Abstract
An injection model of the pre-clinical-stage of Alzheimer’s disease has been reproduced in rats. Experiments have shown that a decrease in the latent period of the conditioned avoidance response (CAR) is accompanied by the increase in endogenous β-amyloid peptide 1–40 and activation of inflammatory cytokines (IL-1β, TNFα, IL-6, IL-10) in the cerebral cortex, hippocampus and blood serum of experimental animals. We do believe that the changes detected at the biochemical level are an important precondition for modulating neuronal function in rats induced by administration of human β-amyloid peptide 1–40. The toxic effects of the exogenous of β-amyloid peptide 1–40 homoaggregates induced intensification of the cytokine response, while the liposomal form of this peptide determined a mild signal causes to the activation of innate immunity. TNFα and endogenous β-amyloid peptide 1–40 servers as the most informative markers for the presence neuroinflammation and amyloidogenic status, respectively.
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Original Russian Text © V.V. Sokolik, A.V. Maltsev, 2015, published in Biomeditsinskaya Khimiya.
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Sokolik, V.V., Maltsev, A.V. Cytokines neuroinflammatory reaction to the action of β-amyloid 1–40 administered to rats in homoaggregated and liposomal forms. Biochem. Moscow Suppl. Ser. B 9, 355–361 (2015). https://doi.org/10.1134/S1990750815040058
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DOI: https://doi.org/10.1134/S1990750815040058