ИСТИНА

A protective effect of a mitochondria-targeted antioxidant SkQR1 was studied in models of focal trauma of rat brain sensorimotor cortex, amyloid-beta (Abeta)-induced impairment of hippocampal longterm potentiation (LTP), a kind of synaptic plasticity associated with learning and memory and streptozotocin-induced memory impairment. It was found that daily intraperitoneal injection of SkQR1 after trauma or streptozotocin treatment improves performance in a test characterizing neurological deficit, decreases the damaged cortical zone and significantly attenuated streptozotocin-induced memory impairment which was evaluated by behavioral test "passive avoidance". Single intraperitoneal injection into the rat of SkQR1 abolishes the deleterious effect of Abeta on LTP, significantly increases of long-term potentiation amplitude of the population spike in pyramidal layer of the CA1 field of the hippocampus and the animals treated by SkQR1 performed better results in the behavioral tests «passive avoidance. Our results suggest that SkQR1 may be considered as a promising candidate for the treatment of traumatic brain injury and early-stage Alzheimer's disease.