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  • 1
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We studied the targeting of spongiform lesions within the visual pathways after intraocular injection with the Fujisaki strain of Creutzfeldt-Jakob disease (CJD) virus. The first lesions were observed 18 weeks postinoculation in the most superficial layer of the superior colliculus and in the lateral geniculate body contralateral to the side of the inoculation. Asymmetrical lesions in the superior colliculus were found also in mice sacrificed at 19, 22, and 27 weeks postinoculation. These results demonstrate that CJD virus spreads within the CNS via central axons of the visual pathways following intraocular inoculation.
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  • 2
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Rabbits were infected successfully with two strains of human T-cell leukemia virus type I (HTLV-I), one isolated from a Colombian patient with HTLV-I associated myelopathy/tropical spastic paraparesis (HAM/TSP) and the other from an asymptomatic carrier. HTLV-I was repeatedly demonstrated in peripheral blood mononuclear cells (PBMNC) of infected rabbits, and the rabbits had elevated antibodies against the various structural proteins of HTLV-I. Four rabbits inoculated with HTLV-I-infected autologous lymphoid cells intravenously (i.v.) and intracerebrally (i.c.) had virus present in their PBMNC for more than 40 weeks, while those that were inoculated either with HTLV-I-infected human lymphoid cells or with autologous rabbit lymphoid cells intraperitoneally (i.p.) had episodes during which virus was not recovered from their PBMNC. The one rabbit inoculated i.p. developed antibodies to viral envelope glycoproteins earlier than did those inoculated i.v. and i.c. Rabbit lymphoid cell lines persistently infected with HTLV-I were established by cocultivating the rabbit PBMNC with HTLV-I-infected human lymphoid cells that had been irradiated or by inoculation with cell-free supernatant fluids of HTLV-I infected non-irradiated lymphoid cell cultures. HTLV-I-infected rabbit cell lines were of T-cell origin and expressed HTLV-I antigens by immunofluorescence. Electron microscopy revealed type-C retrovirus particles.
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  • 3
    ISSN: 1432-0533
    Keywords: Scrapie ; Dystrophic neurites ; Vacuolation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Numbers of dystrophic neurites, seen with the electron microscope, in CA1 of the hippocampus of either C3H mice infected with 22C or 79A strains of scrapie, or LM mice infected with strain ME7 were greater than in age-matched control mice. Vacuolation, seen by light microscopy in CA1 of the hippocampus of mice infected with either 22C or 79A, preceded the increase in dystrophic neurites by up to about 20 days. In mice infected with ME7, however, the vacuolation followed the increase in dystrophic neurites by some 20 to 40 days. In view of the differences in the times at which dystrophic neurites and vacuolation were seen, no causative relationship between the two lesions appeared to exist.
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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: 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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  • 6
    ISSN: 1432-0533
    Keywords: Key words Tubulovesicular structures ; Prion protein ; Transmissible spongiform encephalopathy ; Immunogold ; electron microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Tubulovesicular structures (TVS) are disease-specific, intraneuronal particles found by thin-section electron microscopy in all of the transmissible spongiform encephalopathies. We used immunogold (both 10 nm immunogold and 1 nm immunogold silver enhanced) methods for ultrastructural localization of prion protein (PrP). In all scrapie models examined (263 K and 22CH in hamsters and 87V and ME7 in mice), TVS-containing processes were readily detected but neither these processes nor TVS themselves were decorated with gold particles. Even when amyloid plaques were observed in a close contact with TVS-containing neuronal processes, the processes remained unstained, while the plaques were decorated with gold particles. TVS located in areas adjacent to plaques in the 87V model and in areas of diffuse PrP immunolabelling in ME7 were also unlabelled with anti-PrP sera. Using immunogold techniques we were unable to label TVS with anti-PrP antibodies. As these technique proved to be sensitive enough to immunolabel not only amyloid plaques but also pre-amyloid accumulations of PrP, we strongly believe that the absence of staining reflects the structure of TVS and that they are not composed of PrP. That TVS are PrP negative may have several important implications for hypotheses about their nature. Principally, it does not support the suggestion that TVS are cross-sections of “thick tubules” visualized by touch-preparations of scrapie-affected mouse and hamster brains. If PrP is the infectious agent, as suggested by the prion hypothesis, the absence of stainable PrP in TVS would indicate that these are not the ultrastructural correlate of the agent. If, however, TVS turn out to be more than merely a useful ultrastructural marker for the whole group of transmissible spongiform encephalopathies, it may suggest that PrP and the agent are two separate entities.
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  • 7
    ISSN: 1432-0533
    Keywords: Creutzfeldt ; Jakob disease ; Tubulovesicular structures ; Prion diseases ; Ultrastructure ; Transmissible spongiform encephalopathies
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary By electron microscopy tubulovesicular structures (TVS) have been consistently observed in brain tissue of transmissible spongiform encephalopathies such as natural and experimental scrapie, bovine spongiform encephalopathy and experimentally induced, but not naturally occurring, Creutzfeldt-Jakob disease (CJD). For the first time we report here the presence of TVS in human brains with CJD as detected by transmission electron microscopy. TVS were observed in all three CJD specimens (two biopsies, one autopsy), but they were rare and were found only in one or two location(s) per grid. TVS were seen in distended pre- and postsynaptic terminals and measured approximately 35 nm in diameter; they were smaller and of higher electron density than synaptic vesicles. Their occurrence in all types of transmissible spongiform encephalopathies irrespective of the affected host and the strain of the infectious agent suggests their biological significance.
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  • 8
    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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  • 9
    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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  • 10
    ISSN: 1432-0533
    Keywords: Key words Prions ; Creutzfeldt-Jakob disease ; Gerstmann-Sträussler-Scheinker disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We report here an unusual sporadic case of Creutzfeldt-Jakob disease (CJD) characterized by an abundance of prion protein (PrP)-immunopositive kuru and multicentric but not florid plaques. Molecular genetic analysis of the PRNP open reading frame region spanning codons 8–221 was performed. Neither deletion nor insertion mutations were detected in the repeat area of the PRNP. No pathogenic mutation was found in the sequenced region between codon 108–221. Restriction analysis of the amplified fragment using restriction endonucleases DdeI, PvuII and AluI did not show any of the previously described pathogenic mutations at codon 102, 105, and 117 associated with Gerstmann-Sträussler-Scheinker (GSS). The patient was heterozygous for the methionine/valine coding triplet at polymorphic codon 129 of the PRNP gene by sequence, restriction endonuclease analysis and hybridization with allele-specific nucleotides. Furthermore, hybridization with 32P-labeled allele-specific oligonucleotides confirmed the absence of pathogenic mutations at codons 102, 200 and 178. Such a case may present a missing “link” between sporadic CJD and familial GSS.
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