Alterations in Serum MAO Activity and Tau Levels in β-Thalassemia

β-Thalassemia is a hereditary hemoglobinopathy characterized by chronic anemia, iron overload, and sustained oxidative stress, leading to progressive multisystem complications. Although oxidative stress is well documented in β-thalassemia, its association with peripheral biomarkers reflecting mitochondrial oxidative metabolism and neuroaxonal protein homeostasis has not been sufficiently investigated. This study aimed to evaluate serum monoamine oxidase (MAO) activity and total Tau protein levels in patients with β-thalassemia major and minor compared with healthy controls, with an emphasis on phenotype-dependent peripheral biochemical alterations related to disease severity. A total of 90 participants were enrolled, including 20 patients with β-thalassemia major, 30 with β-thalassemia minor, and 40 healthy controls. Serum MAO activity and total Tau protein concentrations were measured using ELISA-based assays. Intergroup comparisons were performed using one-way analysis of variance followed by Tukey's post hoc test. Serum MAO activity was significantly higher in the β-thalassemia major group compared with both β-thalassemia minor patients and controls (p < 0.001). Total Tau protein levels were significantly reduced in β-thalassemia major patients, whereas no significant difference was observed between β-thalassemia minor patients and healthy controls. Subgroup analyses revealed positive correlations within both β-thalassemia major and minor groups, consistent with a phenotype-dependent divergence and indicative of Simpson's paradox. In conclusion, β-thalassemia major is characterized by elevated serum MAO activity and reduced total Tau protein levels, reflecting concurrent alterations in systemic oxidative metabolism and peripheral Tau homeostasis. These findings represent peripheral biochemical signatures associated with disease severity rather than direct evidence of central nervous system pathology.