[Biomarkers of neuroinflammation in patients with chronic cerebral ischemia during the therapy with vinpocetine (study INFLAMARK)].

OBJECTIVE

To evaluate the effect of vinpocetine therapy on clinical manifestations of chronic cerebral ischemia (CCI) and the blood concentrations of neuroinflammation markers (S100B, IL-1β).

MATERIAL AND METHODS

The study included 30 patients (mean age 61.6 [56.9; 67.9] years) with CCI that received vinpocetine (30 mg/day) for 3 months. Brain changes according to magnetic resonance imaging data were assessed using the STRIVE protocol. We analyzed the dynamics of changes in the clinical questionnaires: Montreal Cognitive Assessment Scale (MoCA), Hospital Anxiety and Depression Scale (HADS), Asthenic State Scale (ASS), Epworth Sleepiness Scale (ESS), general impressions of treatment (Global Rating of Change Scale, GRC).

RESULTS

In 3 months after vinpocetine therapy there was a significant improvement in cognitive status (MoCA: 25.1±2.1 vs 26.6±1.4 <0.05), emotional state (HADS: 8.4±1.4 vs 7.1±1.8 (<0.05)), daytime sleep parameters (ESS 8.4±2.1 vs 6.2±2.3 <0.05) and reduction in asthenia (ASS: 72.2±18.1 vs 52.3±9.3, <0.05). A significantly larger proportion of patients assessed the improvement from therapy as «moderate» and «pronounced» (GRC, =22, 73.3%). Concentrations of S100B and IL-1β decreased significantly by the time therapy was completed. The overall severity of cerebrovascular changes according to MRI was significantly associated with blood levels of S100β, but not IL-1β: β=0.504, =0.026, 95% CI 0.149-0.901, mainly due to periventricular changes in white matter (β=0.562, =0.035, 95% CI (-0.024-0.820). Blood levels of S100β correlated with MoCA test results (=0.6795), and IL-1β correlated with ESS scores (=0. 6657).

CONCLUSIONS

The use of vinpocetine can significantly reduce the severity of cognitive and affective disorders, asthenia, normalize the circadian rhythm of sleep, suppress the expression S100β and IL-1β in patients with CCI. One of the vinpocetine's mechanisms of action may be the inhibition of neuroinflammation.