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  • 1
    ISSN: 1432-0533
    Keywords: Key words Basic fibroblast growth factor ; Complement-activated oligodendrocytes ; Gangliosides ; Glial fibrillary tangles ; Heparin-binding growth factors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Pick's disease (PD) brains were examined immunohistochemically for the expression of antigens known to be associated with Alzheimer's disease (AD) lesions. Most antibodies which label intracellular neurofibrillary tangles (NFTs) in AD were found to stain Pick bodies (PBs). Among them was the monoclonal antibody A2B5, which is known to recognize neuronal surface gangliosides. This result indicates that membrane proteins are probably incorporated int o PBs as into NFTs. However, PBs, in contrast to NFTs, showed a paucity of staining for heparan sulfate glycosaminoglycan and basic fibroblast growth factor (bFGF). Staining for midkine, seen in senile plaques in AD, was not seen in PD. The relative lack of staining for these two neurotrophic factors in PD brain may reflect underlying mechanisms which are distinct from those in AD. We also describe two glial abnormalities in PD: glial fibrillary tangles and clusters of granules positive for the complement protein C4d in the hippocampal dentate fascia. These are presumably related to complement-activated oligodendroglia, and both pathological structures are more abundant in advanced cases, suggesting that they may be hallmarks of the disease progression.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 84 (1992), S. 100-104 
    ISSN: 1432-0533
    Keywords: Parkinson's disease ; Complement ; Lewy bodies ; Oligodendrocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The substantia nigra (SN) in 11 Parkinson's disease (PD) patients and 5 neurologically normal controls was examined immunohistochemically using antibodies to various proteins of the complement system. In PD, but not in control SN, intra-and extraneuronal Lewy bodies and dendritic spheroid bodies were stained with anti-human C3d, C4d, C7 and C9 antibodies, but not with antibodies to C1q, fraction Bb of factor B or properdin. Axonal spheroid bodies in the nigrostriatal tract were not stained by any of the complement antibodies. However, complement-activated oligodendroglia were revealed by anti-C3d and anti-C4d antibodies in the PD substantia nigral area. These data indicate that some pathological structures in PD activate the classical complement pathway.
    Type of Medium: Electronic Resource
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