Peculiarity of Inflammatory Process Generalization in the Rats Brain depending on β--amyloid Peptides Site of Action and Age

According to the amyloid cascade hypothesis, β-amyloid peptides are the main pathogenetic link in the development of amyloidosis in neurodegenerative pathology. It is shown that the deposition of β-amyloid and the formation of senile plaques accompany the activation of the congenital immune system. Material and methods. We studied the propagation of the proinflammatory effect of β-amyloid peptides in phylogenetically different brain regions of male rats aged 6- and 18-months of age (n = 55). Foci of inflammation were created by administering a suspension of aggregates of Human Amyloid β Protein Fragment 1-40 or 1-42 (15 nM) into the neocortex, hippocampus, or olfactory bulbs. The animals of the comparison groups were infused with an appropriate volume of the solvent. The controls were intact rats of representative age and sex. Results and discussion. One month after the creation of the neuronality models, the cytokine concentration: TNFα, IL-6, IL-10 was established in supernatants of the nervous tissue. It was found that irrespective of the localization (neocortical, hippocampal or bulbar) of the inflammatory focus caused by toxic effects of aggregates of β-amyloid peptides, activation of the cytokine link of inflammation occurred directly in the area of direct action of proinflammatory factors and spread from phylogenetically young brain structures to more ancient: neocortex → hippocampus → olfactory bulbs. The age-related prerequisites for chronic neuroinflammation are probably related to the overload of neuronal neocortical and hippocampal networks. Conclusions. Growing with age, the overload of the neural networks of the cortex and the hippocampus of the brain may be a prerequisite for the occurrence of non-specific chronic inflammation. Regardless of the location of the focal point of the inflammatory process (neocortical, hypocampal or bulbar), activation of the cytokine link occurs directly in the area of direct influence of the proinflammatory factor and extends in the direction from the phylogenetically younger structures of the brain to the more ancient ones.