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Pathology of SSLOW, a transmissible and fatal synthetic prion protein disorder, and comparison with naturally occurring classical transmissible spongiform encephalopathies
Version of Record online: 13 MAR 2014
© 2013 Crown copyright. Neuropathology and Applied Neurobiology © 2013 British Neuropathological Society
Neuropathology and Applied Neurobiology
Volume 40, Issue 3, pages 296–310, April 2014
How to Cite
Jeffrey, M., McGovern, G., Makarava, N., González, L., Kim, Y.-S., Rohwer, R. G. and Baskakov, I. V. (2014), Pathology of SSLOW, a transmissible and fatal synthetic prion protein disorder, and comparison with naturally occurring classical transmissible spongiform encephalopathies. Neuropathology and Applied Neurobiology, 40: 296–310. doi: 10.1111/nan.12053
- Issue online: 13 MAR 2014
- Version of Record online: 13 MAR 2014
- Accepted manuscript online: 12 APR 2013 03:28AM EST
- Manuscript Accepted: 24 MAR 2013
- Manuscript Received: 1 NOV 2012
- National Institutes of Health (NIH). Grant Number: NS045585
- Veterans Affairs Merit Award
Figure S1. Astrocytic and microglial activation. (a) Stratum lacunosum-moleculare (SL) showing moderate astrocytosis and mild vacuolation. Bar = 200 μm. Immunohistochemistry for GFAP. (b) Stratum lacunosum-moleculare showing mild microglial activation and mild vacuolation. Bar = 100 μm. Immunohistochemistry for coronin. (c) Severe astrocytosis in the superior colliculus associated with marked vacuolation. Bar = 200 μm. Immunohistochemistry for GFAP. (d) Severe microgliosis associated with marked vacuolation in the midbrain tectum. Bar = 100 μm. Immunohistochemistry for coronin. (e) Marked astrocytosis is present around several sub-ependymal plaques (arrowheads). Bar = 100 μm. Immunohistochemistry for GFAP. (f) Small numbers of activated microglia are present in the neuropil adjacent to amyloid plaques (arrowheads) in the periventricular glial limitans. Bar = 100 μm. Immunohistochemistry for coronin.
Figure S2. Tau immunolabelling: cerebral cortex showing moderate vacuolation and punctuate tau immunolabelled structures. Bar = 50 μm. Immunohistochemistry for tau.
Figure S3. Area postrema. (a) A large areas of neuropil surrounding a blood vessel shows loss of normal architecture, increased extracellular space and a dystrophic neurite (d). Bar = 3 μm. Uranyl acetate/lead citrate. (b) Detail of an area similar to the above, showing loss of normal cellular processes and replacement by poorly defined fibrillar (arrowheads) PrPSSLOW amyloid fibrils. Bar = 0.5 μm. Immunogold for PrPSSLOW. (c) Accumulation of PrPSSLOW in association with convoluted and microfolded processes, and poorly defined fibrils (arrowheads) surrounding a large astrocytic process (A). Bar = 1 μm. Immunogold for PrPSSLOW.
Figure S4. Enlarged mitochondria: enlarged mitochondria with abnormal christae were mostly located in glial cell cytoplasm. A normal mitochondrion is present at M. Bar = −0.5 μm. Uranyl acetate/lead citrate.
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