The potential role of serum and urine galectin-3 values in the diagnosis and staging of Parkinson’s disease

Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterised by both motor and nonmotor symptoms. Galectin-3, a protein involved in the regulation of inflammatory responses, has emerged as a potential contributor to neurodegenerative processes. This study aimed to measure serum and urinary galectin-3 levels in patients with PD and to evaluate the associations of this biomarker with disease stages and clinical symptoms. The present cross-sectional study included 30 PD patients and 29 healthy controls. Galectin-3 levels in serum and urine samples were measured via Enzyme-Linked Immunosorbent Assay (ELISA). The clinical data recorded included demographic information, Hoehn and Yahr (H&Y) stage, Unified Parkinson’s Disease Rating Scale (UPDRS) motor score, nonmotor symptom score (NMS), and total dopaminergic treatment dose parameters. Multivariate analyses were adjusted for age and sex due to demographic differences between groups. Serum galectin-3 optical density (OD) levels (0.2 [0.1–1.4]) and urinary galectin-3 OD levels (0.2 [0.1–0.6]) were significantly higher in PD patients than in controls (p < 0.050). Serum and urinary galectin-3 concentration (C) values were also elevated in the PD group. A moderate negative correlation was observed between serum galectin-3 levels and both the H&Y stage (r = − 0.418, p = 0.021) and the UPDRS motor score (r = − 0.541, p = 0.002). After adjusting for age and sex, serum galectin-3 C remained independently associated with motor severity. ROC analysis revealed that serum galectin-3 levels demonstrated promising diagnostic performance, with high specificity and sensitivity in distinguishing patients with PD from healthy controls (AUC = 0.716, p = 0.001). The serum/urine galectin-3 concentration ratio also showed significant discriminative value (AUC = 0.722, p = 0.035). Our findings suggest that elevated levels of galectin-3 in serum and urine are associated with Parkinson’s disease and may reflect underlying neuroinflammatory mechanisms contributing to its pathophysiology. The diagnostic performance of galectin-3 markers remained robust even after adjusting for age and sex. However, the strict exclusion criteria and the age imbalance between groups may limit the generalizability of these results to broader clinical populations. Therefore, these findings should be considered exploratory and require confirmation through larger, longitudinal studies to determine their diagnostic and prognostic utility.