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  • 1
    Electronic Resource
    Electronic Resource
    Intermitochondrial septate structures in dystrophic axons (1980)
    Springer
    Acta neuropathologica 52 (1980), S. 105-109 
    Details
    ISSN: 1432-0533
    Keywords: Neuroaxonal dystrophy ; Mitochondria ; Membranes ; Junctions
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Intermitochondrial septate structures were found in the dystrophic axons of two cases of infantile neuroaxonal dystrophy. Septate structures were previously seen in some tumors (glioblastomas and Schwannomas) and several organs of vertebrates and invertebrates, but never in human central nervous system (CNS). The structures were studied by transmission and transmission tilt electron microscopy. A proposed model was constructed and X-rayed. Artist's depictions are shown and described. The intermitochondrial septate structures have a periodicity of 120 Å which puts them within the range of those structures previously reported. It was found that our structures are not true junctions, but a complex interdigitation of the outer membranes of the involved mitochondria.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688007
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Cholinesterases colocalize with sites of neurofibrillary degeneration in aged and Alzheimer's brains (1994)
    Springer
    Acta neuropathologica 87 (1994), S. 284-292 
    Details
    ISSN: 1432-0533
    Keywords: Acetylcholinesterase ; Butyrylcholinesterase ; Tau protein ; Tangle ; Degenerated neurites
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Acetylcholinesterase and butyrylcholinesterase have been associated with structures undergoing neurofibrillary degeneration, as well as with all types of senile plaques, in non-demented aged and Alzheimer's brains. At the electron microscope level, the reaction product of both enzymes, appeared to decorate paired helical filaments, straight filaments and βA4 amyloid fibrils. Recent studies showed that cholinesterases were associated with amyloid at early stages, e.g., in diffuse plaques. In the present study, the interrelationship of cholinesterases to structures undergoing neurofibrillary degeneration was analyzed further. Tau immunoreactivity was compared to the staining pattern observed with the two esterases. Double protocols consecutively performed on the same sections, and counterstaining with thioflavin-S, confirmed the presence of cholinesterases in all structures with neurofibrillary degeneration. The conclusion that cholinesterases consistently colocalize with both neurofibrillary bundles and βA4 amyloid fibrils at all stages of their accumulation, allows us to speculate on the possible role that these enzymes may play in either the formation or the consolidation of fibrillary aggregates.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296744
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Alzheimer's disease-type neurofibrillary degeneration in verrucose dysplasias of the cerebral cortex (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 356-365 
    Details
    ISSN: 1432-0533
    Keywords: Tangle ; Nodule ; Cortical development ; Ischemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Verrucose dysplasias, found at autopsy in the cerebral cortex of three elderly individuals (two without neurological disorders and one with motor neuron disease), are shown to present neurofibrillary degeneration of Alzheimer's disease type. This neurofibrillary degeneration immunoreacted with antibodies against abnormally phosphorylated tau (5E2 and AT8), disclosed acetyland butyrylcholinesterase activity, and was consistently stained with thioflavin-S. Cortical dysplasias, found either as isolated verrucose nodules or comprising multiple nodules, contained cell-sparse areas around which a peak of neurofibrillary changes was seen. Cell-sparse areas were sometimes bridged by stripes of neurons and fibers arranged in a radial fashion, and many of these neurons showed neurofibrillary degeneration. Cytoskeletal abnormalities were conspicuous in layers II and III at the external borders of the dysplasias, as well as in neurons located in layers V and VI, and in the white matter beneath layer VI in central zones of each lesion. The morphology of cells undergoing neurofibrillary changes (from early nonfibrillar stages to late extracellular ones) suggests that neurons disturbed in their migration toward the site to which they had been committed may become vulnerable to cytoskeletal changes. Micro-environmental disturbances related to hypoxia-ischemia in the affected cortex are proposed as likely contributing factors for the longterm production of this neurofibrillary degeneration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00315009
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    Paper (German National Licenses)
    Fulltext
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