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Biomedical subjects

A N Samokhin

Publications and source records attributed to A N Samokhin.

7 recordsLinked to original sources
PubMed2005

Cholinopositive effect of dilept (neurotensin peptidomimetic) as the basis of its mnemotropic effect.

Dilept eliminated learning disturbances in the extrapolation avoidance test, caused by chronic injections of scopolamine alone and in combination with madopar to rats. Dilept improved the dynamics of training and parameters of spatial memory impaired by olfactory bulbectomy (operation causing hypofunction of the central cholinergic system). The detected choline-positive effect of dilept together with pronounced dopaminergic activity necessitate its further development as a drug effective in positive and negative symptoms of schizophrenia and psychotic manifestations of Alzheimer's disease.

Alzheimer Disease↗
PubMed2004

Increased level of beta-amyloid in the brain of bulbectomized mice.

Six weeks after bilateral olfactory bulbectomy, a peptide with molecular weight of 4 kD was revealed in extracts of the neocortex and hippocampus from mice. Using monoclonal antibodies 4G8, this peptide was identified as beta-amyloid. Its level was significantly higher in the bulbectomized animals than in sham-operated mice. The bulbectomized mice displayed sharp impairment in spatial memory when tested in the Morris water maze. The results suggest that bulbectomy initiates in the brain a pathological process similar to human Alzheimer's disease in location, biochemistry, and behavioral manifestations.

Alzheimer Disease↗
PubMed2004

Morphofunctional changes in neurons in the temporal cortex of the brain in relation to spatial memory in bulbectomized mice after treatment with mineral ascorbates.

The effects of an antioxidant mixture of mineral ascorbates (MA) on the state of neurons in the temporal area of the cortex and the behavior of mice subjected to bulbectomy (BE) were studied; these mice, as demonstrated previously, are characterized by deficiency of spatial memory and the development of a neurodegenerative process in brain structures showing pathological changes in Alzheimer's disease. One month after BE, there were abnormalities in the cytoarchitectonics of the temporal area of the cortex, with loss of clarity of the boundaries between its layers because of dystrophy of pyramidal neurons and foci of loss of these cells. There were sharp increases in the numbers of neurons showing pyknosis, karyolysis, and vacuolysis on the background of decreases in neuronal density. Three weeks of treatment by addition of MA to the diet prevented the degradation of spatial memory in mice after BE and protected neurons in the temporal area of the cortex from degenerative changes. These results provide evidence for the possibility of prophylaxis of neurodestructive changes of the Alzheimer's type.

Animals↗
PubMed2003

[Morpho-functional changes of neurons in temporal cortex in comparison with spatial memory in bulbectomized mice after treatment with minerals and ascorbates].

The effect of antioxidant mixture of mineralascorbates (MA) on the status of neurons of brain temporal cortex and behavior of mice after olfactory bulbectomy (BE) was studied, as it was previously shown by us that these animals were characterized by a deficit of spatial memory and development of neurodegenerative process in brain structures, which are affected by Alzheimer disease. Disorganization of cytoarchitectonics of temporal cortex with the deletion of its layers as a result of dystrophy of pyramidal neurons and foci of their complete disappearance were shown 1 month after BE. The increased number of neurons with the phenomena of karyopyknosis, karyolysis and vacuolysis was observed with a concomitant reduction in neuronal density. Addition of MA to the diet for three weeks prevented the development of deterioration of spatial memory in mice after BE and protected the neurons of brain temporal cortex from the degenerative changes. The results obtained suggest the possibility of realization of prophylaxis aimed at the prevention of the development of Alzheimer-type neurodestructive processes.

Animals↗
PubMedDate not supplied

[Immunodepressed status of mice after bulbectomy].

We studied the immune response in lymphoid cells of mice subjected to bilateral olfactory bulbectomy in comparison with sham-operated animals 1.5 and 13 months after surgery. The concentration of tumor necrosis factor decreased threefold in the peripheral blood of bulbectomized mice 1.5 months after surgery. Signs of immunodepression were also observed 13 months after surgery: suppression of mitogen-stimulated proliferation of T and B lymphocytes in the spleen, inhibition of synthesis of tumor necrosis factor in peritoneal macrophages and splenocytes, and decreased macrophage NO production. According to the immune status indices and our previous data on behavioral, biochemical, and morphological changes induced in bulbectomized mice, they have common symptoms with the Alzheimer's disease. This allows us to consider such animals as a model of sporadic form of this disease rather than of a depression.

Alzheimer Disease↗
PubMedDate not supplied

[Noopept improves the spatial memory and stimulates prefibrillar beta-amyloid(25-35) antibody production in mice].

The effects of the novel proline-containing nootropic and neuroprotective dipeptide noopept (GVS-111, N-phenylacetyl-L-prolylglycine ethyl ester) were studied on NMRI mice upon olfactory bulbectomy, which had been previously shown to imitate the main morphological and biochemical signs of Alzheimer's disease (AD). The spatial memory was assessed using the Morris (water maze) test; the immunological status was characterized by ELISA with antibodies to prefibrillar beta-amyloid(25-35), S100b protein, and protofilaments of equine lysozyme, which are the molecular factors involved in the pathogenesis of AD. The control (sham-operated) animals during the Morris test preferred a sector where the safety platform was placed during the learning session. Bulbectomized animals treated with saline failed to recognize this sector, while bulbectomized animals treated with noopept (0.01 mg/kg for 21 days) restored this predominance, thus demonstrating the improvement of the spatial memory. These animals also demonstrated an increase in the level of antibodies to beta-amyloid(25-35)--the effect, which was more pronounced in the sham-operated than in bulbectomized mice. The latter demonstrated a profound decrease of immunological reactivity in a large number of tests. Noopept, stimulating the production of antibodies to beta-amyloid(25-35), can attenuate the well-known neurotoxic effects of beta-amyloid. The obtained data on the mnemotropic and immunostimulant effects noopept are indicative of good prospects for the clinical usage of this drug in the therapy of patients with neurodegenerative diseases.

Alzheimer Disease↗