Serum Galectin‐1 and Galectin‐3 Levels and Their Relationship With Executive Functions and Memory in Patients With Major Depressive Disorder

ABSTRACT Objective Neuroinflammation is increasingly recognized as a key mechanism in the pathophysiology of Major Depressive Disorder (MDD). Galectin‐1 and Galectin‐3, β ‐galactoside‐binding lectins involved in immune regulation and neuroprotection, may serve as biomarkers linking inflammation to cognitive dysfunction. However, no previous study has simultaneously examined serum levels of these galectins alongside detailed cognitive assessments in MDD. This study aimed to determine whether Galectin‐1 and Galectin‐3 are altered in MDD and to explore their association with disease severity and cognitive performance. Method Forty patients with MDD and 40 matched healthy controls were assessed. Depressive and anxiety symptoms were measured using the Hamilton Depression (HAM‐D) and Anxiety (HAM‐A) Rating Scales. Cognitive performance was evaluated with the Rey Auditory Verbal Learning Test, Go/No‐Go Test, and Stroop Test. Serum Galectin‐1, Galectin‐3, Glomerular Filtration Rate (GFR), and C‐reactive protein (CRP) levels were determined. Results Serum Galectin‐1 and Galectin‐3 levels were significantly lower in the MDD group compared to controls ( p < 0.05). Galectin‐1 levels showed a negative correlation with HAM‐D and HAM‐A scores, indicating an inverse association with symptom severity (i.e., lower Galectin‐1 levels were associated with higher symptom severity). Patients exhibited impaired verbal learning, while no significant group differences were found in Go/No‐Go or Stroop performance. Galectin levels did not correlate with any cognitive test scores. Conclusion Reduced Galectin‐1 and Galectin‐3 levels in MDD support their involvement in neuroinflammatory mechanisms. The inverse association between Galectin‐1 and symptom severity suggests that Galectin‐1 may be associated with symptom severity; however, the direction of this relationship remains unclear. The lack of associations with cognitive performance implies that cognitive deficits in MDD may be mediated by other immunometabolic pathways. These findings highlight galectins as promising but complex biomarkers, warranting further investigation in larger and longitudinal studies.