Circulating nerve growth factor as a neuroimmune biomarker in first-episode major depressive disorder: Integrative analysis of serum levels and NGF Ala273Val (rs6330) polymorphism
2026· Journal of Medical Biochemistry· pp. 159-159· 0 citations· 24 references
TL;DR
Circulating NGF is significantly altered in first-episode MDD, supporting its role as a neuroimmunerelated biochemical marker associated with disease presence rather than symptom severity, and highlighting the potential utility of serum NGF as a laboratory biomarker in the biochemical characterization of MDD.
Abstract
Background: Major depressive disorder (MDD) has been
increasingly recognized as a systemic disorder involving
neuroimmune and biochemical dysregulation. Circulating neurotrophic factors, particularly nerve growth factor
(NGF), may serve as potential laboratory biomarkers reflecting neurobiological alterations.
Methods: This case–control study enrolled 47 drug-naïve
patients with first-episode MDD and 40 age- and sexmatched healthy controls. Serum NGF concentrations
were quantified using enzyme-linked immunosorbent assay (ELISA). The NGF Ala273Val (rs6330) polymorphism
was genotyped via polymerase chain reaction and direct
sequencing. Statistical analyses included group comparisons, correlation analysis, and genotype–phenotype association evaluation.
Results: Serum NGF levels were significantly elevated
in patients with MDD compared with controls (36.81 ±
7.11 vs. 29.74 ± 5.69 pg/mL, P < 0.001). However, no
significant correlation was observed between NGF concentrations and HAMD-17 scores (r = 0.12, P = 0.42).
Genotype and allele distributions of the NGF Ala273Val
polymorphism did not differ significantly between groups
(P > 0.05), and no genotype-dependent differences in
serum NGF levels were detected. Conclusion: Circulating NGF is significantly altered in
first-episode MDD, supporting its role as a neuroimmunerelated biochemical marker associated with disease
presence rather than symptom severity. The NGF
Ala273Val polymorphism does not appear to influence
susceptibility or peripheral NGF expression. These
findings highlight the potential utility of serum NGF as a
laboratory biomarker in the biochemical characterization
of MDD.
Background: Type 2 Diabetes Mellitus (T2DM) is associated with cognitive decline, potentially mediated by neuroinflammatory processes and altered neuroplasticity. This study investigated cerebrospinal fluid (CSF) biomarkers of neuroinflammation and neuroplasticity in T2DM individuals versus controls, and their relationship with cognitive performance. Methods: This cross-sectional study included 56 T2DM individuals and 26 controls (aged 37–70 years; 48% male). CSF concentrations of leptin, IL-6, VEGF, BDNF, TNF-α, IGF-1, and IL-1β were measured using ELISA. Cognitive function was assessed using MMSE, the Stroop test, SDMT, RCFT, and TAAV. Group comparisons used Mann–Whitney U or t-tests; Spearman correlations examined variable relationships. Results: No statistically significant differences in CSF biomarkers were observed between groups. However, T2DM patients showed lower word recall (4.66 ± 1.48 vs. 5.81 ± 1.52; p = 0.002), reduced Symbol–Digit performance (17.82 ± 12.16 vs. 24.92 ± 12.10; p = 0.016), and higher Complex Figure Test scores (19.94 ± 9.32 vs. 15.94 ± 5.02; p = 0.009). IL-6 was negatively correlated with MMSE (r = −0.33, p = 0.005). Significant correlations emerged between MMSE and Symbol–Digit scores (r = 0.40, p < 0.001) and among biomarkers. Conclusions: “No statistically significant differences in CSF biomarkers were observed between groups and unadjusted CSF biomarker concentrations did not differ significantly between groups; however, after adjustment for age and BMI, IL-6 was significantly elevated in T2DM patients, indicating that covariate-adjusted analyses may be more sensitive for detecting subtle neuroinflammatory differences in this population.
César Mauricio Baracaldo Barrera, M. C. Jiménez Martínez, Sandra Rojas Vega· Diabetology· 0 citations
It is demonstrated that decreased serum BDNF levels are associated with the presence and symptom severity of anxiety disorders, and the Val66Met polymorphism does not appear to be a primary determinant of serum BDNF levels in this population, suggesting that other genetic or environmental factors may be involved.
Dicle Yilmaz Uyanik, Merve Şahin Can, O. Baykan et al.· Molecular Biology Reports· 0 citations
HS-CRP shows potential as an adjunct inflammatory marker in assessing depression and IL-1β demonstrated poor performance, while composite biomarker approach combined with clinical tools should enhance diagnostic and treatment strategies.
Aiusha Mawlong, Rinchen D. Bhutia, S. S. Bhandari et al.· Indian Journal of Biochemist...· 0 citations
The biological distinction between first-episode psychosis (FEP) and chronic schizophrenia remains unclear. This study investigated a panel of non-canonical serum biomarkers related to neurodegeneration, neuroinflammation, and neurotrophic signaling across these clinical stages. In a cross-sectional design, serum concentrations of 18 biomarkers were measured using multiplex immunoassay in 49 FEP patients, 80 patients with chronic schizophrenia (SCH), and 80 healthy controls (CON). Principal component analysis identified two major axes (neuroinflammatory-neurotrophic and synaptic), but the distributions of diagnostic groups overlapped substantially. A distinct biomarker profile was identified in FEP, characterized by significantly lower levels of YKL-40 and BDNF, elevated NCAM-1, decreased TDP-43, and a higher frequency of detectable Aβ1‑42 compared to both SCH and CON groups. In contrast, the SCH group did not differ from CON on most of these markers. Correlation analysis revealed a dense, interconnected biomarker network in SCH, centered on MIF and BDNF, while FEP exhibited a single strong correlation between TDP-43 and YKL-40. Principal component analysis identified two major axes (neuroinflammatory-neurotrophic and synaptic) but showed substantial overlap between diagnostic groups. The findings reveal a unique, stage-dependent biological signature in early psychosis, differentiating FEP from both health and the chronic phase of illness. This supports the view of FEP as a distinct pathophysiological state involving dysregulated neuroinflammation, synaptic plasticity, and protein homeostasis, rather than merely a prodromal stage of chronic schizophrenia. Not applicable.
V. Zakurazhnaya, Y. Zorkina, O. Abramova et al.· BMC Psychiatry· 0 citations
Inflammation contributes to MDD in some patients, but single-marker diagnosis and routine anti-inflammatory treatment are not currently justified, and biomarker-stratified trials are needed to develop precision therapies.
Emilia Włoszek, Bartosz Mikołajek, Anita Godlewska et al.· African Journal of Biomedica...· 0 citations
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