Neuronal plasticity and astrocytic reaction in Down syndrome and Alzheimer disease.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Standard

Neuronal plasticity and astrocytic reaction in Down syndrome and Alzheimer disease. / Jørgensen, Ole Steen; Brooksbank, B W; Balázs, R.

I: Journal of the Neurological Sciences, Bind 98, Nr. 1, 1990, s. 63-79.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Jørgensen, OS, Brooksbank, BW & Balázs, R 1990, 'Neuronal plasticity and astrocytic reaction in Down syndrome and Alzheimer disease.', Journal of the Neurological Sciences, bind 98, nr. 1, s. 63-79.

APA

Jørgensen, O. S., Brooksbank, B. W., & Balázs, R. (1990). Neuronal plasticity and astrocytic reaction in Down syndrome and Alzheimer disease. Journal of the Neurological Sciences, 98(1), 63-79.

Vancouver

Jørgensen OS, Brooksbank BW, Balázs R. Neuronal plasticity and astrocytic reaction in Down syndrome and Alzheimer disease. Journal of the Neurological Sciences. 1990;98(1):63-79.

Author

Jørgensen, Ole Steen ; Brooksbank, B W ; Balázs, R. / Neuronal plasticity and astrocytic reaction in Down syndrome and Alzheimer disease. I: Journal of the Neurological Sciences. 1990 ; Bind 98, Nr. 1. s. 63-79.

Bibtex

@article{f92b75f07d9f11dd81b0000ea68e967b,
title = "Neuronal plasticity and astrocytic reaction in Down syndrome and Alzheimer disease.",
abstract = "Proteins relatively enriched in neurons (neural cell adhesion molecule (NCAM) and D3-protein) or in glia (glutamine synthetase, glial fibrillary acidic protein (GFAP) and S100) were measured by quantitative immunochemical methods in autopsy samples of the cerebral cortex of subjects with Alzheimer disease (AD) and adults with Down syndrome (DS), the latter also presenting manifest signs of Alzheimer type of neuropathology. The trend of changes was similar in AD and DS, but more marked in the latter. The biochemical make-up of astrocytes was differentially affected: in both the frontal and DS temporal cortex the specific concentration of glutamine synthetase was unaltered, while that of S100 and the soluble form of GFAP was markedly elevated (about 260% and 690% of control values, respectively). In the AD frontal cortex the estimates for glutamine synthetase were normal, while S100 and GFAP were about 180% and 230% of control. The observations (normal GS and elevated levels of the other markers) might suggest that the pathological changes involve a differentiated astrocytic reaction and that the astrocytic reaction is more marked in DS than in AD. In DS the increase in S100 could be explained, in part, by a gene dosage effect and in part by reactive gliosis. The neuronal markers were also differentially affected. In comparison with appropriate controls, the concentration of D3-protein in frontal cortex was decreased by 24% in DS and by 14% in AD, whereas NCAM levels were not significantly affected. The ratio of NCAM to D3-protein was significantly increased by 32% and 8.5% in DS and AD, respectively. These observations are consistent with the view that the destruction of mature neuronal structures (as marked by the D-3 protein) coincides with the formation of new neuronal membranes (as indicated by NCAM), i.e. in these degenerative disorders plastic changes are taking place involving cerebral cortex neurons in which trophic substances may be instrumental.",
author = "J{\o}rgensen, {Ole Steen} and Brooksbank, {B W} and R Bal{\'a}zs",
note = "Keywords: Aged; Alzheimer Disease; Astrocytes; Cell Adhesion Molecules, Neuronal; Down Syndrome; Frontal Lobe; Glial Fibrillary Acidic Protein; Glutamate-Ammonia Ligase; Humans; Immunodiffusion; Immunoelectrophoresis, Two-Dimensional; Middle Aged; Nerve Tissue Proteins; Neuronal Plasticity; S100 Proteins",
year = "1990",
language = "English",
volume = "98",
pages = "63--79",
journal = "Journal of the Neurological Sciences",
issn = "0022-510X",
publisher = "Elsevier",
number = "1",

}

RIS

TY - JOUR

T1 - Neuronal plasticity and astrocytic reaction in Down syndrome and Alzheimer disease.

AU - Jørgensen, Ole Steen

AU - Brooksbank, B W

AU - Balázs, R

N1 - Keywords: Aged; Alzheimer Disease; Astrocytes; Cell Adhesion Molecules, Neuronal; Down Syndrome; Frontal Lobe; Glial Fibrillary Acidic Protein; Glutamate-Ammonia Ligase; Humans; Immunodiffusion; Immunoelectrophoresis, Two-Dimensional; Middle Aged; Nerve Tissue Proteins; Neuronal Plasticity; S100 Proteins

PY - 1990

Y1 - 1990

N2 - Proteins relatively enriched in neurons (neural cell adhesion molecule (NCAM) and D3-protein) or in glia (glutamine synthetase, glial fibrillary acidic protein (GFAP) and S100) were measured by quantitative immunochemical methods in autopsy samples of the cerebral cortex of subjects with Alzheimer disease (AD) and adults with Down syndrome (DS), the latter also presenting manifest signs of Alzheimer type of neuropathology. The trend of changes was similar in AD and DS, but more marked in the latter. The biochemical make-up of astrocytes was differentially affected: in both the frontal and DS temporal cortex the specific concentration of glutamine synthetase was unaltered, while that of S100 and the soluble form of GFAP was markedly elevated (about 260% and 690% of control values, respectively). In the AD frontal cortex the estimates for glutamine synthetase were normal, while S100 and GFAP were about 180% and 230% of control. The observations (normal GS and elevated levels of the other markers) might suggest that the pathological changes involve a differentiated astrocytic reaction and that the astrocytic reaction is more marked in DS than in AD. In DS the increase in S100 could be explained, in part, by a gene dosage effect and in part by reactive gliosis. The neuronal markers were also differentially affected. In comparison with appropriate controls, the concentration of D3-protein in frontal cortex was decreased by 24% in DS and by 14% in AD, whereas NCAM levels were not significantly affected. The ratio of NCAM to D3-protein was significantly increased by 32% and 8.5% in DS and AD, respectively. These observations are consistent with the view that the destruction of mature neuronal structures (as marked by the D-3 protein) coincides with the formation of new neuronal membranes (as indicated by NCAM), i.e. in these degenerative disorders plastic changes are taking place involving cerebral cortex neurons in which trophic substances may be instrumental.

AB - Proteins relatively enriched in neurons (neural cell adhesion molecule (NCAM) and D3-protein) or in glia (glutamine synthetase, glial fibrillary acidic protein (GFAP) and S100) were measured by quantitative immunochemical methods in autopsy samples of the cerebral cortex of subjects with Alzheimer disease (AD) and adults with Down syndrome (DS), the latter also presenting manifest signs of Alzheimer type of neuropathology. The trend of changes was similar in AD and DS, but more marked in the latter. The biochemical make-up of astrocytes was differentially affected: in both the frontal and DS temporal cortex the specific concentration of glutamine synthetase was unaltered, while that of S100 and the soluble form of GFAP was markedly elevated (about 260% and 690% of control values, respectively). In the AD frontal cortex the estimates for glutamine synthetase were normal, while S100 and GFAP were about 180% and 230% of control. The observations (normal GS and elevated levels of the other markers) might suggest that the pathological changes involve a differentiated astrocytic reaction and that the astrocytic reaction is more marked in DS than in AD. In DS the increase in S100 could be explained, in part, by a gene dosage effect and in part by reactive gliosis. The neuronal markers were also differentially affected. In comparison with appropriate controls, the concentration of D3-protein in frontal cortex was decreased by 24% in DS and by 14% in AD, whereas NCAM levels were not significantly affected. The ratio of NCAM to D3-protein was significantly increased by 32% and 8.5% in DS and AD, respectively. These observations are consistent with the view that the destruction of mature neuronal structures (as marked by the D-3 protein) coincides with the formation of new neuronal membranes (as indicated by NCAM), i.e. in these degenerative disorders plastic changes are taking place involving cerebral cortex neurons in which trophic substances may be instrumental.

M3 - Journal article

C2 - 1977892

VL - 98

SP - 63

EP - 79

JO - Journal of the Neurological Sciences

JF - Journal of the Neurological Sciences

SN - 0022-510X

IS - 1

ER -

ID: 5941288