摘要:

Studies have shown that the parent myelin basic protein (MBP) is a more potent antigen than its disease-inducing fragments. Based on equimolar ratios, 10–15 times more peptide is required to induce experimental allergic encephalomyelitis (EAE) with the same severity as that induced by the intact MBP. In this report, we show that 2 epitopes are required for EAE in Lewis rats; that which induces T cell-mediated immunity requires the expression of a B cell epitope for the development of full spectrum of clinical and histopathological signs of disease. Thus, the development of disease may be related to the magnitude of the humoral and cellular responses to particular B and T cell epitopes. Whether more than 1 epitope, over 30 of which have been located in the MBP, contribute to the development of MBP-induced disease is not clear; but what is clear is that the EAE-inducing peptide sequence, unlike the MBP, is restricted in terms of the number of recognizable epitope

ISSN:0304-324X    

DOI:10.1159/000212873

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

Cellular and humoral immunoreactivity to neuronal antigens was investigated in patients with motor neurone disease (MND). Lymphocytes from patients with MND and normal healthy controls were cultured with a membrane fraction prepared from cultured spinal cord neurones. 4 out of 14 patients with MND and 0 out of 9 normal controls showed a significantly increased stimulation index. An enzyme-linked immunoabsorbent assay (ELISA) was established to detect antibodies to synaptic membrane fraction prepared from human motor cortex. Sera from MND patients showed a significantly increased immuno-globulin binding with respect to normal control sera. Antineuronal antibody production by MND lymphocytes was studied by using Epstein-Barr virus transformation followed by fusion with a mouse myeloma cell line. Antibody-producing clones were isolated. This procedure would allow a more detailed analysis of the antineuronal antibody production in MND.

ISSN:0304-324X    

DOI:10.1159/000212874

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

The glial fibrillary acidic protein (GFAP), myelin basic protein (MBP), S100 protein (S100), γγ-enolase and neurofilament proteins were determined in the CSF of neurological patients. In Alzheimer’s disease (AD), the GFAP values were very often increased but this was not specific to this disease. In 2 cases of familial AD, increases in neurofilament protein were detected. The determination of autoantibodies against neurofilament proteins in blood showed rather low values in AD, although they were higher than in subacute sclerosing panencephalitis (SSPE) and Chagas’ disease. Increases were observed in diseases not related to AD such as vascular disorders and Parkinson’s disease.

ISSN:0304-324X    

DOI:10.1159/000212875

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

The intralaminar distribution of choline acetyltransferase, galactocerebrosides, gangliosides and proteins were determined in frontal (Brodmann’s area 9) and temporal (Brodmann’s area 22) cortices from subjects with autopsy-proven Alzheimer’s disease and controls matched for sex, age and postmortem delay. In normal brain choline acetyltransferase (CAT) activity was higher in the II and IV layers in the temporal cortex, while in frontal cortex CAT activity was relatively high in the II–III layer, appearing as a single peak. The intracortical distribution of galactocerebrosides normally shows a trend to a higher activity from the pial surface to white matter either in frontal or temporal cortices. Higher concentrations of gangliosides were associated with the cell body layers in either frontal or temporal cortices. In either frontal and temporal cortices from 5 patients with Alzheimer’s disease the pattern of intralaminar distribution of CAT activity was completely disrupted and it was significantly lower than in all cortical layers of the controls. Galactocerebrosides concentration was significantly decreased in the lower layers (IV, V and VI) in both frontal and temporal cortices and ganglioside sialic acid concentration was also decreased in the Alzheimer brain consistently in the lower (III–IV) layers of the frontal and temporal cortices. These observations indicate a widespread involvement of cholinergic activities through all cortical layers. However, the selective decrease in galactocerebroside concentration in the lower layers (IV–VI) suggests a selective loss of ascending fibers from subcortical nuclei. The decreased concentration of ganglioside sialic acid in lower layers suggests a selective axo-dendritic degeneration in these laminae of frontal association and temporal cortex in Alzhei

ISSN:0304-324X    

DOI:10.1159/000212876

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

A 15-min complete cerebral ischemia, and repetitive ischemic insults of 15-min duration each cause changes in brain cortical glucose and energy metabolism which are similar in quality but different in quantity. Abnormalities in glycolytic flux, lactate production, cessation of oxidation and energy production were found to be more pronounced with advancing age, thus indicating a reduced biological plasticity of the brain to meet emergency conditions. Repeatedly occurring ischemic insults may damage energy metabolism in particular.

ISSN:0304-324X    

DOI:10.1159/000212877

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

Synaptosomes isolated from the forebrain of rats of different ages (20, 60, 100 and 140 weeks of age) and incubated in Krebs-Henseleit-Hepes pH 7.4 buffer (for 10 min at 24 °C) were utilized to define the redox state of the intramitochondrial NAD couple (ΔGox-red) and the phosphorylation state of adenine nucleotide system (ΔGATP). The free-energy change (ΔΔG) for the coupled reactions was calculated. The animals were subjected for 10 min to different degrees of in vivo hypoxia (52 ≥ PaO2 ≥ 11 mm Hg). In synaptosomes isolated from the forebrain of animals submitted to moderate degrees of hypoxia, the trend of ΔΔG was quite similar to that observed in normoxia. In synaptosomes isolated from the forebrain of rats submitted to severe degrees of hypoxia, the ΔΔG was markedly altered as function of both aging and severity of hypoxemia. The extensive ΔΔG changes were largely supported by alteration of the phosphorylation state of adenine nucleotides. However, in synaptosomes from severely hypoxic rats, aging affected the re

ISSN:0304-324X    

DOI:10.1159/000212879

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

The potentials of postischemic functional recovery were studied in cats submitted to 1 h of complete cerebrocirculatory arrest in normothermia. Neuronal activity was estimated by recording the electroencephalogram (EEG), the pyramidal response following stimulation of the motor cortex and the somatosensorily evoked cortical potentials. During ischemia EEG was suppressed within 12–15 s, evoked potentials within 2 min, and the pyramidal response within 5 min. After recirculation following ischemia, the electrically evoked D wave of the paramidal response began to reappear between 7 and 9 min and the synaptically evoked I wave between 25 and 60 min. The evoked cortical potentials returned in parallel with the I wave of the pyramidal response but control amplitude was not reached before 3 h. The peak latencies of the evoked potentials were consistently prolonged for at least 24 h but normalized after a few days, provided secondary postischemic circulatory disturbances could be prevented. EEG began to recover after the beginning appearance of the somatosensorily evoked cortical potentials; initially it exhibited a burst-suppression pattern but it gradually progressed to continuous activity. The frequency pattern of the EEG normalized within 24 h and the amplitude after a few days. After recovery, the behavior of the pyramidal response and of evoked potentials to repetitive stimulation was the same as under control condition

ISSN:0304-324X    

DOI:10.1159/000212880

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

Incomplete ischemia of the spinal cord of rabbits was produced by a 40-min occlusion of the abdominal aorta followed by 1 and 4 days of recirculation. Regional evaluation of ATP-induced bioluminescence after 20 min of ischemia revealed ATP depletion mainly in the gray matter of the spinal cord. After 40 min of ischemia, ATP-induced bioluminescence was too faint to expose the photographic film. Within 1 and 4 days of recovery following 40 min of ischemia, restitution of ATP was regionally heterogeneous, reduced predominantly in the anterior horns of gray matter. Polysome profiles remained unaltered during the ischemic period, but a marked disaggregation of polyribosomes occurred after 10 min of recirculation. Protein synthesis in a cell-free system was inhibited by the addition of a postischemic cytosol or protein fraction isolated from cytosols on a DEAE column. The inhibition can be overcome by the addition of each initiation factor 2 (eIF-2), GTP and GDP exchange factor (GEF). Occlusion of abdominal aorta for 40 min results in decrease in monoamine oxidase accumulation in both proximal and distal ligature placed on sciatic nerve. Within 4 days of recovery the transport was progressively depressed to 22 and 21 % in the proximal and distal direction, respectively.

ISSN:0304-324X    

DOI:10.1159/000212881

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

Endogenous neurotrophic factors have been proposed to play an important role in degenerative diseases and aging. In aged rats, neurotrophic activity induced by partial lesion of nigro-striatal pathways seems to be lower compared to young rats when assayed in vitro on cultured mesencephalic dissociated neuronal cells. In parallel experiments, we could also observe an age-dependent delay in spontaneous recovery of striatal tyrosine hydroxylase activity after lesion. Both experimental evidences suggest a low-potential neuroplasticity in aged rats. Nevertheless, the aging brain seems to be responsive to pharmacological manipulation. Long-term phosphatidylserine treatment has been shown to maintain the integrity of neuronal structures altered by the aging process. Putative mechanisms of action underlying these effects are presented.

ISSN:0304-324X    

DOI:10.1159/000212882

出版商:S. Karger AG    

年代:1987

数据来源: Karger

ISSN:0304-324X    

DOI:10.1159/000212883

出版商:S. Karger AG    

年代:1987

数据来源: Karger