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An injection model of preclinical stages of Alzheimer's disease has been reproduced in rats. It was accompanied by the decrease in the latent period of conditioned reflex avoidance, increasing levels of endogenous b-amyloid peptide 1-40 and activation of inflammatory cytokines (IL-1b, TNF-a, IL-6, IL-10) in the cerebral cortex, hippocampus and blood serum of experimental animals. We belive that changes identified at the biochemical level are prerequisite to modulate neuronal functions in rats induced by Ab40_Human administration. The toxic effect of exogenous b-amyloid 1-40 homoaggregates caused intense response of the cytokine system, while its liposomal form caused the soft information signal to the activation of innate immunity.V issledovanii na krysakh byla vosproizvedena in"ektsionnaia model' doklinicheskogo étapa bolezni Al'tsgeĭmera. Pokazali, chto umen'shenie latentnogo perioda uslovno-reflektornoĭ reaktsii izbeganiia soprovozhdaet povyshenie urovnia éndogennogo b-amiloidnogo peptida 1-40 i aktivatsiia tsitokinovogo zvena vospaleniia (IL-1b, TNF-a, IL-6, IL-10) v kore golovnogo mozga, gippokampe i syvorotke krovi éksperimental'nykh zhivotnykh. My polagaem, chto vyiavlennye na biokhimicheskom urovne izmeneniia sluzhat usloviem modulirovaniia neĭronal'noĭ funktsii u krys pod deĭstviem Ab40_Human. Toksicheskiĭ éffekt gomoagregatnoĭ formy ékzogennogo b-amiloidnogo peptida 1-40 vyzyval intensivnyĭ otvet tsitokinovoĭ sistemy, togda kak ego liposomnaia forma obuslovlivala miagkiĭ informatsionnyĭ signal k aktivatsii vrozhdennogo immuniteta. Samym informativnym markerom nalichiia neĭrovospaleniia okazalsia faktor nekroza opukholi-a, a amiloidogennogo statusa – éndogennyĭ b-amiloidnyĭ peptid 1-40.