Glutamate antibodies repress expression of Dffb gene in brain of rats in experimental Alzheimer's disease

The rat model of Alzheimer's disease including injection of neurotoxic fragment of beta-amyloid protein A beta(25-35) into giant-cell nuclei basalis of Meynert was used for experiments. We have investigated the influence of glutamate antibodies administered intranasally in a dose of 300 mu g/kg after 1 h of the mentioned alteration on the level of expression of Dffb mRNA. Dffb gene codes caspase-dependent DNase, which participates in the internucleosomal fragmentation of genome DNA during apoptosis. On the third day after the injection of A beta(25-35), we obtained a significant decrease in Dffb gene expression in the prefrontal cortex (37% decrease) and hippocampus (62% decrease) in the group of experimental animals compared to the control group. In the hypothalamus, there were no such differences. Seemingly, the repressing action of glutamate antibodies on the mRNA expression of the Dffb gene reflects the stabilization of processes that take place in the brain cells during experimental Alzheimer's disease; meanwhile, the intensity of the apoptotic death of neurons and glial cells decreases.