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10.1111/nan.12053 http://scihub22266oqcxt.onion/10.1111/nan.12053 C3783560!3783560!23578208     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=23578208&cmd=llinks): Failed to open stream: HTTP request failed! 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Pathology of SSLOW, a transmissible and fatal synthetic prion protein disorder and comparison with naturally occurring classical Transmissible Spongiform Encephalopathies |pdf=|usr=}}{{23578208}} gab.com Text Pathology of SSLOW, a transmissible and fatal synthetic prion protein disorder and comparison with naturally occurring classical Transmissible Spongiform Encephalopathies JO: Neuropathol Appl Neurobiol http://www.kidney.de/pget.php?&tw=1&pmid=23578208 #FOAvip Aims: Naturally occurring transmissible spongiform encephalopathies (TSEs) accumulate disease specific forms of prion protein on cell membranes in association with pathognomonic lesions. We wished to determine whether synthetic prion protein disorders recapitulated these and other sub-cellular TSE specific changes. Methods: SSLOW is a TSE initiated with refolded synthetic prion protein. Five terminally sick hamsters previously intra-cerebrally inoculated with 3rd passage SSLOW were examined using light and immunogold electron microscopy. Results: SSLOW affected hamsters showed widespread abnormal prion protein (PrPSSLOW) and amyloid plaques. PrPSSLOW accumulated on plasma-lemmas of neurites and glia without pathological changes. PrPSSLOW also co-localised with increased coated vesicles and pits, coated spiral membrane invaginations and membrane microfolding. PrPSSLOW was additionally observed in lysosomes of microglial cells but not of neurons or astrocytes. Conclusions: PrPSSLOW is propagated by cell membrane conversion of normal PrP and lethal disease may be linked to the progressive growth of amyloid plaques. Cell membrane changes present in SSLOW are indistinguishable from those of naturally occurring TSEs. However, some lesions found in SSLOW are absent in natural animal TSEs and vice versa. SSLOW may not entirely recapitulate neuropathological features previously described for natural disease. End?stage neuropathology in SSLOW, particularly the nature and distribution of amyloid plaques may be significantly influenced by the early re-distribution of seeds within the inoculum and its recirculation following interstitial, perivascular and other drainage pathways. The way in which seeds are distributed and aggregate into plaques in SSLOW has significant overlap with murine APP overexpressing mice challenged with A?. Twit Text FOAVip Pathology of SSLOW, a transmissible and fatal synthetic prion protein disorder and comparison with naturally occurring classical Transmissible Spongiform Encephalopathies ????Neuropathol Appl Neurobiol http://www.kidney.de/pget.php?&tw=1&pmid=23578208 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23578208 #FOAvip English Wikipedia <ref>{{Cite pmid|23578208}}</ref> Pathology of SSLOW, a transmissible and fatal synthetic prion protein disorder and comparison with naturally occurring classical Transmissible Spongiform Encephalopathies #MMPMID23578208 Jeffrey M; McGovern G; Makarava N; González L; Kim JS; Rohwer RG; Baskakov IV Neuropathol Appl Neurobiol 2014[Apr]; 40 (3): 296-310 PMID23578208show ga Aims: Naturally occurring transmissible spongiform encephalopathies (TSEs) accumulate disease specific forms of prion protein on cell membranes in association with pathognomonic lesions. We wished to determine whether synthetic prion protein disorders recapitulated these and other sub-cellular TSE specific changes. Methods: SSLOW is a TSE initiated with refolded synthetic prion protein. Five terminally sick hamsters previously intra-cerebrally inoculated with 3rd passage SSLOW were examined using light and immunogold electron microscopy. Results: SSLOW affected hamsters showed widespread abnormal prion protein (PrPSSLOW) and amyloid plaques. PrPSSLOW accumulated on plasma-lemmas of neurites and glia without pathological changes. PrPSSLOW also co-localised with increased coated vesicles and pits, coated spiral membrane invaginations and membrane microfolding. PrPSSLOW was additionally observed in lysosomes of microglial cells but not of neurons or astrocytes. Conclusions: PrPSSLOW is propagated by cell membrane conversion of normal PrP and lethal disease may be linked to the progressive growth of amyloid plaques. Cell membrane changes present in SSLOW are indistinguishable from those of naturally occurring TSEs. However, some lesions found in SSLOW are absent in natural animal TSEs and vice versa. SSLOW may not entirely recapitulate neuropathological features previously described for natural disease. End?stage neuropathology in SSLOW, particularly the nature and distribution of amyloid plaques may be significantly influenced by the early re-distribution of seeds within the inoculum and its recirculation following interstitial, perivascular and other drainage pathways. The way in which seeds are distributed and aggregate into plaques in SSLOW has significant overlap with murine APP overexpressing mice challenged with A?. äPathology of SSLOW, a transmissible and fatal synthetic prion protein (epmc).pdf DeepDyve Pubget Overpricing