Biomarkers For Depressive Disorder Research Articles

Serum lipid level as a biomarker in depressive disorder: A cross-sectional case control study

Objectives: This study investigates the potential of serum lipids as markers for depression, specifically focusing on symptoms such as suicidal ideation and anhedonia. In the context of advancing psychiatric biomarker research, this study aims to identify lipid-related markers and their underlying biological connections to depression, offering valuable insights for clinical practice and patient outcomes. Material and Methods: This case-control observational study was conducted over 18 months at a tertiary care center. The study enrolled patients aged 18–60 years diagnosed with depression attending outpatient and inpatient departments, totaling 100 subjects, including 100 cases and 100 controls, with gender and body mass index (BMI)-matched controls. Inclusion criteria for cases required depression diagnosis using the International Classification of Diseases-10-Diagnostic Criteria for Research criteria, while controls comprised healthy individuals within the same age range. Exclusion criteria encompassed comorbid psychiatric illnesses, substance use disorders (except tobacco), unstable medical conditions, lipid-lowering agent use, and a BMI over 30. Clinical assessments, including the Hamilton Depression Rating Scale-17 item scale, Modified Scale for Suicidal Ideation, and Snaith-Hamilton Pleasure Scale-Clinician administered, were administered. Serum lipid parameters, including triglycerides (TG), total cholesterol (TC), and high-density lipoprotein (HDL)-cholesterol, were measured. Results: In a cross-sectional case-control study (n = 200), we examined serum lipids as potential depression biomarkers. Cases (n = 100) matched controls in age, BMI, and gender. Cases had lower TC (153.27 mg/dL vs. 171.34 mg/dL, P < 0.01*). Serum TG and low-density lipoprotein also varied significantly with depression severity (P < 0.01*). However, HDL levels remained consistent. No significant associations were found between suicidal ideation and anhedonia, and post hoc analyses revealed significant differences (P ≤ 0.05) in lipid parameters across various depression severity levels. Conclusion: These findings suggest a complex relationship between serum lipids and depression, with potential implications for understanding the biological underpinnings of depression and its severity. However, there was no such relationship that was observed between serum lipids and anhedonia or suicidal ideation. These insights could inform clinical practices and improve patient outcomes in depression management.

Clinical Utility of Fluid Biomarker in Depressive Disorder.

Major depressive disorders are ranked as the single largest contributor to non-fatal health loss and biomarkers could largely improve our routine clinical activity by predicting disease course and guiding treatment. However there is still a dearth of valid biomarkers in the field of psychiatry. The initial assumption that a single biomarker can capture the myriad of complex processes proved to be naive. The purpose of this paper is to critically review the field and to illustrate the possible practical application for routine clinical care. Biomarkers derived from DNA analysis are the ones that have received the most attention. Other potential candidates include circulating transcription products, proteins, and inflammatory markers. DNA polygenic risk scores proved to be useful in other fields of medicine and preliminary results suggest that they could be useful both as risk and diagnostic biomarkers also in depression and for the choice of treatment. A number of other possible fluid biomarkers are currently under investigation for diagnosis, outcome prediction, staging, and stratification of interventions, however research is still needed before they can be used for routine clinical care. When available, clinicians may be able to receive a lab report with detailed information about disease risk, outcome prediction, and specific indications about preferred treatments.

Integrating Endocannabinoid Signalling In Depression.

Depression is a common mental disorder and is the leading cause of suicide globally. Because of the significant diversity in mental disorders, accurate diagnosis is difficult. Hence, the investigation of novel biomarkers is a key research perspective in psychotherapy to enable an individually tailored treatment approach. The prefrontal cortex (PFC) is a vital cortical region whose circuitry has been implicated in the development of depressive disorder. The endocannabinoid system (ECS) has garnered increasing attention because of its involvement in several diverse physiological brain processes including regulation of emotional, motivational and cognitive functions. The current review article explores the function of the key elements of the ECS as a biomarker in depressive disorder. The activity of endocannabinoids is thought to be moderated by the CB1 receptors in the central nervous system (CNS). Variations in the concentration of endocannabinoids and the binding affinity of CB1 receptors and their density have been identified in the PFC of persons with depression. Such discoveries support our theory that alteration in endocannabinoid function leads to the pathophysiological features of depressive disorders. Moreover, evidence from animal and human studies has revealed that dysfunction in endocannabinoid signalling can produce depression-like behaviours; therefore, improvement of endocannabinoid signalling may represent a new therapeutic approach for the management of depressive disorders.

Cerebrospinal fluid monoamine metabolite concentrations in depressive disorder: A meta-analysis of historic evidence

Altered monoaminergic functions have been implicated in the pathophysiology of depressive disorder. However, previously reported cerebrospinal fluid (CSF) monoamine metabolite concentrations in major depression have been inconsistent. We performed a meta-analysis of historic evidence to determine whether CSF monoamine metabolite levels were different between patients with depression and normal controls, and could be used as depression biomarkers. Relevant studies that investigated CSF 5-hydroxyindoleacetic acid (5-HIAA), homovanillic acid (HVA), and 3-methoxy-4-hydroxyphenylglycol (MHPG) levels in patients with depression and normal controls were identified in PubMed, Web of Science, PsycINFO, and Embase databases through September 5, 2017, using a synonymous search for depression, CSF, normal, control, and each monoamine metabolite name, and in the reference lists of the acquired articles. Obtained records were individually scrutinized for eligibility. Our search strategy identified 26 studies, including our own. We employed random effects modeling and adopted “Hedges's g” as an index of effect size. In the meta-analyses, no significant difference was observed in CSF 5-HIAA or MHPG levels between patients with depressive disorder and controls. In contrast, CSF HVA was significantly decreased in patients with depression (Hedges's g = −0.30, P = 0.0000025), and these results remained significant after patients with bipolar disorder were excluded (Hedges's g = −0.37, P = 0.000061). In the meta-regression, sex was significantly associated with the Hedges's g of CSF HVA (Q = 4.41, P = 0.036). This meta-analysis revealed that only CSF HVA, and not 5-HIAA or MHPG, levels were decreased in depressive disorder. The reduction in the CSF HVA concentration in patients with depression may guide future studies on depression and serve as a useful biomarker of depressive disorder.

Predictive value of homocysteine for depression after acute coronary syndrome.

We investigated roles of plasma homocysteine and MTHFR gene in relation to risks and treatment responses of depression in ACS. A sample of 969 patients with recent ACS were recruited and 711 followed 1 year later. In addition, of 378 baseline participants with depressive disorder, 255 were randomized to a 24-week double blind trial of escitalopram (N = 127) or placebo (N = 128). A higher homocysteine concentration was independently associated with prevalent depressive disorder at baseline irrespective of MTHFR genotype; and with both incident and persistent depressive disorder at follow-up only in the presence of TT genotype. MTHFR genotype was not itself associated with depressive disorder after ACS. No associations were found with 24-week antidepressant treatment responses. Plasma homocysteine could be a biomarker for depressive disorder particularly in the acute phase of ACS. Focused interventions for those with higher homocysteine level and MTHFR TT genotype might reduce the risk of later depressive disorder.

Relationship between interleukin-1β and depressive disorder after acute coronary syndrome

This study was aimed to investigate the effect of serum interleukin (IL)-1β in the depression trajectory after acute coronary syndrome (ACS) considering two IL-1β polymorphisms: −511C/T or +3953C/T. A total of 969 patients were evaluated within 2weeks after ACS and of these, 711 were followed-up 1year later. Depressive disorders were evaluated at baseline and 1year after ACS, using the Mini-International Neuropsychiatric Interview. Serum IL-1β levels and IL-1β genotypes were investigated at baseline. Covariates on socio-demographic and clinical characteristics including depressive symptoms, cardiovascular risk factors, and current cardiac status were assessed. Depression during the acute ACS was significantly associated with the IL-1β levels and the −511T allele. The interaction of the IL-1β level with depression at baseline in the presence of the −511T allele was also significant. No associations were found with depression during the chronic ACS. For the +3953C/T genotype, there was no association with depression in either the acute or chronic phase. The IL-1β level and −511C/T genotype, separately or interactively, could be a biomarker for depressive disorder in the acute phase of ACS. Focused interventions for those with higher IL-1β level and −511T allele might reduce the risk of depressive disorder.

Cytokines as biomarkers in depressive disorder: Current standing and prospects

The frequently observed co-occurrence of depressive disorders and inflammatory diseases suggests a close connection between the nervous and the immune systems. Increased pro-inflammatory and type 1 cytokines, such as interleukin (IL)-1, tumour necrosis factor (TNF)-α and interferon (IFN)-γ, appear to be an important link. Cytokines are synthesized by immune cells in the blood and peripheral tissues and by glial cells in the central nervous system (CNS). Evidence suggests that the blood–brain barrier (BBB) is permeable to cytokines and immune cells, and that afferent nerves, e.g. the vagus nerve, mediate the communication between peripheral inflammatory processes and CNS. Cytokines such as IL-1ß, TNF-α and IFN-γ seem to contribute to the pathophysiology of depression by activating monoamine reuptake, stimulating the hypothalamic–pituitary–adrenocortical (HPA) axis and decreasing production of serotonin due to increased activity of indolamine-2,3-dioxygenase (IDO). However, critical appraisal of these hypotheses is required, because cytokine elevation is not specific to depression. Moreover, several effective antidepressants such as amitriptyline and mirtazapine have been shown to increase cytokine production. When applying immunomodulatory therapies, these drugs may increase the risk of specific side effects such as infections or interact with antidepressant drugs on important functions of the body such as the coagulation system.