Thursday, October 27, 2011

Squirrel Monkeys (Saimiri sciureus) Infected with the Agent of Bovine Spongiform Encephalopathy Develop Tau Pathology

doi:10.1016/j.jcpa.2011.09.004 | How to Cite or Link Using DOI

Experimentally induced disease


Squirrel Monkeys (Saimiri sciureus) Infected with the Agent of Bovine Spongiform Encephalopathy Develop Tau Pathology


P. Piccardo*, †, , , J. Cervenak*, O. Yakovleva‡, L. Gregori*, K. Pomeroy*, A. Cook§, F.S. Muhammad§, T. Seuberlich¶, L. Cervenakova‡, D.M. Asher*

Laboratory of Bacterial and TSE Agents, Center for Biologics Evaluation and Research, United States Food and Drug Administration, Rockville, MD, USA



Neuropathogenesis Division, Roslin Institute, University of Edinburgh, Easter Bush, Midlothian, UK



Transmissible Diseases Department, Jerome H. Holland Laboratory for the Biomedical Sciences, American Red Cross, Rockville, MD, USA,

§

BIOQUAL Inc., Rockville, MD, USA



NeuroCentre, National and OIE Reference Laboratories for BSE and Scrapie, Vetsuisse Faculty, University of Bern, Bern, Switzerland

Received 28 June 2011; Accepted 8 September 2011. Available online 19 October 2011.


Summary


Squirrel monkeys (Saimiri sciureus) were infected experimentally with the agent of classical bovine spongiform encephalopathy (BSE). Two to four years later, six of the monkeys developed alterations in interactive behaviour and cognition and other neurological signs typical of transmissible spongiform encephalopathy (TSE). At necropsy examination, the brains from all of the monkeys showed pathological changes similar to those described in variant Creutzfeldt–Jakob disease (vCJD) of man, except that the squirrel monkey brains contained no PrP-amyloid plaques typical of that disease. Constant neuropathological features included spongiform degeneration, gliosis, deposition of abnormal prion protein (PrPTSE) and many deposits of abnormally phosphorylated tau protein (p-Tau) in several areas of the cerebrum and cerebellum. Western blots showed large amounts of proteinase K-resistant prion protein in the central nervous system. The striking absence of PrP plaques (prominent in brains of cynomolgus macaques [Macaca fascicularis] with experimentally-induced BSE and vCJD and in human patients with vCJD) reinforces the conclusion that the host plays a major role in determining the neuropathology of TSEs. Results of this study suggest that p-Tau, found in the brains of all BSE-infected monkeys, might play a role in the pathogenesis of TSEs. Whether p-Tau contributes to development of disease or appears as a secondary change late in the course of illness remains to be determined.

Keywords: bovine spongiform encephalopathy; prion protein; squirrel monkey; tau protein



http://www.sciencedirect.com/science/article/pii/S002199751100137X




Monday, September 26, 2011

Variably Protease-Sensitive Prionopathy, Prionpathy, Prionopathy, FFI, GSS, gCJD, hvCJD, sCJD, TSE, PRION, update 2011

http://prionopathy.blogspot.com/2011/09/variably-protease-sensitive-prionopathy.html




http://prionopathy.blogspot.com/





http://prionpathy.blogspot.com/





Tuesday, October 4, 2011

De novo induction of amyloid-ß deposition in vivo

Molecular Psychiatry advance online publication 4 October 2011; doi: 10.1038/mp.2011.120

http://betaamyloidcjd.blogspot.com/2011/10/de-novo-induction-of-amyloid-deposition.html





http://betaamyloidcjd.blogspot.com/





Saturday, June 18, 2011

Self-propagation and transmission of misfolded mutant SOD1 Prion or Prion-like phenomenon?

http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/self-propagation-and-transmission-of.html





EFSA Journal 2011 The European Response to BSE: A Success Story

This is an interesting editorial about the Mad Cow Disease debacle, and it's ramifications that will continue to play out for decades to come ;

Monday, October 10, 2011

EFSA Journal 2011 The European Response to BSE: A Success Story

snip...

EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.

snip...

http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1





http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf




see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;

http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html





Thursday, August 4, 2011

Terry Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis, Date aired: 27 Jun 2011 (SEE VIDEO)

http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/terry-singeltary-sr-on-creutzfeldt.html





Sunday, September 25, 2011

Mad Cow Scaremongers by Terry S. Singeltary Sr. a review of the TSE prion agent 2003-2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/09/mad-cow-scaremongers.html





http://transmissiblespongiformencephalopathy.blogspot.com/





http://bse-atypical.blogspot.com/





http://scrapie-usa.blogspot.com/





http://nor-98.blogspot.com/





http://chronic-wasting-disease.blogspot.com/





http://creutzfeldt-jakob-disease.blogspot.com/





TSS

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