Highly selective sodium glucose cotransporter type 2 inhibitor empagliflozin neuroprotective potential in chronic brain dyscirculation

Background. Chronic brain dyscirculation occurs in type 2 diabetes mellitus (DM2) with a high frequency and leads to patients disability. The early diagnosis of this disorder is difficult. Sodium-glucose cotransporter type 2 inhibitors are among the priority antidiabetic drugs due to their pronounced cardioprotective effect, but their effect on the central nervous system has not been studied enough. Aim. To study empagliflozin effect on clinical and laboratory parameters of brain damage in patients with DM2. Materials and methods. The study included patients with DM2 on metformin therapy (n=52). Patients with target glycated hemoglobin level formed the MET group (n=18), in those with non-target glycated hemoglobin level empagliflozin was added for 6 months (group MET+EMPA; n=19). A healthy control group was also created (n=15). The cognitive status and concentration of neurofilament light chains were studied. Results. In patients of the MET group, despite the target level of glycated hemoglobin, there was a cognitive deficit, according to the Montreal Cognitive Assessment: 25.0 (21.0; 27.0) points with a norm of 26 points or more. Therapy with empagliflozin led to the normalization of cognitive status after 6 months: 26.5 (24.0; 27.0) points. Initially, all patients had an increased neurofilament light chains level: 4.50 (3.31; 5.56) ng/ml in the MET group, 5.25 (3.75; 6.25) ng/ml in the MET+EMPA comparing with 3.50 (2.25; 3.50) ng/ml in the Control group. Empagliflozin therapy led to a decrease in this parameter after 3 months: 3.80 (3.25; 3.87) ng/ml and maintenance of this level after 6 months. Conclusion. DM2 is accompanied by pathological changes in the central nervous system even under satisfactory glycemic control. Empagliflozin therapy causes an improvement in cognitive status and a decrease in the level of neurofilament light chains.