1. [Repressional effects of the glutamate antibodies on expression of Dffb gene in the brain of rats with experimental Alzheimer's disease].
- Author
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Kolobov VV, Davydova TV, Zakharova IA, Gorbatov VIu, and Fomina VG
- Subjects
- Administration, Intranasal, Alzheimer Disease chemically induced, Alzheimer Disease metabolism, Amyloid beta-Peptides administration & dosage, Animals, Antibodies immunology, Apoptosis drug effects, Basal Nucleus of Meynert drug effects, Basal Nucleus of Meynert pathology, Cerebral Cortex metabolism, Deoxyribonucleases genetics, Deoxyribonucleases metabolism, Disease Models, Animal, Gene Expression drug effects, Glutamic Acid immunology, Hippocampus metabolism, Hypothalamus drug effects, Hypothalamus metabolism, Injections, Intraventricular, Male, Poly-ADP-Ribose Binding Proteins, RNA, Messenger biosynthesis, Rats, Rats, Wistar, Alzheimer Disease drug therapy, Antibodies therapeutic use, Cerebral Cortex drug effects, Deoxyribonucleases antagonists & inhibitors, Hippocampus drug effects, RNA, Messenger antagonists & inhibitors
- Abstract
The intranasal administration of glutamate antibodies in the dose of 300 microg/kg one hour after damage on the level of mRNA expression of Dffb gene which codes caspase-activated DNase which participates in intranucleosome fragmentation of genome DNA in apoptosis was investigated in experimental Alzheimer's disease induced by injection of neurotoxic fragment of beta-amyloid protein Abeta25-35 in Meynert basal magnocellular nuclei on rats. On the Day 3 after Abeta25-35 injection is observed significant decrease of the level of mRNA expression of Dffb gene in prefrontal cortex in 37%, and in hippocampus in 62% in the experiment group versus the control group. These differences were not found in the hypothalamus when comparing the experimental and control animals. It was suggested that repressive effect of glutamate antibodies on the level of mRNA expression of Dffb gene reflects stabilization of processes taking place in brain cells in experimental Alzheimer's disease, and in its turn the intensiveness of nerve and glial cells apoptotic death is decreased.
- Published
- 2012