ИСТИНА

Bath application of 200 nM amyloid-ß 1-42 (Aß) to rat hippocampal slices impairs induction of long-term potentiation (LTP) of the population spike (PS) in pyramidal layer of the CA1 field of the hippocampus. Intraperitoneal injection of mitochondria-targeted plastoquinone derivative SkQ1at very low concentrations (250 nmol/kg body weight) given 24 h before the slice preparation or 1 h treatment of hippocampal slices with 250 nM SkQ1 prevents the deleterious effect of Aß on LTP. To elucidate which part of the molecule is responsible for this type of neuroprotective activity, the effect of the analog of SkQ1 lacking plastoquinone (C12TPP) was studied. It was found that C12TPP was much less efficient in LTP protection than SkQ1 itself. It means that plastoquinone part of SkQ1 molecule is responsible for the LTP rescue. To summarize, in vivo and in vitro injection of SkQ1 compensates for Aß-induced oxidative damage of long-term synaptic plasticity in the hippocampus, which is considered to be the main reason of memory loss and impairment of other cognitive functions associated with Alzheimer?s disease (AD). Therefore, SkQ1 may be considered as a promising candidate for the treatment of early-stage of AD.