STANLEY PRUSINER AND THE DINOSAUR END OF TIME SCENARIO WITH TSE PRION aka mad cow type disease

STANLEY PRUSINER AND THE DINOSAUR END OF TIME SCENARIO WITH TSE PRION aka mad cow type disease



The BSE Inquiry



Dr. Stanley Prusiner (scheduled to give oral evidence 06/06/98)


TRANSCRIPT OF A LECTURE BY DR STANLEY PRUSINER

GIVEN AT COLUMBIA UNIVERSITY, NEW YORK CITY

(OCTOBER 1997)


{2 MONTHS BEFORE MY MOM DIED FROM HVCJD confirmed...tss}


snip...


111. So we are very enthusiastic about that line of approach, to get at the structure of PrP Scrapie.

112. Let me summarise. What I have told you today is that sporadic and infectious forms of the disease have PrPc being converted into PrP Scrapie. This is wild type PrPc being converted into wild type PrP Scrapie. The inherited forms of the disease: it is mutant PrPc which is converted into mutant PrP Scrapie.

113. Now, that is me many years later.

What I have told you today is that prions contain only protein called PrP Scrapie and no nucleic acid has been found.

114. A chromosomal gene encodes PrP Scrapie and its precursor PrPc.

115. Mutations in the PrP gene cause inherited prion diseases. PrP Scrapie is formed from PrPc as the protein changes its conformation.

116. Prion strain specific properties are encripted in the conformation of PrP Scrapie and in caveoiae-like domains PrP Scrapie acts as a template directing the conversion of PrPc into nascent PrP Scrapie. I think there are many implications for the future from these studies. First of all, I think that we will, in the future, learn about profound effects of conformational changes regulating metabolism. We will learn much more about the dynamic plasticity of protein structure as better technologies become available to study this. We will learn about transient metabolic regulation through conformational changes.

117. In some fascinating work started by Reid Wickner, and then carried on by many other people now, it appears that there are some prion like phenomena in yeast, and also in fungi that regulates stable metabolic states. I would not be surprised if protein polymerization might not be partially under the control of these kinds of conformational shifts.

118. The prion diseases are clearly disorders of protein conformation; and they share many features with the common neurodegenerative illnesses: age dependence, progressive fatal course, the majority are sporadic, about 15 per cent of these are familial diseases that are autosomal dominant; the pathologic protein deposits are found. These diseases progress in the absence of any recognition by the immune system.

119. If you take all of the descriptors they equally well apply to Alzheimers' disease, Parkinson's disease, and ALS. What is different, of course, is that attempts to transmit these diseases to experimental animals have failed in the past. I do not think that is an important aspect of what I am talking about.

120. How do we treat these diseases? I think we can use what we have been learning about protein X to develop transgenic animals that will be resistant to prions, where we take advantage of the dominant negative experiments that nature has already done both in sheep and in humans. But for humans, of course, we need peptidomimetic drugs that will attach either to PrPc at the protein X binding site or attach to protein X at the PrPc binding site; and I think such drugs will be highly effective.

121. I am hopeful that this work will progress relatively rapidly in the near future. Both Fred Cohen and I are putting a large amount of effort into such studies.

122. Now, do not look at the bottom of the slide, only look at the top. This is from the Chicago Tribune, October 12th 1997. This is a quiz to see whether you guys have been alert. So what was this Nobel Prize awarded for, a new type of germ that was described as being like which of the following? Dracula, Jekyll and Hyde, Wolfman, Xena: The Warrior Princess.

123. Okay. How many people vote for A? How many for 8? So the answer, this is great, Jekyll and Hyde. When shaped one way the germ is benign, but if it is folded differently it causes disease.

124. I thought I would end with this. Many of you probably have children who have seen 'The Lost World', and some of you have even gone to see this.

125. What you did not learn in 'The Lost Wortd' was that the dinosaurs were dying of a disease called "OX". The reason is that the scriptwriters left out the whole story of prions from Michael Crichton's book; and I tried, with the producers, to get it reinstated, but I failed.

126. But at the end of the book, just like in 'Jurassic Park' where the good guys survive, the bad guys are eaten by the dinosaurs. This all takes place on an island off the coast of Costa Rica, where the Germans have produced a big plant to make dinosaurs all based on technology from Menlow Parke?), California.

127. The good guys are now leaving. The boat left the jungle river behind, and they moved into darkness '" Sarah Harding - she is a wonderful character in the book; you have to read about her - stared at him ... "They made a mistake on that island many years ago ... They were manufacturing infant dinosaurs ... And as the carnivores grew they fed them a special animal protein extract. And the extract was made of ground up sheep."

128. Now Levine -- you must understand that Levine is a Harvard professor --: "So? What's wrong with that?" "In a zoo, they never use sheep extract", she said, "because of the danger of infection",

129. "Infection", Levine repeated .. .'What kind of infection?" (Harvard). "Prions," Malcom said, from the other side of the boat .... "Prions •• , Harding said, "are the simplest disease causing entities known, even simpler than viruses. They're just protein fragments. They're so simple they can't even invade a body - they have to be passively ingested. But once eaten, they cause disease; Scrapie, in sheep; mad cow disease, and Kuru, a brain disease of human beings. And the dinosaurs developed a prion disease called DX" - that is a medical student question in San Francisco -- "from a bad batch of sheep protein extract. The lab battled it for years, trying to get rid of it." "You're saying they didn't?" "For a while it seemed they did. The dinosaurs were flourishing. But then something happened. The disease began to spread."

130. And with that I will end.

Media enquiries for Dr Prusiner: UIVERSITY OF CALIFORNIA, SAN FRANCISCO Telephone number 001 4154764482 Fascimile number 001 4154768386 Issued on behalf of the witness by: The SSE Inquiry Press Office 6th Floor Hercules House Hercules Road London SE1 7DU Tel: 0171 261 8377/8383 Fax: 0171 8030893 Website: http://www.bse.org.uk email: inquiry@bse.org.uk



bseinquiry.gov.uk/





Subject: Louping-ill vaccine documents from November 23rd, 1946




Date: Sat, 9 Sep 2000 17:44:57 -0700



From: "Terry S. Singeltary Sr."



Reply-To: Bovine Spongiform Encephalopathy



To: BSE-L@uni-karlsruhe.de



######### Bovine Spongiform Encephalopathy #########



THE VETERINARY RECORD 516 No 47. Vol. 58 November 23rd, 1946



NATIONAL VETERINARY MEDICAL ASSOCIATION OF GREAT BRITAIN AND IRELAND



ANNUAL CONGRESS, 1946



The annual Congress, 1946, was held at the Royal Veterinary College, Royal College Street, London, N.W.I. from September 22nd to September 27th.



Opening Meeting



[skip to scrapie vaccine issue...tss]



Papers Presented to Congress



The papers presented to this year's Congress had as their general theme the progressive work of the profession during the war years. Their appeal was clearly demonstrated by the large and remarkably uniform attendance in the Grand Hall of the Royal Veterinary College throughout the series; between 200 and 250 members were present and they showed a keen interest in every paper, which was reflected in the expression of some disappointment that the time available for discussion did not permit of the participation of more than a small proportion of would-be contributors.



In this issue we publish (below) the first to be read and discussed, that by Dr. W. S. Gordon, M.R.C.V.S., F.R.S.E., "Advances in Veterinary Research." Next week's issue will contain the paper on "Some Recent Advances in Veterinary Medicine and Surgery in Large-Animal Practice" by Mr. T. Norman Gold, M.R.C.V.S. In succeeding numbers of the Record will be reproduced, also with reports of discussions, that by Mr. W. L. Weipers, M.R.C.V.S., D.V.S.M., on the same subject as relating to small-animal practice, and the papers by Mr. J. N. Ritchie, B.SC., M.R.C.V.S., D.V.S.M., and Mr. H.W. Steele-Bodger, M.R.C.V.S., on "War-time Achievements of the British Home Veterinary Services."



The first scientific paper of Congress was read by Dr. W. S. Gordon, M.R.C.V.S., F.R.S.E. on Monday, September 23rd, 1946, when Professor J. Basil Buxton, M.A., F.R.C.V.S, D.V.H., Prinicipal of the Royal Veterinary College, presided.



Advances in Veterinary Research



by



W.S. GORDON, PH.D., M.R.C.V.S., F.R.S.E.



Agriculteral Research Council, Field Station, Compton, Berks.



Louping-ill, Tick-borne Fever and Scrapie



In 1930 Pool, Browniee; Wilson recorded that louping-ill was a transmissible disease. Greig et al, (1931) showed that the infective agent was a filter-passing virus with neurotropic characters and Browniee & Wilson (1932) that the essential pathology was that of an encephalomyelitis. Gordon, Browniee, Wilson & MacLeod (1932) and MacLeod & Gordon (1932) confirmed and extended this work. It was shown that on louping-ill farms the virus was present in the blood of many sheep which did not show clinical symptoms indicating involvement of the central nervous system and that for the perpetuation and spread of the disease these subclinical cases were probably of greater importance that the frank clinical cases because, in Nature, the disease was spread by the tick, lxodes ricinus L. More recently Wilson (1945, 1946) has described the cultivation of the virus in a chick embryo medium, the pathogenic properties of this culture virus and the preparation of louping-ill antiserum.



Between 1931 and 1934 I carried out experiments which resulted in the development of an effective vaccine for the prevention of louping-ill.* This vaccine has been in general use since 1935 and in his annual report to the Animal Diseases Research Association this year, Dr. Greig stated that about 227,000 doses of vaccine had been issued from Moredun alone.



Dr. Gordon illustrated this portion of his paper by means of graphs and diagrams projected by the epidiascope.



This investigation, however, did not begin and end with the study of louping-ill; it had, by good fortune, a more romantic turn and less fortunately a final dramatic twist which led almost to catastrophe. After it had been established that a solid immunity to louping-ill could be induced in sheep, a group of immunized and a group of susceptible animals were placed together on the tick-infected pasture of a louping-ill farm. Each day all the animals were gathered and their temperatures were recorded. It was anticipated that febrile reactions with some fatalities would develop in the controls while the louping-ill immunes would remain normal. Contrary to expectation, however, every sheep, both immune and control, developed a febrile reaction. This unexpected result made necessary further investigation which showed that the febrile reaction in the louping-ill immunes was due to a hitherto undescribed infective agent, a Rickettsia-like organism which could be observed in the cytoplasm of the granular leucocytes, especially the neutrophil polymorphs (MacLeod (1932), Gordon, Browniee, Wilson & MacLeod. MacLeod & Gordon (1933). MacLeod (1936). MacLeod collected ticks over many widely separated parts of Scotland and all were found to harbour the infective agent of tick-borne fever, and it is probable that all sheep on tick-infested farms develop this disease, at least on the first occasion that they become infested with ticks. When the infection is passed in series through susceptible adult sheep it causes a sever, febrile reaction, dullness and loss of bodily condition but it rarely, if ever, proves fatal. It is clear, however, that it aggravates the harmful effects of a louping-ill infection and it is a serious additional complication to such infections as pyaemia and the anacrobic infections which beset lambs on the hill farms of Northern Britain.



Studying the epidemiology of louping-ill on hill farms it became obvious that the pyaemic condition of lambs described by M'Fadyean (1894) was very prevalent on tick infested farms Pyaemia is a crippling condition of lambs associated with tick-bite and is often confused with louping-ill. It is caused by infection with Staphylococcus aureus and affected animals may show abscess formation on the skin, in the joints, viscera, meninges and elsewhere in the body. It was thought that tick-borne fever might have been a predisposing factor in this disease and unsuccessful attempts were made by Taylor, Holman & Gordon (1941) to reproduce the condition by infecting lambs subcutaneously with the staphylococcus and concurrently producing infections with tickborne fever and louping-ill in the same lambs. Work on pyaemia was then continued by McDiarmid (1946a, 1946b, 1946c), who succeeded in reproducing a pyaemic disease in mice, guinea-pigs and lambs similar to the naturally occurring condition by intravenous inoculation of Staphylococcus aureus. He also found a bacteraemic form of the disease in which no gross pyaemic lesions were observed. The prevention or treatment of this condition presents a formidable problem. It is unlikely that staphylococcal ???oid will provide an effective immunity and even if penicillin proved to be a successful treatment, the difficulty of applying it in adequate and sustained dosage to young lambs on hill farms would be almost insurmountable.



From 1931 to 1934 field trials to test the immunizing value and harmlessness of the loup-ill vaccine were carried out on a gradually increasing scale. Many thousands of sheep were vaccinated and similar numbers, living under identical conditions were left as controls. The end result showed that an average mortability of about 9 percent in the controls was reduced to less than 1 percent in the vaccinated animals. While the efficiency of the vaccine was obvious after the second year of work, previous bitter experience had shown the wisdom of withholding a biological product from widespread use until it had been successfully produced in bulk, as opposed to small-scale experimental production and until it had been thoroughly tested for immunizing efficiency and freedom from harmful effects. It was thought that after four years testing this stage had been reached in 1935, and in the spring of that year the vaccine was issued for general use. It comprised a 10 percent saline suspension of brain, spinal cord and spleen tissues taken from sheep five days after infection with louping-ill virus by intracerebral inoculation. To this suspension 0-35 percent of formalin was added to inactivate the virus and its safety for use as a vaccine was checked by intracerbral inoculation of mice and sheep and by the inoculation of culture medium. Its protective power was proved by vaccination sheep and later subjecting them, along with controls, to a test dose of living virus.



Vaccine for issue had to be free from detectable, living virus and capable of protecting sheep against a test dose of virus applied subcutaneously. The 1935 vaccine conformed to these standards and was issued for inoculation in March as three separate batches labelled 1, 2, and 3. The tissues of 140 sheep were employed to make batch 1 of which 22,270 doses were used; 114 to make batch 2 of which 18,000 doses were used and 44 to make batch 3 of which 4,360 doses were used. All the sheep tissues incorporated in the vaccine were obtained from yearling sheep. During 1935 and 1936 the vaccine proved highly efficient in the prevention of loup-ill and no user observed an ill-effect in the inoculated animals. In September, 1937, two and a half years after vaccinating the sheep, two owners complained that scrapie, a disease which had not before been observed in the Blackface breed, was appearing in their stock of Blackface sheep and further that it was confined to animals vaccinated with louping-ill vaccine in 1935. At that stage it was difficult to conceive that the occurrence could be associated with the injection of the vaccine but in view of the implications, I visited most of the farms on which sheep had been vaccinated in 1935. It was at this point that the investigation reached its dramatic phase; I shall not forget the profound effect on my emotions when I visited these farms and was warmly welcomed because of the great benefits resulting from the application of louping-ill vaccine, wheras the chief purpose of my visit was to determine if scrapie was appearing in the inoculated sheep. The enquiry made the position clear. Scrapie was developing in the sheep vaccinated in 1935 and it was only in a few instances that the owner was associating the occurrence with louping-ill vaccination. The disease was affecting all breeds and it was confined to the animals vaccinated with batch 2. This was clearly demonstrated on a number of farms on which batch 1 had been used to inoculate the hoggs in 1935 and batch 2 to inoculate the ewes. None of the hoggs, which at this time were three- year-old ewes. At this time it was difficult to forecast whether all of the 18,000 sheep which had received batch 2 vaccine would develop scrapie. It was fortunate, however, that the majority of the sheep vaccinated with batch 2 were ewes and therfore all that were four years old and upwards at the time of vaccination had already been disposed of and there only remained the ewes which had been two to three years old at the time of vaccination, consequently no accurate assessment of the incidence of scrapie could be made. On a few farms, however, where vaccination was confined to hoggs, the incidence ranged from 1 percent, to 35 percent, with an average of about 5 percent. Since batch 2 vaccine had been incriminated as a probable source of scrapie infection, an attempt was made to trace the origin of the 112 sheep whose tissues had been included in the vaccine. It was found that they had been supplied by three owners and that all were of the Blackface or Greyface breed with the exception of eight which were Cheviot lambs born in 1935 from ewes which had been in contact with scrapie infection. Some of these contact ewes developed scrapie in 1936-37 and three surviving fellow lambs to the eight included in the batch 2 vaccine of 1935 developed scrapie, one in September, 1936, one in February, 1937, and one in November, 1937. There was, therefore, strong presumptive evidence that the eight Cheviot lambs included in the vaccine although apparently healthy were, in fact, in the incubative stage of a scrapie infection and that in their tissues there was an infective agent which had contaminated the batch 2 vaccine, rendering it liable to set up scrapie. If that assumption was correct then the evidence indicated that:-



(1) the infective agent of scrapie was present in the brain, spinal cord and or spleen of infected sheep: (2) it could withstand a concentration of formalin of 0-35 percent, which inactivated the virus of louping-ill: (3) it could be transmitted by subcutaneous inoculation; (4) it had an incubative period of two years and longer.



Two Frenchmen, Cuille & Chelle (1939) as the result of experiments commenced in 1932, reported the successful infection of sheep by inoculation of emulsions of spinal cord or brain material by the intracerebral, epidural, intraocular and subcutaneous routes The incubation period varied according to the route employed, being one year intracerebrally, 15 months intraocularly and 20 months subcutaneously. They failed to infect rabbits but succeeded in infecting goats. Another important part of their work showed that the infective agent could pass through a chamberland 1.3 filter, thus demonstrating that the infective agent was a filtrable virus. It was a curious coincidence that while they were doing their transmission experiments their work was being confirmed by the unforeseeable infectivity of a formalinized tissue vaccine.



As a result of this experience a large-scale transmission experiment involving the ue of 788 sheep was commenced in 1938 on a farm specially taken for the purpose by the Animal Diseases Research Association with funds provided by the Agricultural Research Council. The experiment was designed to determine the nature of the infective agent and the pathogenesis of the disease. It is only possible here to give a summary of the result which showed that (1) saline suspensions of brain and spinal cord tissue of sheep affected with scrapie were infective to normal sheep when inoculated intracerebrally or subcutaneously; (2) the incubation period after intracerebral inoculation was seven months and upwards and only 60 percent of the inoculated sheep developed scrapie during a period of four and a half years; (3) the incubation period after subcutaneous inoculation was 15 months and upwards and only about 30 percent of the inoculated sheep developed the disease during the four and a half years: (4) the infective agent was of small size and probably a filtrable virus.



The prolonged incubative period of the disease and the remarkable resistance of the causal agent to formalin are features of distinct interest. It still remains to determine if a biological test can be devised to detect infected animals so that they can be killed for food before they develop clinical symptoms and to explore the possibilities of producing an immunity to the disease.



==================================================================



Scrapie Louping-ill Vaccine



‘There has been one instance of inadvertant [sic] transmission of the scrapie agent to sheep through louping ill vaccine (Gordon, Bronlee and Wilson 1939). One of the three batches of vaccine made in 1935 at the Moredun Institute contained the scrapie agent resulting in 7% of the recipients of the 18, 000 doses in the batch developing scrapie. This vaccine was made from formalin-inactivated sheep brain, and brought to the attention of research workers that formalin, at a concentration of 0.35% for at least 3 months, which inactivated conventional viruses, did not totally inactivate the scrapie agent.



----------------------------



4. Questions we might want to have answered are:



the highest risk would be from parenterals prepared from brain (eg rabies vaccine). Any species in which transmissible spongiform encephalopathies have been described would be suspect (“natural” infections in sheep, goats, cattle, deer, mink, but can be transmitted to hamster, mouse, guinea-pig etc). Are sterilisation processes adequate for the most resistant strain of scrapie agent or for CJD agent? Should companies be asked to include investigation for inclusion of scrapie agent (eg mouse innoculation [sic]) in at least some batches? If BSE behaves like scrapie, then we might expect other nervous tissue, spleen, lymph nodes and placenta to be contaminated. Infection has been described in other tissues too, eg gut wall, and we can not [sic] be sure blood is free. Do we know what bovine materials are used in which products, both as the active ingredient and in production? Bovine active ingredients in human products include insulin, vasopressin, bone, immune globulins, fibrin, dermal collagen, albumin. Bovine serum albumin and fetal calf serum must be used in preparation of very many products. For each of these products would any “BSE agent” be destroyed or eliminated in processing? If not, and the product is administered parenterally or topically into an open wound, might there be a risk? [For oral products, there would only be a trivially increased load on top of that taken in food in omnivores/carnivores including man. But for some herbivores, this might allow the agent to be introduced into yet another species].



--------------------------







http://www.whale.to/v/singeltary7.html








Sunday, May 18, 2008



MAD COW DISEASE BSE CJD CHILDREN VACCINES



http://bseinquiry.blogspot.com/2008/05/mad-cow-disease-bse-cjd-children.html













US SENATOR AND STAN THE MAN SLAM USDA ''DAMNING TESTIMONY''

Senator Michael Machado from California

''USDA does not know what's going on''.

''USDA is protecting the industry''.

''SHOULD the state of California step in''

Stanley Prusiner

''nobody has ever ask us to comment''

''they don't want us to comment''

''they never ask''

i tried to see Venemon, after Candian cow was discovered with BSE. went to see lyle. after talking with him... absolute ignorance... then thought I should see Venemon... it was clear his entire policy was to get cattle bonless beef prods across the border... nothing else mattered...

his aids confirmed this... 5 times i tried to see Venemon, never worked... eventually met with carl rove the political... he is the one that arranged meeting with Venemon... just trying to give you a sense of the distance... healh public safety...

was never contacted...

yes i believe that prions are bad to eat and you can die from them... END

Dr. Stan bashing Ann Veneman - 3 minutes

http://maddeer.org/video/embedded/08snip.ram



Recall Authority and Mad Cow Disease: Is the Current System Good for Californians?

Tuesday, February 24, 2004

JOINT HEARING

AGRICULTURE AND WATER RESOURCES HEALTH AND HUMAN SERVICES AND SELECT COMMITTEE ON GOVERNMENT OVERSIGHT - MACHADO, ORTIZ, and SPEIER, Chairs

ALL VIDEOS OF THIS HEARING HAVE BEEN REMOVED FROM THE WWW, LIKE IT NEVER HAPPENED...but we know different...TSS



Monday, March 19, 2012



Infectivity in Skeletal Muscle of Cattle with Atypical Bovine Spongiform Encephalopathy


PLoS One. 2012; 7(2): e31449.

http://transmissiblespongiformencephalopathy.blogspot.com/2012/03/infectivity-in-skeletal-muscle-of.html




Saturday, March 5, 2011



MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA



http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html




Sunday, February 12, 2012



National Prion Disease Pathology Surveillance Center Cases Examined1 (August 19, 2011) including Texas



http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/national-prion-disease-pathology.html







CJD1/9 0185

Ref: 1M51A


IN STRICT CONFIDENCE


Dr McGovern From: Dr A Wight

Date: 5 January 1993

Copies: Dr Metters

Dr Skinner

Dr Pickles

Dr Morris

Mr Murray


TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES


1. CMO will wish to be aware that a meeting was held at DH yesterday, 4 January, to discuss the above findings. It was chaired by Professor Murray (Chairman of the MRC Co-ordinating Committee on Research in the Spongiform Encephalopathies in Man), and attended by relevant experts in the fields of Neurology, Neuropathology, molecular biology, amyloid biochemistry, and the spongiform encephalopathies, and by representatives of the MRC and AFRC.
2. Briefly, the meeting agreed that:


i) Dr Ridley et als findings of experimental induction of p amyloid in primates were valid, interesting and a significant advance in the understanding of neurodegenerative disorders;


ii) there were no immediate implications for the public health, and no further safeguards were thought to be necessary at present; and


iii) additional research was desirable, both epidemiological and at the molecular level. Possible avenues are being followed up by DH and the MRC, but the details will require further discussion.
93/01.05/4.1


http://collections.europarchive.org/tna/20080102191246/http://www.bseinquiry.gov.uk/files/yb/1993/01/05004001.pdf






BSE101/1 0136


IN CONFIDENCE


5 NOV 1992


CMO From: Dr J S Metters DCMO 4 November 1992


TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES


1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have recognized the public sensitivity of these findings and intend to report them in their proper context. This hopefully will avoid misunderstanding and possible distortion by the media to portray the results as having more greater significance than the findings so far justify.


2. Using a highly unusual route of transmission (intra-cerebral injection) the researchers have demonstrated the transmission of a pathological process from two cases one of severe Alzheimer's disease the other of Gerstmann-Straussler disease to marmosets. However they have not demonstrated the transmission of either clinical condition as the "animals were behaving normally when killed'. As the report emphasizes the unanswered question is whether the disease condition would have revealed itself if the marmosets had lived longer. They are planning further research to see if the conditions, as opposed to the partial pathological process, is transmissible.


What are the implications for public health?


3. . The route of transmission is very specific and in the natural state of things highly unusual. However it could be argued that the results reveal a potential risk, in that brain tissue from these two patients has been shown to transmit a pathological process. Should therefore brain tissue from such cases be regarded as potentially infective? Pathologists, morticians, neuro surgeons and those assisting at neuro surgical procedures and others coming into contact with "raw" human brain tissue could in theory be at risk. However, on a priori grounds given the highly specific route of transmission in these experiments that risk must be negligible if the usual precautions for handling brain tissue are observed.


92/11.4/1-1


BSE101/1 0137


4. The other dimension to consider is the public reaction. To some extent the GSS case demonstrates little more than the transmission of BSE to a pig by intra-cerebral injection. If other prion diseases can be transmitted in this way it is little surprise that some pathological findings observed in GSS were also transmissible to a marmoset. But the transmission of features of Alzheimer's pathology is a different matter, given the much greater frequency of this disease and raises the unanswered question whether some cases are the result of a transmissible prion. The only tenable public line will be that "more research is required" before that hypothesis could be evaluated. The possibility on a transmissible prion remains open. In the meantime MRC needs carefully to consider the range and sequence of studies needed to follow through from the preliminary observations in these two cases. Not a particularly comfortable message, but until we know more about the causation of Alzheimer's disease the total reassurance is not practical.


JS METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832


121/YdeS


92/11.4/1.2



http://collections.europarchive.org/tna/20080102232842/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf







Wednesday, January 18, 2012


Government seeking $1T campaign against Alzheimer's


http://betaamyloidcjd.blogspot.com/2012/01/government-seeking-1t-campaign-against.html







Tuesday, October 4, 2011


De novo induction of amyloid-β 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





amyloid; prion; protein misfolding; disease transmission



http://betaamyloidcjd.blogspot.com/2011_06_01_archive.html



http://betaamyloidcjd.blogspot.com/2011_04_01_archive.html



http://betaamyloidcjd.blogspot.com/2011_01_01_archive.html





http://betaamyloidcjd.blogspot.com/





right after the first mad cow in the USA was finally _documented_, this came out;



December 20, 2003


Mad Cow Scaremongers


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




Terry Singletary -- A retired machinist and high school dropout, Terry Singletary suffered the tragic loss of his mother to “sporadic” Creutzfeldt-Jakob disease (CJD) in 1997. Desperate to find an explanation for his mother’s death, he has devoted himself to the sad and fruitless task of connecting her death to her diet. Various reports confirm that Mrs. Singletary’s life was claimed by the most common sub-type of CJD (one that accounts for 70 percent of “sporadic” cases). Sporadic CJD, unlike its newer “variant,” is not linked to meat.

As the self-appointed international coordinator of CJD Watch, an organization he co-founded with social worker Deborah Oney, Singletary is cited in media reports as an apparent expert on tracking mad cow disease. This despite his lack of formal education and the absence for support from any credible academic, medical or scientific authority. His sensationalist allegations about the safety of U.S. beef have found their way into hundreds of newspapers and broadcasts. Singletary moderates a mad-cow discussion forum run by a vegetarian activist group; his contributions account for more than half the traffic on the “BSE-L” mailing list, which is generally read by real scientists. Animal rights activists and other food-scare artists frequently refer to him as “Dr. Terry Singletary,” apparently an honorary degree as he has yet to finish high school.

Like many activists, Singletary ignores overwhelming epidemiological and laboratory evidence that rules out a connection between sporadic CJD and beef. Relying entirely on shallow circumstantial evidence and frequent repetition of claims which have been publicly refuted as false, he also blindly insists upon a mad-cow with Alzheimer’s, Parkinson’s, and Lou Gehrig’s disease. His specific allegations have been clearly refuted by Centers for Disease Countrol and Prevention scientists in the journal Neurology.






http://www.consumerfreedom.com/2003/12/138-mad-cow-scaremongers/





sporadic cjd USA via cjd usa prion unit and cjd foundation et al = 1 in 9,000, in age groups of 55 years and older. see ;




> The Akron, Ohio-based CJD Foundation said the Center for Disease Control revised that number in October of 2004 to about one in 9,000 CJD cases per year in the population group age 55 and older.






Sunday, February 12, 2012


National Prion Disease Pathology Surveillance Center Cases Examined1 (August 19, 2011) including Texas



http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/national-prion-disease-pathology.html






I lost my mom to the Heidenhain Variant of Creutzfeldt Jakob disease on December 14, 1997.



am I still angry?



YOU BETCHA !!!



TSS



Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
flounder9@verizon.net