Experimental evidences of calcium-dependent proteolysis dysregulation in brain of murine model of Alzheimer disease were obtained. Experimental treatment consisted in intra-hippocampal injection of amyloid beta-peptide (AP1-40) promoted activation of main calpain forms in murine brain along with decrease incontent of natural calpain inhibitor, calpastatin. As a result of prognostic experiment on the correction of neurodegeneration induced in murine the neuroprotective properties of steroid hormone estradiol were confirmed and one of the possible protective action mechanisms was suggested. Obtained results allow considering both biochemical modifications in protein facilities of pathology-affected brain and the mechanisms of neurodegeneration and neuroprotection.
On the basis of experimental series with murine models there was obtained the evidence on calcium-dependent protease activity changes in rat brain at induced neurodegeneration. The properties of the proteolytic and regulatory components of calpain system under the effect of neurotoxic stimuli--amyloid beta-peptide or glutamate--were characterized; the basic endogenous regulatory mechanisms of calcium-dependent proteolysis modulation were determined as well. Neuroprotective properties of exogenous calpain regulators differing in the mechanisms of action (sex steroids, calcium regulators) were tested on studied neurodegeneration models.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.