatment with serotonin reuptake inhibitors [43], and is altered in medicated patients with depression [31]. Mental stress has been shown to increase platelet assessed the amount of platelet P-selectin independent of granule or surface association.…”

Section: Accepted Manuscriptmentioning

confidence: 99%

“…The adhesion molecules PECAM-1 and soluble ICAM might be altered in depression and also contribute to the link with cardiovascular disease [31,32]. -TG and PF-4 are standard markers of platelet reactivity and have been analyzed in depressed patients, cardiovascular patients as well as in various mental stress conditions [33,34].…”

Section: Introductionmentioning

confidence: 99%

Differential changes in platelet reactivity induced by acute physical compared to persistent mental stress

Hüfner

Koudouovoh-Tripp

Kandler

et al. 2015

Physiology & Behavior

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Bioprofiling of platelets in medicated patients with depression

Cited by 17 publications

References 52 publications

Peripheral tryptophan, serotonin, kynurenine, and their metabolites in major depression: A case–control study

Peripheral tryptophan, serotonin, kynurenine, and their metabolites in major depression: A case–control study

Consensus paper of the WFSBP Task Force on Genetics: Genetics, epigenetics and gene expression markers of major depressive disorder and antidepressant response

Differential changes in platelet reactivity induced by acute physical compared to persistent mental stress

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