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  • 1
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Inorganic chemistry 25 (1986), S. 3570-3572 
    ISSN: 1520-510X
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Analytical chemistry 67 (1995), S. 2635-2643 
    ISSN: 1520-6882
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1520-6882
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Analytical chemistry 60 (1988), S. 169-172 
    ISSN: 1520-6882
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 55 (1981), S. 39-46 
    ISSN: 1432-0533
    Keywords: Polyneuropathy ; Intermediate filaments ; Connatal diseases ; Schwann cells ; Demyelination
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A case of connatal polyneuropathy is described in a boy who died of pneumonia at the age of 2 years, and from whom sural nerve biopsies had been taken when he was 4 and 16 months old. Clinically, his disease was characterized by motor weakness and muscular flaccidity in the presence of normal intellectual development. The evolution of the connatal peripheral nerve lesion could be followed from the age of 4 months to death: The first biopsy evidenced the most serious pathologic changes. The findings were reminiscent of those encountered in a fetal nerve at 18 weeks of gestation. Furthermore, it showed numerous filamentous inclusions in Schwann cells. The second biopsy showed a sparsely myelinated nerve with bands of basement membrane apparently unrelated to cells arranged around the nerve's fibers. A few Schwann cells containing filamentous inclusions were still present. At autopsy, the findings were identical to those of the second biopsy. The possibility that this patient was transitionally exposed to a neurotoxic agent during pregnancy and that the biopsy findings represent a lesion that is still florid in the first and in a residual state in the second biopsy is considered.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0533
    Keywords: Senile dementia of Alzheimer type ; Neurofibrillary tangles ; Fibrous astrocytes ; Immunocytochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Two types of Alzheimer neurofibrillary tangles may be found in the hippocampus in senile dementia of the Alzheimer type. Besides classical flameshaped intraneuronal tangles, there are less compact tangles representing extracellular remnants of destroyed neurons with neurofibrillary change. Strong immunoreactivity for glial fibrillary acidic protein (GFA) was found in the second type of tangles, which was due to penetration of fine processes of fibrous astrocytes into bundles of paired helical filaments (PHF). PHF appear to be a strong stimulus for astrocytic reaction when they are not segregated from the neuropil by the neuronal cell membrane.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-0533
    Keywords: Oculopharyngeal muscular dystrophy ; Chronic axonal atrophy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We report on morphometric investigations of peripheral nerves in a woman, who died at the age of 69, presenting the classical symptoms of oculopharyngeal muscular dystrophy (OPMD) and a typical family history with several members (males and females) affected over three generations. Evidence for chronic axonal atrophy was found in peripheral nerves and especially in oculomotor nerves with severe axon loss in endomysial nervetwigs of extra-ocular, laryngeal, and tongue muscles. Whereas limb muscles presented features of neurogenic atrophy, severe changes of “myopathic” type were evident in extrinsic eye muscles, laryngeal constrictor, tongue, and diaphragma. However, we interpreted these changes as neurogenic in origin in view of the severe denervation found in those muscles. Our findings suggest that OPMD is a disease of primary neurogenic origin rather than a primary myopathic disorder.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 60 (1983), S. 199-206 
    ISSN: 1432-0533
    Keywords: Myelin ; Leukodystrophies ; Immunocytochemistry ; Myelin basic protein ; Myelin associated glycoprotein ; Glial fibrillary protein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary One case of each of the following human leukodystrophies was examined immunocytochemically with antisera against myelin basic protein (MBP), myelin associated glycoprotein (MAG) and gliofibrillary acidic protein (GFA): Metachromatic leukodystrophy (MLD), connatal adrenoleukodystrophy (ALD), sudanophilic leukodystrophy of the adult (SLD) and connatal Pelizaeus-Merzbacher disease (PMD). A case of canine globoid cell leukodystrophy (GLD) was also included under the assumption that this disease was the same in the dog as in man. It was shown that the storage process in MLD and GLD did not involve MBP or MAG and that the breakdown of myelin with the formation of fat granule cells containing droplets of neutral fat in ALD and SLS proceeds in a similar way as in experimental Wallerian degeneration. In PMD, MBP is present in the vicinity of axons not surrounded by a myelin sheath demonstrable with conventional means. The globoid cells of GLD could be demonstrated to be of non-astrocytic origin.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-0533
    Keywords: Alzheimer's disease ; A4 protein ; Acetylcholinesterase ; Senile plaque ; Neuropathology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In 20 unselected autopsy cases tissue blocks from the hippocampus with adjacent entorhinal cortex and neocortex were stained for acetylcholinesterase (AChE). From five brains shown to have large numbers of senile plaques tissue, adjacent to that taken for AChE tissue blocks, was embedded in paraffin and sections were immunostained for the A4 protein. The morphological aspects were compared. Equivalent types of plaques and plaque-like structures were observed in the A4- and ACHE-stained sections. On selected tissue blocks from patients with many senile plaques two immediately adjacent cryostat sections were stained, one for AChE and one for A4 protein. The same individual plaques could be identified on the two sections. These findings suggest that high AChE activity is intimately associated with the process of A4 protein formation and accumulation in plaques and that this association already occurs at a very carly stage of plaque formation.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 83 (1991), S. 21-29 
    ISSN: 1432-0533
    Keywords: Diffuse plaques ; Dendrites ; Synapses ; β/A4 protein ; Amyloid precursor protein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The origin of the extracellular β-amyloid protein (β/A4) found in senile plaques and the cellular mechanisms responsible for its deposition in cerebral tissues are still an unresolved issue in Alzheimer's disease. In this study we analyzed in detail the distribution of various epitopes of β/A4 in relation to local cellular elements in diffuse plaques of the hippocampal region. We also correlated our findings with the presence and distribution of non-β/A4 epitopes of the amyloid precursor protein (APP) and with synaptophysin immunoreactivity in the cortical neuropil. Discontinuous β/A4-immunoreactive deposits were found along dendrites, and around the soma of neurons included in the plaques. Furthermore, increased synaptophysin reactivity with slightly dilated synaptophysin-immunolabeled presynaptic terminals were found in diffuse plaques. APP epitopes could not be found in diffuse plaques. However, some of the APP antibodies, mainly those to the C-terminal portion of APP, and antibodies to β/A4 recognized clusters of flat vesicular profiles (0.6–1.4 μm in width and 2–3 μm in length) in the neuropil of cortical areas where plaques had developed. Our findings are compatible with a neuronal origin of β/A4 in diffuse plaques and with a primary release of β/A4 at synaptic sites along the immunostained neurites. They also suggest that diffuse plaques might be preceded by minute lesions of the neuropil where β/A4 is not yet released from the precursor molecule.
    Type of Medium: Electronic Resource
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