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Ultrastructural studies of experimental scrapie and Creutzfeldt-Jakob disease in hamsters. I. Alterations of myelinated axons

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Liberski P. P., Bratosiewicz-Wasik J., Gajdusek D. C., Brown P.
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EN
Classical and ultrastructural neuropathology of prion diseases are generally well described. Here we report that alterations of myelinated fibres in hamsters infected either with polioencephalopathic strains of scrapie or panencephalopathic strains of CJD (Echigo-1) are virtually identical and differ only quantitatively. In contrast, mice infected with the panencephalopathic Fujisaki strain of CJD exhibited much more elaborate changes of myelinated fibres.
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Ultrastructural studies of experimental scrapie and Creutzfeldt-Jakob disease in hamsters. II. Astrocytic and macrophage reaction toward the axonal destruction

100%
Liberski P. P., Bratosiewicz-Wasik J., Gajdusek D. C., Brown P.
Acta Neurobiologiae Experimentalis
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2002
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vol. 62
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issue 3
131-139
EN
We report here the microglial (macrophage) and astrocytic reaction in several models of transmissible spongiform encephalopathies (TSEs) or prion diseases. With the low power electron microscopy it was readily apparent that myelinated vacuoles were surrounded by cells and their processes. The latter belonged either to hyperplastic reactive astrocytes or to macrophages. Typically reactive astrocytes exhibited cytoplasm filled with innumerable glial filaments and, occasionally, other organelles (like cilia) and abundant tortuous intercellular junctions of adhesive plaque junction type. Desmosome-like junctions connecting astrocytic elements were also seen. As described earlier, astrocytic processes were occasionally interdigitated with oligodendroglial cells and their processes. Two types of macrophages were readily described. The majority of them exhibited electron-dense cytoplasm and numerous ?empty? vacuoles (digestive chambers) containing cellular debris. Occasional vacuoles were surrounded by a thin collar reminiscent of ?lyre-like inclusions? of the second type of macrophages. The latter were rare and characterized by numerous ?lyre-like? inclusions. Several mylinated fibres were clearly engulfed by the cytoplasm of a macrophage containing unusual annulate lamellae.
3
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How do neurons degenerate in prion diseases or transmissible spongiform encephalopathies (TSEs): neuronal autophagy revisited

100%
Liberski P. P., Gajdusek D. C., Brown P.
Acta Neurobiologiae Experimentalis
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2002
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vol. 62
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issue 3
141-147
EN
As in other neurodegenerative diseases such as Alzheimer?s disease, neurons in prion diseases or transmissible spongiform encephalopathies (TSEs) die via programmed cell death of which the apoptotic process is relatively well characterized. A subcellular alteration linked to apoptosis is the formation of autophagic vacuoles, which we and others demonstrated in CJD- and scrapie-affected rodent brains. Autophagy may co-exist with apoptosis or may precede it and the process may be induced by apoptotic stimuli. Here, we extend these observations using different model of scrapie and CJD. Both scrapie models (the 263K and 22C-H) demonstrated autophagic vacuoles with the same frequency; hence, they will be described together. While the following changes had been observed simultaneously in different areas of the same sample, this description is organised as if it followed a sequence of events. First, a part of the neuronal cytoplasm was sequestrated by concentric arrays of membrane; that part of the cytoplasm closed by membranes appeared relatively normal but its density often appeared increased. Next, electron density of the central dramatically increased. Then, membranes proliferated within the cytoplasm in a labyrinth-like manner and an area sequestrated by these membranes enlarged and became more complex structure consisting of vacuoles, electron-dense area and areas of normally-looking cytoplasm connected with convoluted membranes. Finally, a large area of the cytoplasm was transformed into a collection of autophagic vacuoles of different sizes. Virtually identical alterations, albeit with much lower frequency, were seen in terminally ill CJD-affected hamsters.
4
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Molecular analysis of prion protein (PrP) and glial fibrillary acidic protein (GFAP) transcripts in experimental Creutzfeldt Jakob disease in mice

88%
Kordek R., Liberski P. P., Yanagihra R., Isaacson S., Gajdusek D. C.
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EN
Prion protein (PrPsc) which accumulates in the brains affected with subacute spongiform encephalopathies (SSE) is altered isoform of normal, cellular isoform (PrPc), and PrP deposition is accompanied with spongiosis and astrogliosis. To find the amounts of PrP and GFAP transcripts during progression of experimental Creutzfeldt Jakob disease we performed comparative RT PCR on the terminally sick mice brains, 22 weeks following inoculation with Fujisaki strain of CJD agent, and on control brains. The intensity of bands for PrP mRNA and control beta actin were similar for infected and uninfected brains, while amounts of transcripts for GFAP increased as for cytokines released by glial cells TNF-alpha and IL-1 alpha. This study supports thesis that PrPc to PrPsc conversion is post translational process not related to PrP overproduction. Increased amounts of GFAP mRNA during the course of the disease correlated with astrocytosis estimated by immunohistochemistry with anti GFAP antibody.
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