Friday, October 2, 2015

NIH invests $85 million for BRAIN Initiative research (sCJD, TSE, Prion ?)

Sent: Thursday, October 01, 2015 4:44 PM
Subject: NIH invests $85 million for BRAIN Initiative research and not a mention of the TSE prion disease or was it secretly hiden there by Alzheimer's ?
 

Greetings NIH et al,
 
I wish to comment on the good news below, and then, some not so good.
 
just made a promise to mom, never forget, and never you all forget. mom dod 12/14/97 confirmed hvCJD and her brother Alzheimer’s. ...
 
For Immediate Release: Thursday, October 1, 2015
 
NIH invests $85 million for BRAIN Initiative research New round of projects for visualizing the brain in action
 
Share on email The National Institutes of Health announced its second wave of grants to support the goals of the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative, bringing the NIH investment to $85 million in fiscal year 2015. Sixty-seven new awards, totaling more than $38 million, will go to 131 investigators working at 125 institutions in the United States and eight other countries. These awards expand NIH’s efforts to develop new tools and technologies to understand neural circuit function and capture a dynamic view of the brain in action. Projects include proposals to develop soft self-driving electrodes, ultrasound methods for measuring brain activity and the use of deep brain stimulation to treat traumatic brain injuries.
 
In 2014, President Obama launched the BRAIN Initiative as a large-scale effort to equip researchers with fundamental insights necessary for treating a wide variety of brain disorders like Alzheimer’s, schizophrenia, autism, epilepsy, and traumatic brain injury. These new tools and this deeper understanding will ultimately catalyze new treatments and cures for devastating brain disorders and diseases that are estimated by the World Health Organization to affect more than one billion people worldwide.
 
Planning for the NIH component of the BRAIN initiative is guided by the long-term scientific plan, BRAIN 2025: A Scientific Vision that details seven high priority research areas. Last year NIH awarded $46 million to BRAIN Initiative research.
 
For a list of the new grants and more information about the BRAIN Initiative, please visit: http://www.braininitiative.nih.gov.
 
About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.
 
NIH...Turning Discovery Into Health®
 
###
 
 
 
Great news! I was very glad to see Alzheimer’s disease even getting more research funding on top of what they already get.
 
I am however very disappointed that apparently not one cent was earmarked for Transmissible Spongiform Encephalopathy TSE Prion Sporadic Creutzfeldt Jakob disease, and or all the rest of the human TSE prion disease (in this report), and the TSE prion diseases are mounting. with the TSE Prion in cervid aka cwd spreading, science risk factors for human transmission there from increasing. the fact that Texas once again detected another mad cow recently, except this time it was detected by way of one sorghum DDGS sample out of 168 DG samples was contaminated with bovine spongiform encephalopathy, but the transmission route of the bovine spongiform encephalopathy agent could not be clearly defined, (shocking) which shows this damn disease is still out there lingering, spreading, mounting, and the USA government, in my opinion, still acts like (publically), that it’s still not here. I have a serious problem with this. you should too. Bottom line here, I think that whatever the TSE prion funding has come forth to date, needs to be drastically increased, along with Alzheimer’s, one mind find the cause and cure for the other, you never know. but not near enough funding is going toward the sporadic creutzfeldt jakob disease, the 85%+ of all human tse prion.
 
what is Alzheimer’s disease, and is it transmissible? I am going to keep asking this till you folks do the studies...
 
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 ??? ***
 
 
Thursday, October 1, 2015
 
*** Alzheimergate, re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy, Singeltary Submission to Nature ***
 
 
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 ;
 
 
 
*** TEXAS One sorghum DDGS sample out of 168 DG samples was contaminated with bovine spongiform encephalopathy, but the transmission route of the bovine spongiform encephalopathy agent could not be clearly defined. ***
 
 
J Food Prot. 2015 Oct;78(10):1861-9. doi: 10.4315/0362-028X.JFP-15-157.
 
Sunday, September 27, 2015
 
TEXAS CONFIRMATION OF BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION IN ONE SAMPLE OF SORGHUM DDGS OUT OF 168 DG SAMPLES
 
 
 
the fact Texas recently confirmed a case of nvCJD that travel did not include Europe or Saudi;
 
Sunday, November 23, 2014
 
*** Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas in June 2014 confirmed as USA case NOT European ***
 
the patient had resided in Kuwait, Russia and Lebanon. The completed investigation did not support the patient's having had extended travel to European countries, including the United Kingdom, or travel to Saudi Arabia. The specific overseas country where this patient’s infection occurred is less clear largely because the investigation did not definitely link him to a country where other known vCJD cases likely had been infected.
 
 
P.86:
 
Estimating the risk of transmission of BSE and scrapie to ruminants and humans by protein misfolding cyclic amplification
 
Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama National Institute of Animal Health; Tsukuba, Japan
 
To assess the risk of the transmission of ruminant prions to ruminants and humans at the molecular level, we investigated the ability of abnormal prion protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding cyclic amplification (PMCA). Six rounds of serial PMCA was performed using 10% brain homogenates from transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc seed from typical and atypical BSE- or typical scrapie-infected brain homogenates from native host species. In the conventional PMCA, the conversion of PrPC to PrPres was observed only when the species of PrPC source and PrPSc seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested prion strains. On the other hand, human PrPC was converted by PrPSc from typical and H-type BSE in this PMCA condition. Although these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice, ***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
 
================
 
 
 
Thursday, October 1, 2015
 
H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism: clinical and pathologic features in wild-type and E211K cattle following intracranial inoculation
 
 
Saturday, September 12, 2015
 
The Canadian Management of Bovine Spongiform Encephalopathy in Historical and Scientific Perspective, 1990-2014
 
>>>We propose that Canadian policies largely ignored the implicit medical nature of BSE, treating it as a purely agricultural and veterinary issue. In this way, policies to protect Canadians were often delayed and incomplete, in a manner disturbingly reminiscent of Britain’s failed management of BSE. Despite assurances to the contrary, it is premature to conclude that BSE (and with it the risk of variant Creutzfeldt-Jakob disease) is a thing of Canada’s past: BSE remains very much an issue in Canada’s present. <<<
 
 
Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle
 
Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
 
snip...
 
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
 
 
In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells
 
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ...
 
 
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
 
 
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;
 
 
We have shown that cattle-adapted TME is the third cattle prion strain (joining classical and L-type BSE) to be transmissible both to non-human primates and transgenic mice overexpressing human PrP. However, the successful transmission of raccoon TME to primate, inducing a disease with similar features as cattle TME, extends this notion to TME-related strains independent of host origin. Pathological, biochemical and bioassay investigations converged to demonstrate the similarity between cattle-adapted TME and L-BSE.
 
 
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations
 
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France
 
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. *** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, ***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold longe incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), ***is the third potentially zoonotic PD (with BSE and L-type BSE), ***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
 
===============
 
***thus questioning the origin of human sporadic cases...TSS
 
===============
 
 
2014
 
***Moreover, L-BSE has been transmitted more easily to transgenic mice overexpressing a human PrP [13,14] or to primates [15,16] than C-BSE.
 
***It has been suggested that some sporadic CJD subtypes in humans may result from an exposure to the L-BSE agent.
 
*** Lending support to this hypothesis, pathological and biochemical similarities have been observed between L-BSE and an sCJD subtype (MV genotype at codon 129 of PRNP) [17], and between L-BSE infected non-human primate and another sCJD subtype (MM genotype) [15].
 
snip...
 
 
Monday, October 10, 2011
 
EFSA Journal 2011 The European Response to BSE: A Success Story
 
snip...
 
EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far
 
*** but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded.
 
*** Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.
 
snip...
 
 
 
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
 
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
 
O18
 
Zoonotic Potential of CWD Prions
 
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1, Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy, 3Encore Health Resources, Houston, Texas, USA
 
*** These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.
 
==================
 
***These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.***
 
==================
 
P.105: RT-QuIC models trans-species prion transmission
 
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover Prion Research Center; Colorado State University; Fort Collins, CO USA
 
Conversely, FSE maintained sufficient BSE characteristics to more efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was competent for conversion by CWD and fCWD.
 
***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.
 
================
 
***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.***
 
================
 
 
PRION2013 CONGRESSIONAL ABSTRACTS CWD
 
Sunday, August 25, 2013
 
HD.13: CWD infection in the spleen of humanized transgenic mice
 
Liuting Qing and Qingzhong Kong
 
Case Western Reserve University; Cleveland, OH USA
 
Chronic wasting disease (CWD) is a widespread prion disease in free-ranging and captive cervid species in North America, and there is evidence suggesting the existence of multiple CWD strains. The susceptibility of human CNS and peripheral organs to the various CWD prion strains remains largely unclear. Current literature suggests that the classical CWD strain is unlikely to infect human brain, but the potential for peripheral infection by CWD in humans is unknown. We detected protease-resistant PrpSc in the spleens of a few humanized transgenic mice that were intracerebrally inoculated with natural CWD isolates, but PrpSc was not detected in the brains of any of the CWD-inoculated mice. ***Our ongoing bioassays in humanized Tg mice indicate that intracerebral challenge with such PrpSc-positive humanized mouse spleen already led to prion disease in most animals. ***These results indicate that the CWD prion may have the potential to infect human peripheral lymphoid tissues.
 
Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of the ability of sheep, cattle and deer prion disease isolates to convert normal human prion protein to its pathological isoform in a cell-free system
 
Marcelo A.Barria,1 Aru Balachandran,2 Masanori Morita,3 Tetsuyuki Kitamoto,4 Rona Barron,5 Jean Manson,5 Richard Kniqht,1 James W. lronside1 and Mark W. Head1
 
1National CJD Research and Surveillance Unit; Centre for Clinical Brain Sciences; School of Clinical Sciences; The University of Edinburgh; Edinburgh, UK; 2National and OIE Reference Laboratory for Scrapie and CWD; Canadian Food Inspection Agency; Ottawa Laboratory; Fallowfield. ON Canada; 3Infectious Pathogen Research Section; Central Research Laboratory; Japan Blood Products Organization; Kobe, Japan; 4Department of Neurological Science; Tohoku University Graduate School of Medicine; Sendai. Japan; 5Neurobiology Division; The Roslin Institute and R(D)SVS; University of Edinburgh; Easter Bush; Midlothian; Edinburgh, UK
 
Background. Bovine spongiform encephalopathy (BSE) is a known zoonotic prion disease, resulting in variant Creurzfeldt- Jakob disease (vCJD) in humans. In contrast, classical scrapie in sheep is thought to offer little or no danger to human health. However, a widening range of prion diseases have been recognized in cattle, sheep and deer. The risks posed by individual animal prion diseases to human health cannot be determined a priori and are difficult to assess empirically. The fundamemal event in prion disease pathogenesis is thought to be the seeded conversion of normal prion protein (PrPC) to its pathological isoform (PrPSc). Here we report the use of a rapid molecular conversion assay to test whether brain specimens from different animal prion diseases are capable of seeding the conversion of human PrPC ro PrPSc.
 
Material and Methods. Classical BSE (C-type BSE), H-type BSE, L-type BSE, classical scrapie, atypical scrapie, chronic wasting disease and vCJD brain homogenates were tested for their ability to seed conversion of human PrPC to PrPSc in protein misfolding cyclic amplification (PMCA) reactions. Newly formed human PrPSc was detected by protease digestion and western blotting using the antibody 3F4.
 
Results. C-type BSE and vCJD were found to efficiently convert PrPC to PrPSc. Scrapie failed to convert human PrPC to PrPSc. Of the other animal prion diseases tested only chronic wasting disease appeared to have the capability ro convert human PrPC to PrPSc. The results were consistent whether the human PrPC came from human brain, humanised transgenic mouse brain or from cultured human cells and the effect was more pronounced for PrPC with methionine at codon 129 compared with that with valine.
 
Conclusion. Our results show that none of the tested animal prion disease isolates are as efficient as C-type BSE and vCJD in converting human prion protein in this in vitro assay. ***However, they also show that there is no absolute barrier ro conversion of human prion protein in the case of chronic wasting disease.
 
PRION2013 CONGRESSIONAL ABSTRACTS CWD
 
Sunday, August 25, 2013
 
***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission
 
 
cwd to humans ???
 
there has been no official documentation of cwd to humans on paper, to date.
 
cwd transmission studies on humans are illegal.
 
cwd transmits freely to the squirrel monkey, but not yet to the macaque, and the macaque is a bit closer to humans than the squirrel monkey.
 
still, with cwd freely transmitting to the squirrel monkey, scientist are very concerned about the cwd to human risk factor, exposure, and potential iatrogenic transmission there from.
 
85% of human TSE is sporadic cjd, and each and every one of them are up for debate as to route and source. I believe that friendly fire (iatrogenic) or the pass it forward mode of the TSE prion will be a large portion of that. all iatrogenic cjd is, is sporadic cjd until the iatrogenic event is discovered, documented, put into the academic and then the public domain, which very seldom happens due to lack of trace back efforts.
 
see what the authors said about this casual link with cwd to human with the case of Jeffrey Schwan 26 year old, and personal communications years ago with cdc about that case. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”
 
From: Terry S. Singeltary Sr.
 
Sent: Saturday, November 15, 2014 9:29 PM
 
To: Terry S. Singeltary Sr.
 
Subject: THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE R. G. WILL 1984
 
THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE
 
R. G. WILL
 
1984
 
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). (SEE LINK IN REPORT HERE...TSS) PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;
 
snip...
 
 
I urge everyone to watch this video closely...terry
 
*** you can see video here and interview with Jeff's Mom, and scientist telling you to test everything and potential risk factors for humans ***
 
 
July's Milwaukee Journal Sentinel article did prod state officials to ask CDC to investigate the cases of the three men who shared wild game feasts. The two men the CDC is still investigating were 55 and 66 years old. But there's also Kevin Boss, a Minnesota hunter who ate Barron County venison and died of CJD at 41. And there's Jeff Schwan, whose Michigan Tech fraternity brothers used to bring venison sausage back to the frat house. His mother, Terry, says that in May 2001, Jeff, 26, began complaining about his vision. A friend noticed misspellings in his e-mail, which was totally unlike him. Jeff began losing weight. He became irritable and withdrawn. By the end of June, he couldn't remember the four-digit code to open the garage door or when and how to feed his parents' cats. At a family gathering in July, he stuck to his parents and girlfriend, barely talking. "On the night we took him to the hospital, he was speaking like he was drunk or high and I noticed his pupils were so dilated I couldn't see the irises," his mother says. By then, Jeff was no longer able to do even simple things on his computer at work, and "in the hospital, he couldn't drink enough water." When he died on September 27, 2001, an autopsy confirmed he had sporadic CJD.
 
In 2000, Belay looked into three CJD cases reported by The Denver Post, two hunters who ate meat from animals killed in Wyoming and the daughter of a hunter who ate venison from a plant that processed Colorado elk. All three died of CJD before they were 30 years old. The CDC asked the USDA to kill 1,000 deer and elk in the area where the men hunted. Belay and others reported their findings in the Archives of Neurology, writing that although "circumstances suggested a link between the three cases and chronic wasting disease, they could find no 'causal' link." Which means, says Belay, "not a single one of those 1,000 deer tested positive for CWD. For all we know, these cases may be CWD. What we have now doesn't indicate a connection. That's reassuring, but it would be wrong to say it will never happen."
 
So far, says NIH researcher Race, the two Wisconsin cases pinpointed by the newspaper look like spontaneous CJD. "But we don't know how CWD would look in human brains. It probably would look like some garden-variety sporadic CJD." What the CDC will do with these cases and four others (three from Colorado and Schwan from Upper Michigan), Race says, is "sequence the prion protein from these people, inject it into mice and wait to see what the disease looks like in their brains. That will take two years."
 
CJD is so rare in people under age 30, one case in a billion (leaving out medical mishaps), that four cases under 30 is "very high," says Colorado neurologist Bosque. "Then, if you add these other two from Wisconsin [cases in the newspaper], six cases of CJD in people associated with venison is very, very high." Only now, with Mary Riley, there are at least seven, and possibly eight, with Steve, her dining companion. "It's not critical mass that matters," however, Belay says. "One case would do it for me." The chance that two people who know each other would both contact CJD, like the two Wisconsin sportsmen, is so unlikely, experts say, it would happen only once in 140 years.
 
Given the incubation period for TSEs in humans, it may require another generation to write the final chapter on CWD in Wisconsin. "Does chronic wasting disease pass into humans? We'll be able to answer that in 2022," says Race. Meanwhile, the state has become part of an immense experiment.
 
 
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
 
 
*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies. ***
 
 
*** IF CWD is not a risk factor for humans, then I guess the FDA et al recalled all this CWD tainted elk tenderloin (2009 Exotic Meats USA of San Antonio, TX) for the welfare and safety of the dead elk. ...tss
 
Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin Because It May Contain Meat Derived From An Elk Confirmed To Have Chronic Wasting Disease
 
Contact: Exotic Meats USA 1-800-680-4375
 
FOR IMMEDIATE RELEASE -- February 9, 2009 -- Exotic Meats USA of San Antonio, TX is initiating a voluntary recall of Elk Tenderloin because it may contain meat derived from an elk confirmed to have Chronic Wasting Disease (CWD). The meat with production dates of December 29, 30 and 31, 2008 was purchased from Sierra Meat Company in Reno, NV. The infected elk came from Elk Farm LLC in Pine Island, MN and was among animals slaughtered and processed at USDA facility Noah’s Ark Processors LLC.
 
Chronic Wasting Disease (CWD) is a fatal brain and nervous system disease found in elk and deer. The disease is caused by an abnormally shaped protein called a prion, which can damage the brain and nerves of animals in the deer family. Currently, it is believed that the prion responsible for causing CWD in deer and elk is not capable of infecting humans who eat deer or elk contaminated with the prion, but the observation of animal-to-human transmission of other prion-mediated diseases, such as bovine spongiform encephalopathy (BSE), has raised a theoretical concern regarding the transmission of CWD from deer or elk to humans. At the present time, FDA believes the risk of becoming ill from eating CWD-positive elk or deer meat is remote. However, FDA strongly advises consumers to return the product to the place of purchase, rather than disposing of it themselves, due to environmental concerns.
 
Exotic Meats USA purchased 1 case of Elk Tenderloins weighing 16.9 lbs. The Elk Tenderloin was sold from January 16 – 27, 2009. The Elk Tenderloins was packaged in individual vacuum packs weighing approximately 3 pounds each. A total of six packs of the Elk Tenderloins were sold to the public at the Exotic Meats USA retail store. Consumers who still have the Elk Tenderloins should return the product to Exotic Meats USA at 1003 NE Loop 410, San Antonio, TX 78209. Customers with concerns or questions about the Voluntary Elk Recall can call 1-800-680-4375. The safety of our customer has always been and always will be our number one priority.
 
Exotic Meats USA requests that for those customers who have products with the production dates in question, do not consume or sell them and return them to the point of purchase. Customers should return the product to the vendor. The vendor should return it to the distributor and the distributor should work with the state to decide upon how best to dispose. If the consumer is disposing of the product he/she should consult with the local state EPA office.
 
#
 
RSS Feed for FDA Recalls Information11 [what's this?12]
 
 
Thursday, May 26, 2011
 
Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.
 
 
now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”
 
From: TSS (216-119-163-189.ipset45.wt.net)
 
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
 
Date: September 30, 2002 at 7:06 am PST
 
From: "Belay, Ermias"
 
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
 
Sent: Monday, September 30, 2002 9:22 AM
 
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
 
Dear Sir/Madam,
 
In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
 
Ermias Belay, M.D. Centers for Disease Control and Prevention
 
-----Original Message-----
 
From: Sent: Sunday, September 29, 2002 10:15 AM
 
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
 
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
 
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
 
Thursday, April 03, 2008
 
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
 
snip...
 
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
 
snip... full text ;
 
 
==============================
 
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
 
 
*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.
 
 
Tuesday, September 29, 2015
 
*** Transmission of chronic wasting disease to sentinel reindeer (Rangifer tarandus tarandus) can transmit CWD to naive reindeer both directly and indirectly
 
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
 
 
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
 
 
Sunday, July 26, 2015
 
*** TEXAS IN MELT DOWN MODE OVER CAPTIVE CWD AND THEY ARE PUTTING LIPSTICK ON THAT PIG AND TAKING HER TO THE DANCE LIKE MAD COW DISEASE ***
 
 
Sunday, August 02, 2015
 
TEXAS CWD, Have you been ThunderStruck, deer semen, straw bred bucks, super ovulation, and the potential TSE Prion connection, what if?
 
 
*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.
 
 
 
In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells
 
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ...
 
 
PRICE OF PRION POKER WITH CAPTIVE CERVID GOES UP $$$
 
Tuesday, September 29, 2015
 
*** Transmission of chronic wasting disease to sentinel reindeer (Rangifer tarandus tarandus) can transmit CWD to naive reindeer both directly and indirectly
 
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
 
 
I said 15 years ago or so, and I believe it still holds true today ;
 
just speaking of human TSE's; "different strains (of same disease) in different species (of the same disease), different routes of infection (of same disease), different infectivity levels (dose rate) of the (same disease), different parts of the brain affected (of the same disease), different genetic make-up of humans (with same disease) = different symptoms, different lengths of illness from 1st onset of illness to death, (of the same disease) + different cultures = different geographical locations = different strains (of same disease) the TSE. ...TSS
 
Sunday, August 09, 2009
 
*** CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009
 
 
 
Tuesday, August 18, 2009
 
*** BSE-The Untold Story - joe gibbs and singeltary 1999 – 2009 ***
 
 
Saturday, May 09, 2015
 
Psychiatric Symptoms in Patients With Sporadic Creutzfeldt-Jakob Disease...
 
 
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
 
 
NOW THINK EXPOSURE THERE FROM ALL THE ABOVE, AT A HOSPITAL NEAR YOU, what if ???
 
Saturday, December 13, 2014
 
*** Terry S. Singeltary Sr. Publications TSE prion disease Peer Review ***
 
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
 
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
 
 
snip...
 
 
you all know how many folks out there are hunters and consuming sub-clinical cwd tse prion cervid, then going on down the road to have surgical, dental, diagnostic, donating blood, tissue, etc., and then from there, oh...that’s right, it’s just sporadic CJD $$$
 
all iatrogenic cjd is, is sporadic cjd, until the iatrogenic event is discovered, the iatrogenic event is traced back, the iatrogenic event is investigated, the iatrogenic event is documented, the iatrogenic event is then put in the academic domain, and then the iatrogenic event is put into the public domain...how many times doe this happen$$$...LMAO!
 
this stuff ain’t going no where, and the longer we procrastinate instead of acting, with what we know right now today, the more this tse prion disease will spread.
 
wasted days and wasted nights.
 
the late, great, Dr. Joe Gibbs NIH was right all along, he told me.
 
Master Obi-Wan Kenobi, Kemosabe...THIS IS NOT GOOD GOOSE!...grasshopper...tonto...tss
 
 
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
 
on the bottom...Galveston Bay
 
 
Posted by at No comments:

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
 
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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
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“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

 


 
 
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