[The influence of afobazole on biochemical and histo-patho-morphological parameters of endothelial function at experimental diabetes mellitis in rats].

Oxidizing stress in rats with experimental diabetes mellitis is accompanied by endothelial dysfunction develops. Its biochemical markers are the increase of concentration of blood MDA, the impairments of cell antioxidant depence and a decrease in concentration of total metabolites of NO and expression of endothelial NO-synthetase (e-NOS). Biochemical changes are considered with histopathomorphologic impairments of aortic endothelium.

[Compensatory mechanisms to heal neuroplasticity impairment under Alzheiemer's disease neurodegeneration. I: The role of amyloid beta and its' precursor protein].

In-depth scholar literature analysis of Alzheimer's disease neurodegenerative features of amyloid beta protein neurochemistry modification and excessive phosphorylation of tau protein (and associated neuronal cytoskeleton rearrangements) are secondary phenomena. At early disease stage these neurobiochemical mechanisms are reversible and serve to heal an impairment of biophysical properties of neuronal membranes, neurotransmission, basic neuronal function and neuroplasticity, while preserving anatomical and functional brain fields. Abeta and tau could well serve to biochemically restore physico-chemical properties of neual membranes due to a role these proteins play in lipid metabolism.

[Morphological and biochemical features of cerebral beta-amyloidosis in long-livers].

This is the first assessment of the pathogenetic values of some environmental factors in the occurrence and progression of cerebral beta-amyloidosis (Alzheimer's disease, senile dementia) in long-livers of different climatic areas of the Republic of North Ossetia-Alania. New isoenzyme serum assays for determining creatine kinase BB-isoenzyme and the transaminase activity in the spinal fluid are proposed, which may be used as potential markers in the biochemical diagnosis of Alzheimer's disease. They can both provide valuable information on the severity of morphological lesions of cerebral cells in Alzheimer's disease and serve as the basis for the differential diagnosis of different forms of dementia wherein dystrophic changes in CNS cells are absent or slightly pronounced.