Effect of Cyclosporin A on the Viability of Hippocampal Cells Cultured under Conditions of Modeling of Alzheimer’s Disease

The presence of amyloid plaques and neurofibrillary tangles accompanied by manifestations of intense neurodegeneration in the brain is the main syndrome of Alzheimer's disease (AD). Until now, the mechanisms underlying neurotoxic properties of the protein specific with respect to AD (amyloid β_1–42) have not been fully interpreted. There are reasons to believe that the opening of mitochondrial permeability transition pores (MPTPs) may play a significant role in the respective processes. We estimated the impact of the mentioned protein on the viability of cultured hippocampal cells of rats. The use of confocal microscopy after staining of the cells by two dyes, Hoechst 33258 and propidium iodide, allowed us to measure the numbers of viable and necrotized units. When 2.0 μm of amyloid β_1–42 was added to the culturing medium, the cell death index (CDI) of hippocampal cells (number of cells stained by propidium iodide normalized with respect to the number of examined units) on day in vitro (DIV) 14 was 59 ± 4%, on average, as compared with 28 ± 6% under control conditions. When not only amyloid β_1–42 was added to the medium but cells were also treated with 1.25 μM of a MPTP blocker, cyclosporin A (CsA), the mean CDI was significantly smaller than that with no treatment (42 ± 6%; P < 0.05). Thus, changes in the mitochondria resulting in opening of MPTPs can be considerably involved in the process of necrotic death of hippocampal cells under conditions of modeling of AD.

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