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The Diagnostic Value of the Combination of Serum Brain-Derived Neurotrophic Factor and Insulin-Like Growth Factor-1 for Major Depressive Disorder Diagnosis and Treatment Efficacy.

ABSTRACT: Background:Last decades of psychiatric investigations have been marked by a search for biological markers that can clarify etiology and pathogenesis, confirm the diagnosis, screen individuals at risk, define the severity, and predict the course of mental disorders. In our study, we aimed to evaluate if BDNF and IGF-1 serum concentrations separately and in combination might be used as biomarkers for major depressive disorder (MDD) diagnosis and treatment efficacy and to evaluate the relationships among those proteins and clinical parameters of MDD. Methods:Forty-one MDD patients (according to DSM-5) and 32 healthy controls (HC) were included in this study. BDNF and IGF-1 serum concentrations, psychopathological (MADRS, CGI) and neuropsychological parameters (PDQ-5, RAVLT, TMT-B, DSST), functioning according to Sheehan Disability Scale were analyzed in all subjects at admission and 30 MDD patients after 8 weeks of vortioxetine treatment. Correlational analyses were performed to explore relationships between BDNF and IGF-1 and clinical characteristics. AUC-ROCs were calculated to determine if the value of serum BDNF and IGF-1 levels could serve for MDD diagnosis. Results:MDD patients had significantly lower serum BDNF (727.6 ± 87.9 pg/ml vs. 853.0 ± 93.9 pg/ml) and higher serum IGF-1 levels (289.15 ± 125.3 ng/ml vs. 170.2 ± 58.2 ng/ml) compared to HC. Significant correlations were obtained between BDNF levels and MDD status, depressive episode (DE) severity, precipitating factors, executive functions disruption (TMT-B, RAVLT immediate recall scores) and all subdomains of functioning. As for IGF-1, correlations were found between IGF-1 level and MDD status, DE severity, number and duration of DE, parameters of subjective and objective cognitive functioning (PDQ-5, RAVLT, TMT-B, DSST scores), and all subdomains of functioning. The associations between IGF-1 concentrations and cognitive tests' performance were stronger than those of BDNF. Separately both BDNF and IGF-1 demonstrated good discriminating ability for MDD diagnosis with AUC of 0.840 and 0.824, respectively. However, the combination of those neurotrophins had excellent diagnostic power to discriminate MDD patients from HC, providing an AUC of 0.916. Vortioxetine treatment significantly increased BDNF and attenuated IGF-1 serum concentrations, improved all psychopathological and neuropsychological parameters and functioning. Conclusions:The combination of IGF-1 and BDNF might be considered as a diagnostic combination for MDD.

SUBMITTER: Troyan AS

PROVIDER: S-EPMC7457028 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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The Diagnostic Value of the Combination of Serum Brain-Derived Neurotrophic Factor and Insulin-Like Growth Factor-1 for Major Depressive Disorder Diagnosis and Treatment Efficacy.

Troyan Alexandra S AS Levada Oleg A OA

Frontiers in psychiatry 20200813

<h4>Background</h4>Last decades of psychiatric investigations have been marked by a search for biological markers that can clarify etiology and pathogenesis, confirm the diagnosis, screen individuals at risk, define the severity, and predict the course of mental disorders. In our study, we aimed to evaluate if BDNF and IGF-1 serum concentrations separately and in combination might be used as biomarkers for major depressive disorder (MDD) diagnosis and treatment efficacy and to evaluate the relat ...[more]

PMID: 32922315

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Project description:Brain-derived neurotrophic factor (BDNF) is important for neuronal survival and regeneration. We investigated the diagnostic and prognostic values of serum BDNF in traumatic brain injury (TBI). We examined serum BDNF in two independent cohorts of TBI cases presenting to the emergency departments (EDs) of the Johns Hopkins Hospital (JHH; n?=?76) and San Francisco General Hospital (SFGH, n?=?80), and a control group of JHH ED patients without TBI (n?=?150). Findings were subsequently validated in the prospective, multi-center Transforming Research and Clinical Knowledge in TBI (TRACK-TBI) Pilot study (n?=?159). We investigated the association between BDNF, glial fibrillary acidic protein (GFAP), and ubiquitin C-terminal hydrolase-L1 (UCH-L1) and recovery from TBI at 6 months in the TRACK-TBI Pilot cohort. Incomplete recovery was defined as having either post-concussive syndrome or a Glasgow Outcome Scale Extended score <8 at 6 months. Median day-of-injury BDNF concentrations (ng/mL) were lower among TBI cases (JHH TBI, 17.5 and SFGH TBI, 13.8) than in JHH controls (60.3; p?=?0.0001). Among TRACK-TBI Pilot subjects, median BDNF concentrations (ng/mL) were higher in mild (8.3) than in moderate (4.3) or severe TBI (4.0; p?=?0.004. In the TRACK-TBI cohort, the 75 (71.4%) subjects with very low BDNF values (i.e., <the 1st percentile for non-TBI controls, <14.2?ng/mL) had higher odds of incomplete recovery than those who did not have very low values (odds ratio, 4.0; 95% confidence interval [CI]: 1.5-11.0). The area under the receiver operator curve for discriminating complete and incomplete recovery was 0.65 (95% CI: 0.52-0.78) for BDNF, 0.61 (95% CI: 0.49-0.73) for GFAP, and 0.55 (95% CI: 0.43-0.66) for UCH-L1. The addition of GFAP/UCH-L1 to BDNF did not improve outcome prediction significantly. Day-of-injury serum BDNF is associated with TBI diagnosis and also provides 6-month prognostic information regarding recovery from TBI. Thus, day-of-injury BDNF values may aid in TBI risk stratification.

Project description:The subgenual anterior cingulate cortex is implicated in the pathology and treatment response of major depressive disorder. Low levels of brain-derived neurotrophic factor (BDNF) and reduced markers for GABA function, including in the amygdala, are reported in major depression, but their contribution to subgenual anterior cingulate cortex dysfunction is not known.Using polymerase chain reaction, we first assessed the degree to which BDNF controls mRNA expression (defined as BDNF dependency) of 15 genes relating to GABA and neuropeptide functions in the cingulate cortex of mice with reduced BDNF function (BDNF-heterozygous [Bdnf(+/-)] mice and BDNF exon-IV knockout [Bdnf(KIV)] mice). Gene expression was then quantified in the subgenual anterior cingulate cortex of 51 postmortem subjects with major depressive disorder and comparison subjects (total subjects, N=102; 49% were women) and compared with previous amygdala results.Based on the results in Bdnf(+/-) and Bdnf(KIV) mice, genes were sorted into high, intermediate, and no BDNF dependency sets. In postmortem human subjects with major depression, BDNF receptor (TRKB) expression, but not BDNF, was reduced. Postmortem depressed subjects exhibited down-regulation in genes with high and intermediate BDNF dependency, including markers of dendritic targeting interneurons (SST, NPY, and CORT) and a GABA synthesizing enzyme (GAD2). Changes extended to BDNF-independent genes (PVALB and GAD1). Changes were greater in men (potentially because of low baseline expression in women), displayed notable differences from prior amygdala results, and were not explained by demographic or clinical factors other than sex.These parallel human/mouse analyses provide direct (low TRKB) and indirect (low expression of BDNF-dependent genes) evidence in support of decreased BDNF signaling in the subgenual anterior cingulate cortex in individuals with major depressive disorder, implicate dendritic targeting GABA neurons and GABA synthesis, and, together, suggest a common BDNF-/GABA-related pathology in major depression with sex- and brain region-specific features.

Dataset Information

The Diagnostic Value of the Combination of Serum Brain-Derived Neurotrophic Factor and Insulin-Like Growth Factor-1 for Major Depressive Disorder Diagnosis and Treatment Efficacy.

Publications

The Diagnostic Value of the Combination of Serum Brain-Derived Neurotrophic Factor and Insulin-Like Growth Factor-1 for Major Depressive Disorder Diagnosis and Treatment Efficacy.

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