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  • 1
    Electronic Resource
    Electronic Resource
    Phagocytosis of β/A4 amyloid fibrils of the neuritic neocortical plaques (1991)
    Springer
    Acta neuropathologica 81 (1991), S. 588-590 
    Details
    ISSN: 1432-0533
    Keywords: Alzheimer disease ; Amyloid ; Phagocytosis ; Microglia ; beta protein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Immunocytochemistry using monoclonal antibodies to β/A4 protein was applied to study the macrophages involved in the removal of amyloid deposits. The material examined included necrotic brain tissue areas with abundant amyloid deposits collected from 32 autopsy cases. The β/A4-immunoreactive products were found in numerous macrophages, appearing as early as 24 h after the onset of stroke. Immunogold electron microscope studies allowed us to localize the reaction product to the secondary lysosomes. Our study clearly demonstrates the differences between macrophages engaged in amyloid removal and microglial cells associated with amyloid deposits, which according to previous observations contain β/A4 material within endoplasmic reticular channels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00310142
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Ultrastructure of the microglia that phagocytose amyloid and the microglia that produce β-amyloid fibrils (1992)
    Springer
    Acta neuropathologica 84 (1992), S. 225-233 
    Details
    ISSN: 1432-0533
    Keywords: Alzheimer's disease ; Tissue culture ; Microglia ; Amyloid ; Ultrastructure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The function of microglia associated with β-amyloid deposits still remains a controversial issue. On the basis of recent ultrastructural data, microglia were postulated to be cells that form amyloid fibrils, not phagocytes that remove amyloid deposits. In this electron microscopic study, we examined the ability of microglia to ingest and digest exogenous amyloid fibrils in vitro. We demonstrate that amyloid fibrils are ingested by cultured microglial cells and collected and stored in phagosomes. The ingested, nondegraded amyloid remains within phagosomes for up to 20 days, suggesting a very limited effectiveness of microglia in degrading β-amyloid fibrils. On the other hand, we showed that in microglial cells of classical plaques in brain cortex of patients with Alzheimer's disease, amyloid fibrils appear first in altered endoplasmic reticulum and deep infoldings of cell membranes. These differences in intracellular distribution of amyloid fibrils in microglial cells support our observations that microglial cells associated with amyloid plaques are engaged in production of amyloid, but not in phagocytosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00227813
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    The complex of microglial cells and amyloid star in three-dimensional reconstruction (1990)
    Springer
    Acta neuropathologica 81 (1990), S. 116-124 
    Details
    ISSN: 1432-0533
    Keywords: Microglia ; Amyloid star ; Classical plaque ; Three-dimensional reconstruction ; Alzheimer's disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Ultrastructural, three-dimensional reconstruction and morphometric studies of classical plaques from the cortex of a patient with Alzheimer's disease showed five or six microglial cells, which form, together with the amyloid star, the central complex of the classical plaque. Microglial cells associated with the amyloid star show marked polymorphism, but all forms possess an amyloid making pole. The surface of the cell membrane at this pole is extended by apparent connection with membranes of cytoplasmic channels filled with amyloid fibers. The amyloid pole also shows other features of local activation with nuclei translocation, expansion of Golgi apparatus and endoplasmic reticulum, and multiplication of vacuoles and coated vesicles that are in close proximity to channels filled with new polymerized amyloid fibers. On the basis of ultrastructural studies, three forms of microglial cells can be distinguished: macrophage-like, cap-like, and octopus-like cells. The most effective in production of amyloid fibers seem to be cap-like microglial cells, which have the greatest interface with the amyloid star. Octopus-like cells have the least contact with the amyloid star. The size of the surface of the interface with the amyloid star appears to be an indicator of the extent of cell engagement in amyloid fiber formation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00334499
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  • 4
    Electronic Resource
    Electronic Resource
    Ultrastructural studies of the cells forming amyloid in the cortical vessel wall in Alzheimer's disease (1992)
    Springer
    Acta neuropathologica 84 (1992), S. 117-127 
    Details
    ISSN: 1432-0533
    Keywords: Alzheimer disease ; Amyloid angiopathy ; Pericytes ; Microglia ; Ultrastructure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Ultrastructural studies of serial sections of the vessels with amyloid deposits in the brain cortex of patients with Alzheimer's disease showed that cells in the position of pericytes — perivascular cells - and perivascular microglial cells are producers of amyloid fibrils in the vascular wall. Three types of changes from normal are distinguishable in the vessel wall: (1) semicircular or circular thickening of vascular wall containing a large amount of amorphous material and various number of amyloid fibrils, (2) tuberous amyloid deposits containing both amorphous material and amyloid fibrils, some of the fibrils being arranged in strata and others arranged radially, and (3) amyloid star composed of a predominantly radial arrangement of bundles of amyloid fibrils and a less prominent amorphous component. A mixture of amorphous material and amyloid fibrils is present in cell membrane envaginations of perivascular cells, and occasionally perivascular microglial cells. Bundles of amyloid fibrils are found in altered cisternae of the endoplasmic reticulum and in the channels confluent with the infoldings of the plasma membrane of perivascular microglial cells. The amyloid deposition in the wall of the vessel causes degeneration of endothelial cells and the reduction of, and in some vessels obliteration of, the vessel lumen. In areas affected by amyloid angiopathy, extensive degeneration both of the neuropil and of neurons was observed. These changes were accompanied by astrogliosis. This study demonstrates similarities in amyloid formation in amyloid angiopathy and in β-amyloid plaques in the neuropil and suggests that cells of the mononuclear phagocyte system of the brain (perivascular cells and perivascular microglia) are engaged in amyloid fibril formation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00311383
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  • 5
    Electronic Resource
    Electronic Resource
    Migration of perivascular cells into the neuropil and their involvement in β-amyloid plaque formation (1993)
    Springer
    Acta neuropathologica 85 (1993), S. 586-595 
    Details
    ISSN: 1432-0533
    Keywords: Alzheimer's disease ; Perivascular cells ; Microglia ; Plaques ; Amyloid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Our recent ultrastructural studies of amyloid angiopathy in biopsy specimens from Alzheimer's disease patients showed that perivascular cells and perivascular microglia are involved in the production of amyloid fibrils. Further examination of the walls of the vessels with and without amyloid deposits presented in this report reveals numerous mononuclear cells with a broad spectrum of morphological appearances. Some of these cells produce amyloid in the vascular wall and migrate into the neuropil. Others do not produce amyloid in this location but also migrate through the vascular basal lamina and position themselves on the external surface of basal lamina or in the neuropil outside the vascular astrocytic end-feet processes. The presence of clusters or rows of six or more of these cells in the position of perivascular microglial cells suggests their proliferation in the perivascular region. After leaving the perimeter of the vessel wall, perivascular cells become the perivascular, neuropil, and satellite microglia cells. Migrating perivascular cells become the microglia, which are engaged in amyloid fibril formation and development of classical and primitive plaques.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00334667
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  • 6
    Electronic Resource
    Electronic Resource
    Isolation and characterization of macrophages from scrapie-infected mouse brain (1987)
    Springer
    Acta neuropathologica 72 (1987), S. 240-247 
    Details
    ISSN: 1432-0533
    Keywords: Scrapie ; Macrophage ; Microglia ; Amyloid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have isolated and characterized a population of brain macrophages from normal and scrapieinfected mice. The cells are phagocytic, possess Fc-IgG receptors, Mac-1 surface antigen and proliferate in the presence of macrophage colony stimulating factor. They resemble microglia in that they have a plasmalemmal distribution of the enzyme nucleoside diphosphatase, a property that is characteristic of microglia in situ. In two of the three combinations of scrapie agent and mouse strain examined, the number of brain macrophages was several fold higher than in normal control mice. The increase was not observed in mice infected intraperitoneally or in control mice inoculated with normal brain homogenate. The increase is detectable as early as 3–5 weeks postinoculation. The agent/host combination that failed to show an increase in brain macrophages is one that develops large numbers of amyloid plaques. These observations suggest that these cells are closely associated with the scrapie pathogenic process in the CNS. The failure of these cells to increase in the plaque forming model of scrapie disease also suggests that they play a role in the control of CNS amyloidogenesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00691096
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