Thursday, October 1, 2015

Alzheimergate, re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy, Singeltary Submission to Nature

 
updated December 10, 2015

Evidence for human transmission of amyloid-B pathology and cerebral amyloid angiopathy, Singeltary Submission to Nature

2015-12-07 02:27 AM


 

 
Sent: Friday, September 25, 2015 4:17 PM
Subject: re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
 

Subject: re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
 
Greetings Nature et al,
 
WITH relations to the recent paper, and the Lancet paper and the media news articles that followed ;
 
Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
 
Zane Jaunmuktane,1, Simon Mead,2, 3, 4, Matthew Ellis,3, Jonathan D. F. Wadsworth,2, 3, Andrew J. Nicoll,2, 3, Joanna Kenny,2, 4, Francesca Launchbury,3, Jacqueline Linehan,2, Angela Richard-Loendt,3, A. Sarah Walker,5, Peter Rudge,2, 4, John Collinge2, 3, 4, & Sebastian Brandner1, 2, 3, Affiliations Contributions Corresponding authors Journal name: Nature Volume: 525, Pages: 247–250 Date published: (10 September 2015) DOI: doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (September, 2015)
 
 
Alzheimergate? When miscommunication met sensationalism
 
www.thelancet.com Vol 386
 
September 19, 2015 1109
 
 
Wednesday, September 23, 2015
 
Science Government’s top doctor tried to discredit claims Alzheimer's might be infectious Dame Sally Davies
 
 
Dailymail
 
 
Independent
 
 
I would kindly like to comment on the Nature Paper, the Lancet reply, and the newspaper articles.
 
First, I applaud Nature, the Scientist and Authors of the Nature paper, for bringing this important finding to the attention of the public domain, and the media for printing said findings.
 
Secondly, it seems once again, politics is getting in the way possibly of more important Transmissible Spongiform Encephalopathy TSE Prion scientific findings. findings that could have great implications for human health, and great implications for the medical surgical arena. but apparently, the government peer review process, of the peer review science, tries to intervene again to water down said disturbing findings.
 
where have we all heard this before? it’s been well documented via the BSE Inquiry. have they not learned a lesson from the last time?
 
we have seen this time and time again in England (and other Country’s) with the BSE mad cow TSE Prion debacle.
 
That ‘anonymous' Lancet editorial was disgraceful. The editor, Dick Horton is not a scientist.
 
The pituitary cadavers were very likely elderly and among them some were on their way to CJD or Alzheimer's. Not a bit unusual. Then the recipients — who got pooled extracts injected from thousands of cadavers — were 100% certain to have been injected with both seeds. No surprise that they got both diseases going after thirty year incubations.
 
That the UK has a "system in place to assist science journalists" to squash embargoed science reports they find ‘alarming’ is pathetic.
 
Sounds like the journalists had it right in the first place: “Alzheimer’s may be a transmissible infection” in The Independent to “You can catch Alzheimer’s” in The Daily Mirror or “Alzheimer’s bombshell" in The Daily Express
 
if not for the journalist, the layperson would not know about these important findings.
 
where would we be today with sound science, from where we were 30 years ago, if not for the cloak of secrecy and save the industry at all cost mentality?
 
when you have a peer review system for science, from which a government constantly circumvents, then you have a problem with science, and humans die.
 
to date, as far as _documented_ body bag count, with all TSE prion _named_ to date, that count is still relatively low (one was too many in my case, Mom hvCJD), however that changes drastically once the TSE Prion link is made with Alzheimer’s, the price of poker goes up drastically.
 
so, who makes that final decision, and how many more decades do we have to wait?
 
the iatrogenic mode of transmission of TSE prion, the many routes there from, load factor, threshold from said load factor to sub-clinical disease, to clinical disease, to death, much time is there to spread a TSE Prion to anywhere, but whom, by whom, and when, do we make that final decision to do something about it globally? how many _documented_ body bags does it take? how many more decades do we wait? how many names can we make up for one disease, TSE prion?
 
Professor Collinge et al, and others, have had troubles in the past with the Government meddling in scientific findings, that might in some way involve industry, never mind human and or animal health.
 
FOR any government to continue to circumvent science for monetary gain, fear factor, or any reason, shame, shame on you.
 
in my opinion, it’s one of the reasons we are at where we are at to date, with regards to the TSE Prion disease science i.e. money, industry, politics, then comes science, in that order.
 
greed, corporate, lobbyist there from, and government, must be removed from the peer review process of sound science, it’s bad enough having them in the pharmaceutical aspect of healthcare policy making, in my opinion.
 
my mother died from confirmed hvCJD, and her brother (my uncle) Alzheimer’s of some type (no autopsy?). just made a promise, never forget, and never let them forget, before I do.
 
I kindly wish to remind the public of the past, and a possible future we all hopes never happens again. ...
 
 
[9. Whilst this matter is not at the moment directly concerned with the iatrogenic CJD cases from hgH, there remains a possibility of litigation here, and this presents an added complication. There are also results to be made available shortly (1) concerning a farmer with CJD who had BSE animals, (2) on the possible transmissibility of Alzheimer’s and (3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.]
 
 
 
 
2. The Collinge/Will dispute appears to rumble on. Dr. Collinge had told Dr. Tyrrell that Dr. Will's response to his criticism about sharing material had been ''quite unacceptable'' (in spite of it's apparently conciliatory tone). Apparently Professor Allen was now going to try and arrange a meeting to resolve the dispute. No action here for MAFF, although Mr. Murray may be interested.
 
3. Dr. Tyrrell regretted that the Committee had not seen the article on BBD. However he felt that for the time being NO specific action was called for. The most important need was to consider the possibility that the condition might be transmissible. As we have discussed, I suggested that we might circulate a paper to the members of the committee giving our appreciation of this condition (and perhaps of other non-BSE neurological conditions that had been identified in negative cases) and of any necessary follow up action. IF any Committee member felt strongly about this, or if the issue CAME TO A HEAD, we would call an interim meeting. He was happy with this approach. I would be grateful if Mr. Maslin could, in discussion with CVL and veterinary colleagues draft such a note, which will presumably very largely follow what Mr. Bradley's briefing paper has already said, taking account of DOH comments, We can then clear a final version with DOH before circulating it to Committee members.
 
 
IN CONFIDENCE This is a highly competitive field and it really will be a pity if we allow many of the key findings to be published by overseas groups while we are unable to pursue our research findings because of this disagreement, which I hope we can make every effort to solve.
 
 
Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease
 
Received July 24, 2014; Accepted September 16, 2014; Published November 3, 2014
 
Singeltary comment Alzheimer’s, transmission, what if ???
 
 
Received July 24, 2014; Accepted September 16, 2014; Published November 3, 2014
 
*** IN STRICT CONFIDENCE ***
 
Singeltary comment ;
 
it was said long ago ;
 
Ann N Y Acad Sci. 1982;396:131-43.
 
Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob disease).
 
Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.
 
Abstract
 
Ample justification exists on clinical, pathologic, and biologic grounds for considering a similar pathogenesis for AD and the spongiform virus encephalopathies. However, the crux of the comparison rests squarely on results of attempts to transmit AD to experimental animals, and these results have not as yet validated a common etiology. Investigations of the biologic similarities between AD and the spongiform virus encephalopathies proceed in several laboratories, and our own observation of inoculated animals will be continued in the hope that incubation periods for AD may be even longer than those of CJD.
 
 
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
 
see full text and more IN CONFIDENCE ;
 
Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease
 
Received July 24, 2014; Accepted September 16, 2014; Published November 3, 2014
 
Singeltary comment Alzheimer’s, transmission, what if ???
 
 
RE: re-Human Prion Diseases in the United States
 
part 2 flounder replied to flounder on 02 Jan 2010 at 21:26 GMT
 
No competing interests declared.
 
see full text ;
 
 
(It was noted with concern that hormone extracts could be manufactured by a veterinary surgeon for administration to animals under his care without any Medicines Act Control.)
 
PITUITARY EXTRACT
 
This was used to help cows super ovulate.
 
*** This tissue was considered to be of greatest risk of containing BSE and consequently transmitting the disease. ***
 
 
 
LMAO (it will load correctly, but nothing there)
 
COMMERCIAL IN CONFIDENCE NOT FOR PUBLICATION
 
 
 
 
2.1.2 Allergy Products
 
snip...
 
Comment
 
2.1.3 ________________________, England Ltd) ***contains bovine heart and brain sourced from USA***. (It also uses UK derived equine blood.)
 
 
THE VETERINARY RECORD 516 No 47. Vol. 58 November 23rd, 1946
 
NATIONAL VETERINARY MEDICAL ASSOCIATION OF GREAT BRITAIN AND IRELAND ANNUAL CONGRESS, 1946 Advances in Veterinary Research
 
Louping-ill, Tick-borne Fever and Scrapie W.S. GORDON, PH.D., M.R.C.V.S., F.R.S.E. Agriculteral Research Council, Field Station, Compton, Berks.
 
"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 [[eaten for human food]] 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 althought 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."
 
 
see part of old report I received;
 
 
*** An interview with Professor John Collinge: Director of the MRC Prion Unit. Part of the Hayward Gallery's History Is Now.
 
culture of denial...SEE VIDEO ;
 
 
*** see vaccines (I don’t advertise or make money from these blogs, they are for educational use for the TSE Prion disease and to document history) ;
 
 
*** U.S.A. 50 STATE EMERGENCY BSE MAD COW CONFERENCE CALL Jan. 9, 2001
 
 
IBNC Tauopathy or TSE Prion disease, it appears, no one is sure
 
Singeltary et al
 
Posted by flounder on 03 Jul 2015 at 16:53 GMT
 
 
31 Jan 2015 at 20:14 GMT
 
*** Ruminant feed ban for cervids in the United States? ***
 
31 Jan 2015 at 20:14 GMT
 
 
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;
 
 
Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
 
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
 
To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
 
Terry S. Singeltary, Sr Bacliff, Tex
 
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. FREE FULL TEXT
 
 
Views & Reviews
 
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States
 
Ermias D. Belay, MD, Ryan A. Maddox, MPH, Pierluigi Gambetti, MD and Lawrence B. Schonberger, MD
 
+ Author Affiliations
 
From the Division of Viral and Rickettsial Diseases (Drs. Belay and Schonberger and R.A. Maddox), National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA; and National Prion Disease Pathology Surveillance Center (Dr. Gambetti), Division of Neuropathology, Institute of Pathology, Case Western Reserve University, Cleveland, OH.
 
Address correspondence and reprint requests to Dr. Ermias D. Belay, 1600 Clifton Road, Mailstop A-39, Atlanta, GA 30333.
 
 
26 March 2003
 
Terry S. Singeltary, retired (medically) CJD WATCH
 
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?
 
 
The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003 doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI
 
Tracking spongiform encephalopathies in North America
 
Original
 
Xavier Bosch
 
“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.” 49-year—old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt—Jakob ...
 
 
 
2 January 2000
 
British Medical Journal
 
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well
 
 
15 November 1999
 
British Medical Journal
 
vCJD in the USA * BSE in U.S.
 
 
2012 Singeltary
 
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
 
Background
 
Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer (most of the time) than the TSE prion disease. Symptoms are very similar, and pathology is very similar.
 
Methods
 
Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.
 
Results
 
I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease.
 
Conclusions
 
There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics lets science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already.
 
end...tss
 
SEE FULL TEXT AND SOURCE REFERENCES ;
 
Wednesday, May 16, 2012
 
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
 
Proposal ID: 29403
 
 
From:
 
Sent: Saturday, April 07, 2012 8:20 PM
 
To: Terry S. Singeltary Sr.
 
Subject: RE: re-submission
 
Dear Terry,
 
Yes, your proposal was accepted as a poster presentation. Please decline the invitation if appropriate.
 
Best Regards,
 
______________________________________
 
Alzheimer’s Association – National Office
 
225 North Michigan Avenue – Floor 17
 
Chicago, Illinois 60601
 
=============snip...end...source reference...# 29403==========
 
Wednesday, September 2, 2015
 
Clinically Unsuspected Prion Disease Among Patients With Dementia Diagnoses in an Alzheimer’s Disease Database
 
 
Thursday, July 30, 2015
 
Professor Lacey believes sporadic CJD itself originates from a cattle infection number of cattle farmers falling victim to Creutzfeld-Jakob Disease is much too high to be mere chance
 
 
Wednesday, September 23, 2015
 
*** NIH Availability for Licensing AGENCY: [FR Doc. 2015–24117 Filed 9–22–15; 8:45 am] Detection and Discrimination of Classical and Atypical L-Type BSE Strains by RT-QuIC
 
 
Thursday, September 10, 2015
 
TSEAC FDA TSE PRION MAD COW CIRCUS AND TRAVELING ROAD SHOW (their words)
 
25th Meeting of the Transmissible Spongiform Encephalopathies Advisory Committee Food and Drug Administration Silver Spring, Maryland June 1, 2015
 
 
Thursday, August 13, 2015
 
Iatrogenic CJD due to pituitary-derived growth hormone with genetically determined incubation times of up to 40 years
 
 
Monday, August 17, 2015
 
FDA Says Endoscope Makers Failed to Report Superbug Problems OLYMPUS
 
I told Olympus 15 years ago about these risk factors from endoscopy equipment, disinfection, even spoke with the Doctor at Olympus, this was back in 1999. I tried to tell them that they were exposing patients to dangerous pathogens such as the CJD TSE prion, because they could not properly clean them. even presented my concern to a peer review journal GUT, that was going to publish, but then it was pulled by Professor Michael Farthing et al... see ;
 
 
Friday, January 10, 2014
 
vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???
 
 
 
Thursday, September 24, 2015
 
TEXAS Hunters Asked to Submit Samples for Chronic Wasting Disease CWD TSE Prion Testing
 
*** I cannot stress enough to all of you, for the sake of your family and mine, before putting anything in the freezer, have those deer tested for CWD. ...terry
 
 
cwd to humans, iatrogenic, what if ?
 
 
Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.
 
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
 
Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.
 
 
Tuesday, May 26, 2015
 
*** Minimise transmission risk of CJD and vCJD in healthcare settings ***
 
Last updated 15 May 2015
 
 
 
Wednesday, September 23, 2015
 
Alzheimergate? When miscommunication met sensationalism, or just another cover up ?
 
 
Terry S. Singeltary Sr., Bacliff, Texas USA 77518 flounder9@verizon.net
 
Posted by at No comments:

Wednesday, September 23, 2015

Alzheimergate? When miscommunication met sensationalism, or just another cover up ?

Alzheimergate? When miscommunication met sensationalism

 

On Sept 5, The Lancet was alerted by a UK Government source to the impending publication of a Nature paper allegedly about the possible transmission of Alzheimer’s disease. The source was anxious about the likely media coverage and the potential for a public health scare. Although the UK’s Science Media Centre was involved in helping to communicate the findings reported in the paper accurately, our source urged us to consider what we might do to reduce further the risk of a scare. We wrote to the Science Media Centre, explaining our understanding of the potential alarm and asking if we could help in some way. The Science Media Centre did not think the paper by John Collinge and Sebastian Brandner was unduly alarmist. It noted that several highly experienced press officers were working hard on the communication of the research findings to prevent any possibility of a scare. They added that if there were alarmist headlines, it would not be for the want of trying to prevent them.

 

On Sept 10, the UK newspapers took a very different angle than predicted, or hoped for, by our colleagues at the Science Media Centre. Ranging from “Alzheimer’s may be a transmissible infection” in The Independent to “You can catch Alzheimer’s” in The Daily Mirror or “Alzheimer’s bombshell” in The Daily Express, the general tone of the headlines was indeed deeply alarmist. Some news sources tried to redress the harm done. The BBC ran a story on its website saying there was “No evidence to support the headlines”. Meanwhile, in many other countries, the story was either not covered at all, or news headlines at least included a question mark.

 

Question marks were wise and judicious additions, if one reads what the published study actually showed (and did not show). The title promises “Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy”. But the study does not provide evidence of human transmission, as the authors acknowledge themselves in their fi nal paragraph—”there is no suggestion that Alzheimer’s disease is a contagious disease and no supportive evidence from epidemiological studies that Alzheimer’s disease is transmissible.” What John Collinge and Sebastian Brandner’s elegant autopsy study of eight patients shows is that some patients treated with cadaveric human growth hormone who subsequently developed iatrogenic Creutzfeldt-Jakob disease also showed evidence of amyloid β deposition in their pituitary glands. The study does not show whether these patients would have actually developed Alzheimer’s disease had they lived longer (they died from Creutzfeldt-Jakob disease and they had no sign of tau protein pathology characteristic of Alzheimer’s disease). The study does not demonstrate that these patients’ amyloid β deposits were caused by growth hormone contaminated with “amyloid β seeds”. As the authors state in the paper, “Analysis of any residual archival batches of c-hGH [cadaveric-derived human growth hormone] for both prions and Aβ [amyloid β] seeds might be informative in this regard”—informative, and actually crucial to support their hypothesis. Controlled experiments injecting cadaveric human growth hormone into animals to discover whether amyloid deposits develop as a consequence are also needed to support their theory.

 

The much overused phrase “paradigm shift” was quoted in some news reports. But the fi ndings, although certainly interesting, were a long way from a true “paradigm shift”. The use of this phrase likely heightened the interest and attention of journalists—and headline writers. Was “Evidence for human transmission” an appropriate title for this paper? The report does not describe human transmission of amyloid pathology. Rather, it reports amyloid pathology in patients with iatrogenic Creutzfeldt-Jakob disease. Therefore, such a strong statement in a title also seems misleading and potentially alarmist. Neuropathology experts, including those selected by the Science Media Centre, were left with the difficult task of balancing plausible explanations against tenuous extrapolations. The public ended up being warned about “Alzheimer’s link to blood transfusions” or “You can catch Alzheimer’s”, thereby generating unnecessary anxiety and potentially diminishing years of effort against patients’ stigmatisation.

 

Taking these events together, this episode of scientific reporting was handled poorly. One senior protagonist in this affair felt “upset and bewildered” by the outcome. Despite the best efforts of some, the system in place to assist science journalists broke down through a mix of inattention and perhaps even complacency. Preventive actions by the UK’s public health authorities were too weak and too late. The lesson that might be learned from this episode is that goodwill and hope are insufficient to prevent a public health scare. 􀂄 The Lancet

 


 

www.thelancet.com Vol 386 September 19, 2015 1109

 


 

Wednesday, September 23, 2015

 

 Science Government’s top doctor tried to discredit claims Alzheimer's might be infectious Dame Sally Davies

 

 Science Government’s top doctor tried to discredit claims Alzheimer's might be infectious

 

 Dame Sally Davies approached the editor of a rival scientific journal to discredit the study in the eyes of the public, the Independent understands Steve Connor | @SteveAConnor | Wednesday 23 September 2015 18:03 BST| 0 comments |

 

 The study suggests the seeds of Alzheimer’s disease may be transmitted from one person to another during certain medical procedures The study suggests the 'seeds' of Alzheimer’s disease may be transmitted from one person to another during certain medical procedures Corbis

 

 A senior government adviser attempted to undermine a controversial study suggesting that Alzheimer’s is a transmissible disease before it was published in the journal Nature.

 

 Dame Sally Davies, the chief medical officer at the Department of Health, approached the editor of a rival scientific journal, The Lancet, to discredit the study in the eyes of the public, The Independent understands.

 

 Dame Sally told Richard Horton, the editor of The Lancet, that the study on Alzheimer’s was likely to result in a public scare and asked him for advice on how to handle the media reaction before it came out in Nature.

 

 The study, published earlier this month, suggested that the “seeds” of Alzheimer’s disease may be transmitted from one person to another during certain medical procedures.

 

 It was based on the brain autopsies of eight people aged between 36 and 51 who had died of Creutzfeldt-Jakob disease (CJD) after receiving injections of human growth hormone derived from the pituitary glands of dead people.

 

 Seven of the eight has signs of a brain protein linked with Alzheimer’s, although they had no genetic predisposition to the disease and were too young to have developed it naturally – strongly suggesting transmission via contaminated hormone injections.

 

 Dame Sally, a haematologist by training, contacted Dr Horton on the weekend before Nature intended to publish the study having received confidential information under the strict embargo terms of the journal, which prohibit any approaches to third parties unless it is “solely for soliciting informed comment”.

 

 8-Sally-Davies-Get.jpg Dame Sally Davies, chief medical officer at the Department of Health (Getty)

 

 In an unsigned editorial in The Lancet this week, Dr Horton writes that an unnamed government source informed him on the study’s impending publication and urged him to consider what he might do to reduce further the risk of a scare.

 

 Dr Horton then wrote to the Science Media Centre in London, which was coordinating expert reaction to the study with the help of University College London and the Medical Research Council, which funded the work by Professor John Collinge, a world authority on transmissible brain diseases.

 

 Although The Lancet’s source is not identified, The Independent understands that it was Dame Sally, who knows Dr Horton personally and has shared several conference platforms with The Lancet’s outspoken editor.

 

 A spokesman for the Department of Health said last night that the identity of The Lancet’s source is the subject of a freedom of information request and cannot therefore comment.

 

 It is highly unusual for a government science adviser to approach a medical journal for help in media management relating to a controversial study published in a rival journal with its own distinguished track-record of handling contentious research findings.

 


 

hell, this is old news, the government has been trying to cover up that fact since the late 80s, early 90s.

 

 cover up, cover up, cover up at all cost, including human and animal health $$$

 

 AND WE ALL KNEW THIS WAS THE CASE $$$

 

 Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease

 

 Received July 24, 2014; Accepted September 16, 2014; Published November 3, 2014

 

 *** IN STRICT CONFIDENCE ***

 

 Singeltary comment ;

 


 

 Singeltary comment reply to above ‘’Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease’’

 

 Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?

 

 Posted by flounder on 05 Nov 2014 at 21:27 GMT

 

 Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?

 

 Background

 

 Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer (most of the time) than the TSE prion disease. Symptoms are very similar, and pathology is very similar.

 

 Methods

 

 Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.

 

 Results

 

 I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease.

 

 Conclusions

 

 There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics lets science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already.

 

 end...tss

 

 Ann N Y Acad Sci. 1982;396:131-43.

 

 Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob disease).

 

 Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.

 

 Abstract

 

 Ample justification exists on clinical, pathologic, and biologic grounds for considering a similar pathogenesis for AD and the spongiform virus encephalopathies. However, the crux of the comparison rests squarely on results of attempts to transmit AD to experimental animals, and these results have not as yet validated a common etiology. Investigations of the biologic similarities between AD and the spongiform virus encephalopathies proceed in several laboratories, and our own observation of inoculated animals will be continued in the hope that incubation periods for AD may be even longer than those of CJD.

 


 

 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

 


 

 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

 


 

 BSE101/1 0136

 

 IN CONFIDENCE

 

 CMO

 

 From: Dr J S Metters DCMO

 

 4 November 1992

 

 TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES

 


 

 CJD1/9 0185

 

 Ref: 1M51A

 

 IN STRICT CONFIDENCE

 

 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

 


 

 Tuesday, November 26, 2013

 

 Transmission of multiple system atrophy prions to transgenic mice

 

 ‘’Our results provide compelling evidence that α-synuclein aggregates formed in the brains of MSA patients are transmissible and, as such, are prions.’’

 


 

 Transmission of a neurodegenerative disorder from humans to mice

 

 The findings suggest that the α-synuclein deposits that form in the brains of patients with MSA behave like prions and are transmissible under certain circumstances, according to the authors. — N.Z.

 

 α-Synuclein deposits in the brainstems of inoculated mice.

 


 

 kind regards, terry

 

 No competing interests declared.

 

 *** Singeltary comment ***

 


 

 

Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease

 

 Received July 24, 2014; Accepted September 16, 2014; Published November 3, 2014

 

 *** IN STRICT CONFIDENCE ***

 

 Singeltary comment ;

 


 

 

*** NOW PLEASE READ THIS SHORT ABSTRACT FROM DECADES AGO, THE LATE GREAT DR. GIBBS, PLEASE READ THIS 3 TIMES AND THEN PROCEED***

 

 

Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.

 

 Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.

 

 Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.

 

 Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.

 


 

 Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?

 

 Background

 

 Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer (most of the time) than the TSE prion disease. Symptoms are very similar, and pathology is very similar.

 

 Methods

 

 Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.

 

 Results

 

 I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease.

 

 Conclusions

 

 There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics lets science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already.

 

 end...tss

 

 SEE FULL TEXT AND SOURCE REFERENCES ;

 

 Wednesday, May 16, 2012

 

 Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?

 

 Proposal ID: 29403

 


 

 From:

 

 Sent: Saturday, April 07, 2012 8:20 PM

 

 To: Terry S. Singeltary Sr.

 

 Subject: RE: re-submission

 

 Dear Terry,

 

 Yes, your proposal was accepted as a poster presentation. Please decline the invitation if appropriate.

 

 Best Regards,

 

 ______________________________________

 

 Alzheimer’s Association – National Office

 

 225 North Michigan Avenue – Floor 17

 

 Chicago, Illinois 60601

 

 =============snip...end...source reference...# 29403==========

 

 Final Abstract Number: ISE.114

 

 Session: International Scientific Exchange

 

 Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009

 

 T. Singeltary Bacliff, TX, USA

 

 Background: An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and feed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.

 

 Methods: 12 years independent research of available data

 

 Results: I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.

 

 Conclusion: I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.

 


 

 Wednesday, September 9, 2015

 

*** Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy

 


 

Wednesday, September 2, 2015

 

 Clinically Unsuspected Prion Disease Among Patients With Dementia Diagnoses in an Alzheimer’s Disease Database

 


 

 Tuesday, September 1, 2015

 

 Evidence for α-synuclein prions causing multiple system atrophy in humans with parkinsonism

 


 


 

 Thursday, August 13, 2015

 

 Iatrogenic CJD due to pituitary-derived growth hormone with genetically determined incubation times of up to 40 years

 


 

 Friday, January 10, 2014

 

 vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???

 


 

 Tuesday, May 26, 2015

 

 *** Minimise transmission risk of CJD and vCJD in healthcare settings ***

 

 Last updated 15 May 2015

 


 

 Monday, August 17, 2015

 

 FDA Says Endoscope Makers Failed to Report Superbug Problems OLYMPUS

 

 I told Olympus 15 years ago about these risk factors from endoscopy equipment, disinfection, even spoke with the Doctor at Olympus, this was back in 1999. I tried to tell them that they were exposing patients to dangerous pathogens such as the CJD TSE prion, because they could not properly clean them. even presented my concern to a peer review journal GUT, that was going to publish, but then it was pulled by Professor Michael Farthing et al... see ;

 


 

IBNC Tauopathy or TSE Prion disease, it appears, no one is sure

 

 Singeltary et al

 

 Posted by flounder on 03 Jul 2015 at 16:53 GMT

 


 

 Tuesday, September 1, 2015

 

 Evidence for α-synuclein prions causing multiple system atrophy in humans with parkinsonism

 


 

 Wednesday, January 28, 2015

 

 Another new prion disease: relationship with central and peripheral amyloidoses

 

 here we go again...

 


 

 Alzheimer's, iatrogenic, transmissible, tse, prion, what if ?

 

 Wednesday, September 9, 2015

 

 *** Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy

 


 

 Wednesday, September 2, 2015

 

 *** Clinically Unsuspected Prion Disease Among Patients With Dementia Diagnoses in an Alzheimer’s Disease Database

 


 

 Tuesday, September 1, 2015

 

 *** Evidence for α-synuclein prions causing multiple system atrophy in humans with parkinsonism

 


 

 Thursday, September 10, 2015

 

 25th Meeting of the Transmissible Spongiform Encephalopathies Advisory Committee Food and Drug Administration Silver Spring, Maryland June 1, 2015

 


 

 Wednesday, September 23, 2015

 

 NIH Availability for Licensing AGENCY: [FR Doc. 2015–24117 Filed 9–22–15; 8:45 am] Detection and Discrimination of Classical and Atypical L-Type BSE Strains by RT-QuIC

 


 

 SAVE THE INDUSTRIES AT ALL COST, INCLUDING HUMAN AND ANIMAL HEALTH $$$

 

 that’s why we are in this mess...

 

Wednesday, September 23, 2015

 

Science Government’s top doctor tried to discredit claims Alzheimer's might be infectious Dame Sally Davies

 


 

 

Tracking spongiform encephalopathies in North America

Xavier Bosch

DOI: http://dx.doi.org/10.1016/S1473-3099(03)00715-1
Share on mendeleyShare on facebookShare on twitterShare on emailMore Sharing Services




To view the full text, please login as a subscribed user or purchase a subscription. Click here to view the full text on ScienceDirect.
 
“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.”
 
 
http://www.thelancet.com/pdfs/journals/laninf/PIIS1473-3099(03)00715-1.pdf
 


Terry S. Singeltary Sr.



UPDATED DECEMBER 10, 2015


Evidence for human transmission of amyloid-B pathology and cerebral amyloid angiopathy, Singeltary Submission to Nature

 

2015-12-07 02:27 AM

 


 
 
Posted by at No comments:

Science Government’s top doctor tried to discredit claims Alzheimer's might be infectious Dame Sally Davies

Science Government’s top doctor tried to discredit claims Alzheimer's might be infectious

 

Dame Sally Davies approached the editor of a rival scientific journal to discredit the study in the eyes of the public, the Independent understands Steve Connor | @SteveAConnor | Wednesday 23 September 2015 18:03 BST| 0 comments |

 

The study suggests the seeds of Alzheimer’s disease may be transmitted from one person to another during certain medical procedures The study suggests the 'seeds' of Alzheimer’s disease may be transmitted from one person to another during certain medical procedures Corbis

 

A senior government adviser attempted to undermine a controversial study suggesting that Alzheimer’s is a transmissible disease before it was published in the journal Nature.

 

Dame Sally Davies, the chief medical officer at the Department of Health, approached the editor of a rival scientific journal, The Lancet, to discredit the study in the eyes of the public, The Independent understands.

 

Dame Sally told Richard Horton, the editor of The Lancet, that the study on Alzheimer’s was likely to result in a public scare and asked him for advice on how to handle the media reaction before it came out in Nature.

 

The study, published earlier this month, suggested that the “seeds” of Alzheimer’s disease may be transmitted from one person to another during certain medical procedures.

 

It was based on the brain autopsies of eight people aged between 36 and 51 who had died of Creutzfeldt-Jakob disease (CJD) after receiving injections of human growth hormone derived from the pituitary glands of dead people.

 

Seven of the eight has signs of a brain protein linked with Alzheimer’s, although they had no genetic predisposition to the disease and were too young to have developed it naturally – strongly suggesting transmission via contaminated hormone injections.

 

 Dame Sally, a haematologist by training, contacted Dr Horton on the weekend before Nature intended to publish the study having received confidential information under the strict embargo terms of the journal, which prohibit any approaches to third parties unless it is “solely for soliciting informed comment”.

 

8-Sally-Davies-Get.jpg Dame Sally Davies, chief medical officer at the Department of Health (Getty)

 

In an unsigned editorial in The Lancet this week, Dr Horton writes that an unnamed government source informed him on the study’s impending publication and urged him to consider what he might do to reduce further the risk of a scare.

 

Dr Horton then wrote to the Science Media Centre in London, which was coordinating expert reaction to the study with the help of University College London and the Medical Research Council, which funded the work by Professor John Collinge, a world authority on transmissible brain diseases.

 

Although The Lancet’s source is not identified, The Independent understands that it was Dame Sally, who knows Dr Horton personally and has shared several conference platforms with The Lancet’s outspoken editor.

 

A spokesman for the Department of Health said last night that the identity of The Lancet’s source is the subject of a freedom of information request and cannot therefore comment.

 

It is highly unusual for a government science adviser to approach a medical journal for help in media management relating to a controversial study published in a rival journal with its own distinguished track-record of handling contentious research findings.

 


 

 

hell, this is old news, the government has been trying to cover up that fact since the late 80s, early 90s.

 

cover up, cover up, cover up at all cost, including human and animal health $$$

 

AND WE ALL KNEW THIS WAS THE CASE $$$

 

Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease

 

Received July 24, 2014; Accepted September 16, 2014; Published November 3, 2014

 

*** IN STRICT CONFIDENCE ***

 

Singeltary comment ;

 


 

Singeltary comment reply to above ‘’Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease’’

 

Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?

 

Posted by flounder on 05 Nov 2014 at 21:27 GMT

 

Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?

 

Background

 

Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer (most of the time) than the TSE prion disease. Symptoms are very similar, and pathology is very similar.

 

Methods

 

Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.

 

Results

 

I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease.

 

Conclusions

 

There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics lets science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already.

 

end...tss

 

Ann N Y Acad Sci. 1982;396:131-43.

 

Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob disease).

 

Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.

 

Abstract

 

Ample justification exists on clinical, pathologic, and biologic grounds for considering a similar pathogenesis for AD and the spongiform virus encephalopathies. However, the crux of the comparison rests squarely on results of attempts to transmit AD to experimental animals, and these results have not as yet validated a common etiology. Investigations of the biologic similarities between AD and the spongiform virus encephalopathies proceed in several laboratories, and our own observation of inoculated animals will be continued in the hope that incubation periods for AD may be even longer than those of CJD.

 


 

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

 


 

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

 


 

BSE101/1 0136

 

IN CONFIDENCE

 

CMO

 

From: Dr J S Metters DCMO

 

4 November 1992

 

TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES

 


 

CJD1/9 0185

 

Ref: 1M51A

 

IN STRICT CONFIDENCE

 

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

 


 

Tuesday, November 26, 2013

 

Transmission of multiple system atrophy prions to transgenic mice

 

‘’Our results provide compelling evidence that α-synuclein aggregates formed in the brains of MSA patients are transmissible and, as such, are prions.’’

 


 

Transmission of a neurodegenerative disorder from humans to mice

 

The findings suggest that the α-synuclein deposits that form in the brains of patients with MSA behave like prions and are transmissible under certain circumstances, according to the authors. — N.Z.

 

α-Synuclein deposits in the brainstems of inoculated mice.

 


 

kind regards, terry

 

No competing interests declared.

 

*** Singeltary comment ***

 


 

 

Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease

 

Received July 24, 2014; Accepted September 16, 2014; Published November 3, 2014

 

*** IN STRICT CONFIDENCE ***

 

Singeltary comment ;

 


 

 

 

*** NOW PLEASE READ THIS SHORT ABSTRACT FROM DECADES AGO, THE LATE GREAT DR. GIBBS, PLEASE READ THIS 3 TIMES AND THEN PROCEED***

 

 

Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.

 

Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.

 

Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.

 

Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.

 


 

Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?

 

Background

 

Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer (most of the time) than the TSE prion disease. Symptoms are very similar, and pathology is very similar.

 

Methods

 

Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.

 

Results

 

I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease.

 

Conclusions

 

There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics lets science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already.

 

end...tss

 

SEE FULL TEXT AND SOURCE REFERENCES ;

 

Wednesday, May 16, 2012

 

Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?

 

Proposal ID: 29403

 


 

From:

 

Sent: Saturday, April 07, 2012 8:20 PM

 

To: Terry S. Singeltary Sr.

 

Subject: RE: re-submission

 

Dear Terry,

 

Yes, your proposal was accepted as a poster presentation. Please decline the invitation if appropriate.

 

Best Regards,

 

______________________________________

 

Alzheimer’s Association – National Office

 

225 North Michigan Avenue – Floor 17

 

Chicago, Illinois 60601

 

=============snip...end...source reference...# 29403==========

 

Final Abstract Number: ISE.114

 

Session: International Scientific Exchange

 

Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009

 

T. Singeltary Bacliff, TX, USA

 

Background: An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and feed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.

 

Methods: 12 years independent research of available data

 

Results: I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.

 

Conclusion: I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.

 



Wednesday, September 9, 2015

 
Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy

 
 

Wednesday, September 2, 2015

 

Clinically Unsuspected Prion Disease Among Patients With Dementia Diagnoses in an Alzheimer’s Disease Database

 


 

Tuesday, September 1, 2015

 

Evidence for α-synuclein prions causing multiple system atrophy in humans with parkinsonism

 


 


 

Thursday, August 13, 2015

 

Iatrogenic CJD due to pituitary-derived growth hormone with genetically determined incubation times of up to 40 years

 


 

Friday, January 10, 2014

 

vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???

 


 

Tuesday, May 26, 2015

 

*** Minimise transmission risk of CJD and vCJD in healthcare settings ***

 

Last updated 15 May 2015

 


 

Monday, August 17, 2015

 

FDA Says Endoscope Makers Failed to Report Superbug Problems OLYMPUS

 

I told Olympus 15 years ago about these risk factors from endoscopy equipment, disinfection, even spoke with the Doctor at Olympus, this was back in 1999. I tried to tell them that they were exposing patients to dangerous pathogens such as the CJD TSE prion, because they could not properly clean them. even presented my concern to a peer review journal GUT, that was going to publish, but then it was pulled by Professor Michael Farthing et al... see ;

 


 

 

 

IBNC Tauopathy or TSE Prion disease, it appears, no one is sure

 

Singeltary et al

 

Posted by flounder on 03 Jul 2015 at 16:53 GMT

 


 

Tuesday, September 1, 2015

 

Evidence for α-synuclein prions causing multiple system atrophy in humans with parkinsonism

 


 

Wednesday, January 28, 2015

 

Another new prion disease: relationship with central and peripheral amyloidoses

 

here we go again...

 


 

Alzheimer's, iatrogenic, transmissible, tse, prion, what if ?

 

Wednesday, September 9, 2015

 

*** Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy

 


 

Wednesday, September 2, 2015

 

*** Clinically Unsuspected Prion Disease Among Patients With Dementia Diagnoses in an Alzheimer’s Disease Database

 


 

Tuesday, September 1, 2015

 

*** Evidence for α-synuclein prions causing multiple system atrophy in humans with parkinsonism

 


 

Thursday, September 10, 2015

 

25th Meeting of the Transmissible Spongiform Encephalopathies Advisory Committee Food and Drug Administration Silver Spring, Maryland June 1, 2015

 


 

Wednesday, September 23, 2015

 

NIH Availability for Licensing AGENCY: [FR Doc. 2015–24117 Filed 9–22–15; 8:45 am] Detection and Discrimination of Classical and Atypical L-Type BSE Strains by RT-QuIC

 


 

SAVE THE INDUSTRIES AT ALL COST, INCLUDING HUMAN AND ANIMAL HEALTH $$$

 

that’s why we are in this mess...

 

Terry S. Singeltary Sr.
Posted by at No comments:
Subscribe to: Posts (Atom)