Antibodies to Glutamate Reversed the Amnesic Effects of Proinflammatory S100A9 Protein Fibrils in Aged C57Bl/6 Mice.

Chronic intranasal administration of fibrillar structures of proinflammatory S100A9 protein impaired passive avoidance learning in old C57Bl/6 mice. Combined treatment with S100A9 fibrils and antibodies to glutamate was followed by an increase in horizontal locomotor activity of animals in the open-field test and did not disturb spatial memory.

[Autoantibodies to glutamate and GABA in opiate addiction].

Blood serum from 129 patients with opium addiction at different stages of the disease and 63 donors (control group) was examined for the presence of autoantibodies to the exciting and inhibitory amino acids glutamate and GABA. It was shown enhanced production of autoantibodies to glutamate and GABA. Dependence of the level and frequency of detec- tion of autoantibodies to glutamate and GABA on the stage of the disease was revealed.

Ratio of antibodies to neurotransmitters in the serum of students, occasional drug users.

The survey included volunteer students of secondary and higher educational institutions. Two groups have been formed based on the results of clinical and laboratory studies. Group 1 comprised students occasionally using cannabinoids and amphetamines (risk group for psychoactive substances addiction) and group 2 included students who do not use drugs. The serum level of autoantibodies to norepinephrine, dopamine, and serotonin was reduced in the risk group.

[Protective action of glutamate antibodies on increased expression of genes of programmed death of rat brain cells induced by injection of a ß-amyloid fragment (25-35)].

Glutamate antibodies intranasally administered to Wistar rats at a dose of 300 µg/kg reduced the elevated levels of expression of Aifml, Casp3, and Parp 1 genes in the prefrontal cortex and Aifml and Casp3 genes in the hippocampus on the third day after administration of the ß-amyloid fragment Aß25-35 into the Meynert nuclei of the brain. Changes in Aifm1, Bax, Casp3, and Parp 1 gene expression were not found in the hypothalamus, and changes in Bax gene expression were not found in the brain structures studied. The discovered features of gene expression in the prefrontal cortex and hippocampus are considered in terms of development of various cell-death programs, which are modulated by glutamate antibodies.

[Antibodies to neurotransmitters as possible neuroimmune risk markers of formation dependence to psychoactive substances].

In the sera of patients with opioid addiction has been found elevated levels of autoantibodies to the neurotransmitters dopamine, norepinephrine and serotonin in comparison with a control group of healthy people of the same age. In the group of patients with acute withdrawal was showed a reduction of antibody to dopamine, noradrenaline and serotonin in the blood serum when compared with patients in the period of postabstinent disorders. In the group of patients with risk for the formation of substance dependence in serum was observed decrease in autoantibodies to dopamine and norepinephrine compared with the control group.

[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.

[Repressional effects of the glutamate antibodies on expression of Dffb gene in the brain of rats with experimental Alzheimer's disease].

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.

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.

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.

[Glutamate antibodies in the development of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinsonian syndrome in C57B1/6 mice].

The experiments on mice C57B1/6 with MPTP-induced Parkinsonian syndrome have shown that preliminary and simultaneous intranasal injection of glutamate antibodies inhibit development of the syndrome. Administration of glutamate antibodies decreased tremor, rigidity and increased horizontal locomotion, movement velocity in the open field.

Induction of autoantibodies to glutamate in patients with Alzheimer's disease.

Autoantibodies to glutamate were found in blood plasma from patients with Alzheimer's disease. The content of autoantibodies to glutamate in blood plasma from patients with moderate and severe dementia was 2-fold higher compared to patients with mild dementia.

Effect of antibodies against serotonin, bovine serum albumin, and complete Freund's adjuvant on mice subjected to acute immobilization stress.

Nonspecific immunomodulators (complete Freund's adjuvant and bovine serum albumin) produced an antistress effect on mice during immobilization stress. Immunization with a serotonin-protein conjugate produced no antistress effect.

[Common neuroimmunological features of drug addiction, alcoholism, epilepsy, and neurogenic pain syndromes].

In this review the authors analyze neuroimmune aspects of the pathogenesis of such neuropsychic diseases as drug addiction, alcoholism, epilepsy, and pathologic pain. The role of pro-inflammatory cytokines in the development of pathological pain and epilepsy is discussed. The authors analyze their own data on the role of antibodies to neuromediators, such as catecholamines, serotonin, and glutamate, in the development of various forms of neuropathology, and outline the prospects of immunotherapy of the mentioned forms of neuroimmunopathology, including immunotherapy with conjugate on homological protein carrier.

Immunocorrection of alcohol dependence by immunization with a serotonin-homologous protein carrier conjugate.

We demonstrated a possibility of inducing antibody production against serotonin in high titers in rats by active immunization with serotonin conjugated with a homologous protein carrier (rat serum albumin) and with a foreign protein carrier (BSA).

Suppression of alcohol consumption in C57Bl/6 mice after intranasal administration of antiserotonin antibodies.

Experiments on C57Bl/6 mice under conditions of free choice between alcohol and water for 10 months showed that intranasal administration with antiserotonin antibodies in doses of 30 and 15 microg/kg for 2 week decreased alcohol consumption over 1 month after treatment.

Immunotropic effects of active immunization with serotonin-protein conjugate in C57BL/6 mice exposed to immobilization stress.

Immobilization stress for 14 h induced lymphopenia, hypoplasia of the thymus and spleen, and decrease in functional activity of T lymphocytes and macrophages in C57Bl/6 mice. Active induction of antibodies against serotonin during stress decreased functional activity of T lymphocytes and partially recovered phagocytic activity of peritoneal macrophages.

Phagocytic activity and state of bactericidal systems in polymorphonuclear leukocytes from patients with Alzheimer's disease.

Phagocytic activity of peripheral blood neutrophils underwent phase changes in patients with Alzheimer's disease. Neutrophils retained the ability to engulf microbes, but their digestive activity decreased at the early stage of Alzheimer's disease. At the late stage we observed a decrease in the count of phagocytizing neutrophils, reduction of myeloperoxidase activity, and increase in the content of cationic proteins.

Induction of immune complexes and autoantibodies to serotonin and dopamine in patients with Alzheimer's disease.

Plasma concentration of immune complexes and antibodies to serotonin and dopamine were higher in patients with Alzheimer's disease compared to mentally healthy volunteers of the same age. Plasma concentrations of antibodies to serotonin and dopamine decreased with the increase in the duration of this disease.