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  • 1
    ISSN: 1573-7284
    Keywords: PrP-arnyloid ; Creutzfeldt-Jakob disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We report here PrP-immunohistochemistry performed on brains from CJD cases from Poland. Only one of five definitive CJD cases exhibited typical PrP-immunoreactive kuru-like plaques and this was case of a short duration. We thus confirm the low frequency of PrP plaques in CJD of Eastern and Central European origin.
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  • 2
    ISSN: 1573-7284
    Keywords: Creutzfeldt-Jakob disease ; Tubulovesicular structures
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Tubulovesicular structures (TVS) have been consistently observed in brain tissue of animals with transmissible spongiform encephalopathies such as natural and experimental scrapie, bovine spongiform encephalopathy, and experimental Creutzfeldt-Jakob disease (CJD). In this communication we demonstrate for the first time the presence of TVS in natural CJD. TVS were detected in all 3 CJD specimens. However, they were rare and were found only in one or two locations per grid. They were seen in distended pre- and postsynaptic terminals and measured approximately 35 nm in diameter, and they were smaller and of higher electron density than synaptic vesicles. Their occurrence in all types of spongiform encephalopathies irrespective of the affected host and the strain of infectious agent emphasizes their biological significance.
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  • 3
    ISSN: 1573-7284
    Keywords: Creutzfeldt-Jakob disease ; Electron microscopy ; Myelinated axon
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We report the ultrastructural pathology of myelinated axons in mice infected experimentally with the Fujisaki strain of Creutzfeldt-Jakob disease (CJD). Initially the myelin sheath was separated into several concentric bands, and cellular processes penetrated between layers of myelin and lifted away the outermost lamella. Then a complicated labyrinth of the concentric cellular processes, clearly belonging to either astrocytes or macrophages, invested myelinated axons. In terminal stages axons completely denuded of myelin were seen in the center of concentric networks of cellular processes. Myelin remnants were seen within astrocytes and macrophages. We conclude that the mechanism(s) of damage to myelinated axons in CID may be similar to that operating in immunologically mediated demyelinating disorders.
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  • 4
    ISSN: 1432-0533
    Keywords: Creutzfeld ; Jakob disease ; White matter change ; Leukolysins ; Tumor necrosis factor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Creutzfeldt-Jakob disease (CJD), previously regarded as a neurodegenerative disorder strictly of the gray matter, occasionally occurs as a panencephalopathic form which is characterized by severe white matter damage. An ultrastructural study of the white matter pathology in mice experimentally infected with the Fujisaki strain of CJD virus revealed: (1) vacuoles within myelin sheaths, formed by splitting either at the major dense or intraperiod lines, or within axons; (2) macrophages filled with numerous myelin figures, lipid droplets and paracrystalline inclusions; (3) astrocytes actively digesting myelin debris; (4) unusual wrapping of several axons by a common myelin sheath; (5) vesicular degeneration of myelin sheaths; (6) close contact between numerous coated pits and outer myelin lamellae; and (7) proliferation of inner mesaxons. Our data indicate that the damage to myelinated axons in the panencephalopathic type of CJD is accomplished primarily by active degradation of myelin by macrophages and astrocytes and by formation of intra-axonal and intra-myelin vacuoles. The myelin vacuolation is most consistent with that produced by leukolysins released from activated macrophages and astrocytes.
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  • 5
    ISSN: 1432-0533
    Keywords: Creutzfeldt-Jakob disease ; Electron microscopy ; Scrapie ; Tubulovesicular structures
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have consistently observed tubulovesicular structures in brain tissues during the terminal stages of naturally occurring and experimentally induced spongiform encephalopathies, irrespective of the host species and virus strain. In NIH Swiss mice inoculated intracerebrally or intraocularly with the Fujisaki strain of Creutzfeldt-Jakob disease (CJD) virus, tubulovesicular structures, measuring 20–50 nm in diameter, were particularly prominent in dilated, pre-and postsynaptic neuronal processes, occasionally being mixed with synaptic vesicles. These structures appeared 13 weeks following intracerebral inoculation, 5 weeks before the onset of clinical signs, when spongiform changes were also detected. The number and density of tubulovesicular structures increased steadily during the course of clinical disease, and were particularly abundant in mice 47 to 51 weeks after intraocular inoculation. In hamsters infected with the 263 K strain of scrapie virus, these structures were initially detected 3 weeks following intracerebral inoculation and increased dramatically at 10 weeks postinoculation. The appearance of tubulovesicular structures before the onset of overt disease in mice inoculated with CJD virus by either the intracerebral or intraocular route, and before the appearance of other neuropathological changes in hamsters infected with scrapie virus, indicate that they represent either a part or aggregate of the infectious virus or a pathological product of the infection.
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  • 6
    ISSN: 1432-0533
    Keywords: Amyloid β-protein ; Progressive dementia ; Cerebellar plaques
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We report the immunolocalization of extensive amyloid β-protein in senile plaques, cerebrovascular amyloid deposits, neurofibrillary tangles and preamyloid in a 32-year-old man with progressive dementia not to trisomy 21 or trauma. These amyloid deposits were non-reactive to antibodies directed against scrapie amyloid. Our data indicate that the presence of amyloid β-protein is not limited to normal aging, Alzheimer's disease and related disorders but is also found in younger individuals with progressive dementia.
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  • 7
    ISSN: 1432-0533
    Keywords: Scrapie ; Creutzfeldt-Jakob disease ; Neuronal autophagy ; Neuropathology ; Electron microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We report the presence of autophagic vacuoles (AV) in neuronal perikarya and neuronal processes of rodents with experimental scrapie and Creutzfeldt-Jakob disease. AV were composed of sequestrated cytoplasmic areas containing ribosomes and occasionally mitochondria and small secondary vacuoles. The formation of AV may contribute to neuronal degeneration and ultimately to neuronal loss.
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  • 8
    ISSN: 1432-0533
    Keywords: Amyloid ; Microglia ; Prion diseases ; Spongiform encephalopathies ; Gerstmann-Sträussler ; Scheinker syndrome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The microglial cell has been demonstrated as component of the cerebral amyloid plaque of Alzheimer's disease. Involvement of microglia in plaques of another cerebral amyloidosis, the Gerstmann-Sträussler-Scheinker syndrome (GSS), has found little attention. We examine here the presence of microglia in GSS plaques by immunohistochemistry and transmission electron microscopy. Paraffin sections from five brains of patients with GSS were immunolabelled with antibodies against prion protein, A4/β amyloid protein, ferritin, leukocyte common antigen, HLA-DR, CD 68, and the MAC387 epitope for microglia and monocytes/macrophages; microglia was also labelled with the Ricinus communis agglutinin-1 lectin. Such (immuno)labelling demonstrated many delicate cell processes and occasional somata within and around prion protein plaques in all GSS brains. Microglial immunoreactivity was strongest with anti-ferritin and variable with anti-macrophage antibodies. Ultrastructural examination of brain tissue from one autopsy and one biopsy of GSS identified microglial cells in close proximity of amyloid plaque fibrils. Our observations demonstrate microglia as an important component of the amyloid plaque in GSS and suggest a major role for microglia in processing and deposition, or at least organization, of prion protein amyloid. Thus, plaques in both transmissible and nontransmissible cerebral amyloidoses seem to develop via similar pathogenetic mechanisms, irrespective of differences in etiology and molecular composition of the amyloid.
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  • 9
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    Acta neuropathologica 90 (1995), S. 113-125 
    ISSN: 1432-0533
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
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  • 10
    ISSN: 1432-0533
    Keywords: Key words Alzheimer’s disease ; Creutzfeldt-Jakob ; disease ; Dementia ; Neuropathology ; Prion disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Creutzfeldt-Jakob disease (CJD) and Alzheimer’s disease (AD) share clinical, neuropathological, and pathogenetic features. To investigate eventual mutual influences, we screened prominently affected neocortex from 110 neuropathologically proven CJD patients for Alzheimer-type pathology with anti-β/A4, Bielschowsky and anti-tau (immuno)stains. The neuropathological classification of Alzheimer-type pathology was made according to the CERAD criteria. Results were controlled by comparison with Alzheimer-type changes in sections from the same cortical areas in 110 sex- and age-matched non-demented control patients. For comparison, the control patients were also classified according to the CERAD neuropathology criteria as if they had been demented. Alzheimer-type tissue changes as in definite and probable CERAD AD occur in 10.9% of the CJD patients and 19.1% of control patients (P = 0.11). The median age of CJD and control patients with CERAD AD is 72 and 68 years, respectively, which differs significantly from the median ages of 64 and 63 years, respectively, in the non-AD/CJD and non-AD control patients. Since CERAD criteria include “presence of other neuropathological lesions likely to cause dementia”, an AD diagnosis in CJD patients (all of whom are demented) is solely based on densities of neuritic plaques. Similar Alzheimer-type changes in even higher frequency, however, are also present in elderly non-demented controls. Thus, the coexistence of Alzheimer-type pathology in CJD most likely represents an age-related change. Deposits of prion protein (PrP) frequently accumulate at the periphery of β/A4 plaques. The presence of β/A4 amyloid in the brain may influence PrP morphogenesis.
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