[Comparison of the effects of glutamate antibodies on neuronal activity of caspase 3 and memory impairment in rats induced by injection of Abeta(25-35) into the Meynert nuclei].

In experiments on rats showed that intranasal administration of glutamate antibodies in a dose of 300 microg/kg after 1 h after bilateral injection of neurotoxic fragment of beta-amyloid protein (25-35)--Abeta(25-35)--into the Meynert nuclei restores learning ability in the test of passive avoidance on 3 and 14 days of the experiment. Antibodies to glutamate decrease significantly increasing caspase 3 activity, detected on Day 3 after injection of Abeta(25-35), in samples of the prefrontal cortex and hippocampus but not hypothalamus. Intranasal administration of gamma-globulin had no effect on the performance of violations of mnestic functions and caspase 3 activity.

Effect of antibodies to glutamate on caspase-3 activity in brain structures of rats with experimental Alzheimer's disease.

Experiments on rats have showed that neurodegenerative damage to the brain induced by injection of a neurotoxic ß-amyloid protein fragment ß25-35into the basal giant cell nuclei of Meynert activated caspase-3 in the prefrontal cortex and hippocampus on day 3 after injury. Intranasal administration of antibodies to glutamate in a dose of 300 µ g/kg 1 h after damage reduced enzyme activity in these structures in a rat model of Alzheimer's disease.

Antiamnestic effects of antibodies to glutamate in experimental Alzheimer's disease.

Experiments on rats showed that neurodegenerative brain damage caused by administration of neurotoxic fragment of ß-amyloid protein Aß25-35 in a dose of 2 µg into Meynert giant cell nucleus leads to long-term memory impairment in rats. Intranasal administration of antibodies to glutamate in a dose of 300 µg/kg 1 h after damage restores learning capacity of the experimental animals in the conditioned passive avoidance paradigm.

Effect of antibodies to glutamate on retention of conditioned passive avoidance response in rats with ischemic injury of the prefrontal cortex.

Experiments were performed on rats with bilateral photothrombosis of vessels in the prefrontal cortex. Intranasal administration of antibodies to glutamate (1 h after ischemia of the brain cortex) improved retention of conditioned passive avoidance response, which was elicited before ischemic damage. The content of antibodies to glutamate in the serum of rats increased significantly on day 8 after bilateral photochemical thrombosis of vessels in the prefrontal cortex compared to that in the control.

Production of autoantibodies to glutamate during Alzheimer's dementia.

Increased production of autoantibodies to glutamate was found in blood plasma from patients with Alzheimer's dementia. The content of autoantibodies to glutamate in patients with early-onset Alzheimer's disease was much lower than in those with late-onset Alzheimer's disease (1.40+/-0.07 and 1.80+/-0.07 arb. units, p<0.001). The level of autoantibodies to glutamate in patients with mixed - Alzheimer's disease was 1.60+/-0.01 arb. units.