Findings are hypothesis-generating and warrant prospective multicentre validation, as folate, vitamin B12, and lifestyle confounders were unmeasured.
Abstract
Depression is a multifactorial disorder involving neurochemical, metabolic, and inflammatory dysregulation. Elevated homocysteine, a marker of impaired one-carbon metabolism, has been implicated in neurotoxicity and oxidative stress pathways associated with depressive pathology. This study evaluated serum homocysteine levels and their association with body mass index (BMI) in patients with incident drug naiive depression compared to healthy controls. This case-control study enrolled 200 participants: 100 patients with newly diagnosed depressive disorder (DSM-5 criteria) and 100 age- and sex-matched healthy controls recruited from a tertiary psychiatry centre in South India. Serum homocysteine was measured using standard enzymatic assay and BMI was calculated from standardised anthropometric measurements. Independent samples t-test, Pearson’s correlation, ROC analysis and Binomial logistic regression analyses were performed. Serum homocysteine was significantly higher in depressed patients than controls (35.8 ± 7.04 µmol/L vs. 13.6 ± 2.48 µmol/L;
p
< 0.001, Cohen’s d = 4.193; 95% CI for difference: 20.66–23.58 µmol/L). BMI was also significantly elevated in the depression group (25.67 ± 4.97 kg/m
2
vs. 21.92 ± 2.96 kg/m
2
.
p
< 0.001, Cohen’s d = 0.912). A positive homocysteine—BMI correlation was observed in depression(
r
= 0.42,
p
< 0.001) but not in controls (
r
= 0.04,
p
= 0.71). ROC analysis yielded an AUC of 1.000 (optimal cutoff: 20.065 µmol/L, sensitivity: 100%, specificity: 100%), reflecting complete distributional separation in this clinical sample. Binary logistic regression analysis showed homocysteine to be a significant predictor of depression(omnibus χ
2
= 277.26, df = 1,
p
< 0.001; 100% classification accuracy; Nagelkerke R
2
= 1.00), though standard odds ratio estimation was precluded by complete separation. Elevated homocysteine and a group-specific BMI—homocysteine correlation were identified in depressed patients. The AUC of 1.000 reflects complete distributional separation in a tightly controlled institutional sample and requires external validation before clinical application. As folate, vitamin B12, and lifestyle confounders were unmeasured, findings are hypothesis-generating and warrant prospective multicentre validation.
Background: Vitamin D is a Neurosteroid hormone that plays a role in neuroprotection, neurotransmitter modulation, and neurodevelopment. The pathophysiology of schizophrenia and the intensity of related psychotic symptoms have been linked to its insufficiency. Objectives: The purpose of this study is to evaluate blood vitamin D levels between individuals with schizophrenia and age- and sex-matched healthy controls. Additionally, the Positive and Negative Syndrome Scale (PANSS) will be used to correlate vitamin D status with symptom profile. Materials and Methods: At a tertiary care teaching hospital in Tamil Nadu, India, this hospital based case-control study recruited 30 drug-naive patients with schizophrenia (diagnosed according to ICD-10 criteria) and 30 healthy, age- and sex-matched controls between the ages of 25 and 40 over the course of a year. Electrochemiluminescence immunoassay (ECLIA) was used to measure the amount of 25-hydroxyvitamin D in fasting serum. PANSS was used to gauge the severity of the symptoms. For statistical analysis, the chi-square test, independent-samples t-test, one-way ANOVA, and Pearson correlation were employed. Results: Compared to controls (19.57 ± 5.46 ng/mL; t = 4.01, p = 0.001), the mean blood vitamin D was considerably lower in cases (14.13 ± 5.03 ng/mL). Compared to 40.0% of controls, 83.3% of patients had inadequate or deficient vitamin D status (χ² = 12.08, p = 0.002). Positive PANSS scores (r = −0.465, p = 0.010) and total PANSS scores (r = −0.506, p = 0.001) were significantly and negatively linked with vitamin D levels, but not negative PANSS (r = −0.329, p = 0.076) or general psychopathology scores (r = −0.006, p = 0.976).
Conclusion: In this cohort, low blood vitamin D is linked to schizophrenia and corresponds with overall symptom severity and positive symptom load, but not with negative or general psychopathology symptoms. Patients with schizophrenia may benefit from routine metabolic evaluations that include vitamin D assessments, and treating deficiencies may help manage symptoms.
Sudha P, Arivalagan C· NATIONAL BOARD OF EXAMINATIO...· 0 citations
Accumulating evidence has suggested that depression is associated with an increased risk of Parkinson’s disease (PD), yet whether pre-clinical depressive symptoms in PD development and the potential mediating effects of metabolomic profiles remain unclear. We aimed to examine the association between depressive symptoms and PD risk, evaluate effect modification by genetic susceptibility, and assess metabolomic mediation. This prospective study included 451,922 PD-free participants from the UK Biobank. Depressive symptoms were collected by a 2-item Patient Health Questionnaire (range, 0–6; ≥3 indicates possible depressive disorder) at baseline. Identification of PD was based on medical records. PD-related polygenic risk score (PRS
PD
), which incorporates established genes for PD based on external GWAS meta-analyses, was tertiled as low, moderate, and high. Baseline plasma metabolites were quantified via NMR spectroscopy from blood samples. Data were analyzed using Cox regression. Over a median follow-up of 14.6 years, 3108 (0.7%) participants developed PD. Higher depressive symptom severity showed linear association with PD risk (hazard ratio [HR]: 1.11, 95% confidence interval: 1.07–1.15). Participants with possible depressive disorder had 36% higher PD risk (HR: 1.36, 1.15–1.61). Those with both possible depressive disorder and high genetic risk had the highest PD risk (HR 2.15, 1.74–2.65;
P
for interaction = 0.028). Metabolomic signature, incorporating fatty acids and lipoproteins, accounted for 15% (model-based proportion) of the depressive symptoms-PD association. Pre-clinical depressive symptoms are associated with a moderately increased risk of PD, particularly among people with a high genetic susceptibility to PD. Metabolomic profiles account for a significant portion of this relationship.
AIM
To evaluate serum serotonin levels in patients with peptic ulcer disease (PUD) and assess its potential as a biomarker associated with depressive symptoms in patients with PUD.
METHODS
This case-control study included 50 adult male patients with endoscopically confirmed PUD and 50 apparently healthy male controls. Serum serotonin levels were measured using enzyme-linked immunosorbent assay (ELISA). Depression was diagnosed by a psychologist and assessed using the Patient Health Questionnaire-9 (PHQ-9). Statistical analyses included the Mann-Whitney U test, chi-square test, multivariate logistic regression, and receiver operating characteristic (ROC) curve analysis.
RESULTS
Patients with PUD had higher PHQ-9 scores than controls, with a median score of 13.5 (7.0-16.6) versus 4.0 (2.0-8.0) (p<0.001). Serum serotonin levels were lower in patients with PUD than in controls, with a median of 530.086 (435.7-592.8) pg/mL versus 1008.763 (874.89-1120.43) pg/mL (p<0.001). In the adjusted model, lower serotonin levels remained independently associated with comorbid PUD-depression status (OR=0.992; 95% CI 0.988-0.996; p<0.001). ROC analysis showed high diagnostic performance for serotonin in the full sample (AUC=0.920; 95% CI 0.870-0.970; cut-off 803.131 pg/mL; sensitivity 85.0%; specificity 100%).
CONCLUSION
Serum serotonin levels were lower in male patients with PUD and depressive symptoms than in healthy controls. Serotonin may have diagnostic value as a biomarker associated with depressive symptoms in patients with PUD, but longitudinal studies including women and PUD patients without depression are required.
Introduction Anxiety and depression are prevalent, disabling, yet frequently underdiagnosed non-motor symptoms in Parkinson’s disease (PD). This study aimed to develop and validate a non-invasive model predicting these affective disorders by integrating peripheral blood biomarkers with standardized clinical scales to facilitate early screening. Methods We retrospectively analyzed data from 290 patients with PD, who were randomly allocated into a training cohort (n = 203) and a validation cohort (n = 87). Baseline plasma neurofilament light chain (NfL) levels and clinical phenotypes were assessed. Independent risk factors were determined via multivariate logistic regression analysis to construct the clinical prediction nomogram. Model performance was comprehensively evaluated using the area under the receiver operating characteristic curve (AUC) for discrimination, calibration curves for risk consistency, and decision curve analysis (DCA) for clinical utility. Results Multivariate logistic regression identified plasma NfL, Hoehn and Yahr stage, MMSE score, and MDS-UPDRS Part III score as independent predictors for anxiety and depression in PD patients (all p < 0.05). The established model exhibited high discriminative power, achieving an AUC of 0.94 (95% CI: 0.873–0.964) in the training cohort and 0.84 (95% CI: 0.782–0.879) in the validation cohort. Calibration curves demonstrated excellent consistency between predicted and actual probabilities, and DCA confirmed strong clinical net benefits. Discussion In conclusion, combining peripheral plasma NfL levels with standard clinical phenotypes provides an objective, quantifiable, and non-invasive tool for early risk stratification of affective disorders in PD. This multimodal nomogram effectively expands the therapeutic window for timely personalized psychiatric interventions, potentially improving long-term quality of life and clinical outcomes for PD patients.
Guidong Liu, Yan-Qin Geng, Hanwen Zhang et al.· Frontiers in Aging Neuroscie...· 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
Abstract Objectives This study aimed to examine the association of thyroid-stimulating hormone (TSH), interleukin-6 (IL-6), and 3-nitrotyrosine (3-NT) with ApoE gene expression and to evaluate their diagnostic utility in CMS. Methods This case–control study compared hormonal, inflammatory, oxidative stress, and gene expression markers between CMS cases and healthy controls. Group differences were analyzed using non-parametric tests. Diagnostic performance was evaluated using receiver operating characteristic (ROC) analysis, and relationships among variables were assessed using correlation and multivariable logistic regression models. Results CMS cases showed significantly higher levels of TSH, IL-6, 3-NT, and ApoE gene expression compared with controls. TSH demonstrated modest diagnostic accuracy (AUC=0.740), whereas 3-NT exhibited excellent discriminative performance (AUC=0.963). IL-6 also showed good diagnostic accuracy. ApoE gene expression demonstrated strong diagnostic performance and was positively correlated with TSH, 3-NT, and IL-6, with the strongest association observed for IL-6. Multivariable regression analysis confirmed that elevated TSH, IL-6, and 3-NT were independently associated with CMS status. Conclusions CMS is characterized by the convergence of thyroid dysregulation, inflammation, oxidative stress, and increased ApoE gene expression. These findings highlight a coordinated molecular network underlying CMS and support the integration of molecular and inflammatory biomarkers into cardiometabolic risk assessment. Larger longitudinal studies are required to confirm these observations.
Tha-alnoorein Abdulla, T. Kumar D, J. Inbanathan et al.· Hormone Molecular Biology an...· 0 citations