Serum Galectin‐1, Galectin‐9, and YKL‐40 levels in bipolar disorder and their relationship with cognitive functions

Purpose The number of studies conducted on the role of neuroinflammation in the etiopathogenesis of bipolar disorder has been increasing in recent years. The role of Galectin‐1, Galectin‐9, and YKL‐40, which are considered to play roles in neuroinflammation and the etiopathogenesis of bipolar disorder, and the relationship of these parameters with cognitive functions were investigated in the present study. Method Serum Galectin‐1, Galectin‐9, and YKL‐40 levels were measured with the ELISA Method in 64 bipolar euthymic patients and 64 healthy controls. The Stroop and trail‐making tests were administered to assess cognitive functions in all participants. Results Serum Galectin‐1, Galectin‐9, and YKL‐40 levels were statistically and significantly lower in the patient group when compared to the healthy control group. The scores of the Stroop test and trail‐making tests were statistically higher in the patient group than in the healthy control group. There was a weak and positive correlation between serum Galectin‐1, Galectin‐9, and YKL‐40 levels and cognitive performance in all participants. Discussion and conclusion Statistically significant low levels of serum Galectin‐1, Galectin‐9, and YKL‐40 detected in the patient group suggest that these parameters have important roles in neuroinflammation. The statistically higher Stroop and trail‐making test scores of the patient group compared to the control group indicates that the cognitive performance of the patient group was weaker. Also, the positive correlation between Galectin‐1, Galectin‐9, and YKL‐40 levels and cognitive performance suggests that these molecules may have a neuroprotective role. We think that the present study will contribute to this field where there is very limited data in the literature. There are studies reporting that neuroinflammation plays a role in the etiopathogenesis of bipolar disorder. We examined molecules associated with inflammation that have not been studied before in bipolar disorder and their relationship with cognition.