No abstract

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.