Sunday, December 9, 2012

Prions, prionoids and pathogenic proteins in Alzheimer disease

Mini-Review



Prions, prionoids and pathogenic proteins in Alzheimer disease



Volume 7, Issue 1 January/February 2013 Keywords: Alzheimer’s disease, PrP, amyloid-β, pathogenic proteins, prionoids, prions, tau Authors: Karen H. Ashe and Adriano Aguzzi View affiliations Hide affiliations Karen H. Ashe Corresponding author: hsiao005@umn.edu


Adriano Aguzzi Institute of Neuropathology; University Hospital Zurich; Zurich, Switzerland




Abstract:


Like patients with prion disease, Alzheimer patients suffer from a fatal, progressive form of dementia. There is growing evidence that amyloid-β (Aβ) aggregates may be transmissible similar to prions, at least under extreme experimental conditions. However, unlike mice infected with prion protein (PrP) prions, those inoculated with Aβ do not die. The transmission of Aβ and PrP thus differs conspicuously in the neurological effects they induce in their hosts, the difference being no less than a matter of life and death. Far from being a mere academic nuance, this distinction between Aβ and PrP begs the crucial questions of what, exactly, controls prion toxicity and how prion toxicity relates to prion infectivity.



snip...



In prion disease catastrophic brain dysfunction is associated with a global decrease in protein production, resulting from the dysregulation of eIF2a, a mammalian translation initiation factor.23 This fascinating discovery is presumably the mechanism by which PrP prions ultimately induce neurotoxicity.


However, eIF2a is localized within the cytosol whereas infectious prions are extracellular. Therefore, we are still left wondering how prions containing pathologically aggregated PrPSc can possibly exert actions that originate from the extracellular milieu, derange protein folding in the endoplasmic reticulum, induce a surprisingly vigorous unfolded protein response, and eventually quench cytosolic translation of proteins. It is hard not to conclude that eIF2a repression likely represents a downstream effector of a pathogenic cascade that is initiated by molecularly and topologically distant events.


There has been recurrent discussion as to whether the self-replicating material in prion disease (the “prion”) is physically identical with the neurotoxic entity. In this context, John Collinge has recently proposed the term “PrPL” to denote a hypothetical moiety that may be neurotoxic yet differs from PrPSc.24 However, the idea that PrP may produce neurological disease without the generation of infectivity dates back to 1990 when transgenic mice that spontaneously developed prion disease were created. These mice expressed PrP carrying a mutation linked to a familial prion disease, developed ataxia, lethargy and rigidity, and invariably died, but their brains contained few or no infectious prions, suggesting that “an inborn error of PrP metabolism could produce neurologic disease without the generation of infectivity.”25 It is possible, and indeed very likely in our view, that PrPSc and the various non-infectious neurotoxic variants of PrP, which include PrP with supernumerary octapeptide repeats26 and PrP versions with interstitial deletions of the “hinge” region between the unstructured N-terminus and the globular domain,27 activate neurotoxic pathways converging with those triggered by prion infection (Fig. 2).



snip...



In the absence of animal models, harboring Alzheimer-related mutations exclusively, that exhibit the full spectrum of disease, beginning with subtle neuronal dysfunction and culminating with fatal cognitive devastation, the question of whether asymptomatic β-amyloidosis requires Aβ*56 to develop into full-blown Alzheimer disease cannot be addressed experimentally. It is possible that one or more non-prionoid form of Aβ triggers neuronal dysfunction and neurodegeneration in Alzheimer disease. Discovering these pathogenic forms will depend upon the creation of high fidelity model systems of Alzheimer disease.


In bona fide prion diseases, a very large body of evidence links the aggregated form of PrP, PrPSc, to both prion infectivity and prion neurotoxicity. However, non-infectious, yet neurotoxic, variants of PrP occur naturally and more such variants have been constructed experimentally, indicating that the phenotypic expression typical of prion diseases can be triggered by events occurring downstream of prion infection. There is little evidence in mice or humans linking the neurological effects of Aβ to the nucleating forms of this protein, while emerging data point to a specific non-nucleating form of Aβ, Aβ*56, that produces some of the neurological signs of disease. However, Aβ*56 is not sufficient to induce the inexorable neurological deterioration that characterizes Alzheimer disease, indicating that other critical factors or forms of Aβ work in collaboration with Aβ*56 to destroy the brain. Curing prion and Alzheimer disease will depend upon developing a deeper understanding of the pathogenic forms of PrP and Aβ that cause the brain dysfunction underlying these deadly illnesses.




SNIP...SEE FULL TEXT ;












Wednesday, January 18, 2012


Government seeking $1T campaign against Alzheimer's







Monday, September 26, 2011


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







Are some commoner types of neurodegenerative disease (including Alzheimer's disease and Parkinson's disease) also transmissible? Some recent scientific research has suggested this possibility




Wednesday, September 21, 2011


PrioNet Canada researchers in Vancouver confirm prion-like properties in Amyotrophic Lateral Sclerosis (ALS)


Researchers’ Discovery May Revolutionize Treatment of ALS






Friday, September 3, 2010


Alzheimer's, Autism, Amyotrophic Lateral Sclerosis, Parkinson's, Prionoids, Prionpathy, Prionopathy, TSE







Wednesday, September 21, 2011


PrioNet Canada researchers in Vancouver confirm prion-like properties in Amyotrophic Lateral Sclerosis (ALS)









Wednesday, January 5, 2011


ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011 Prions


David W. Colby1,* and Stanley B. Prusiner1,2

















SCENARIO 3: ‘THE THIN STEMMED GLASS’


Sustainable Production and Fragile Markets


Canada


Science


- BSE is not linked to classical CJD, but a TSE is found that is linked to Alzheimer’s disease.


- Science breakthroughs in neurodegenerative diseases.


- New product development continues.








SNIP...SEE FULL TEXT ;



Sunday, December 2, 2012


CANADA 19 cases of mad cow disease SCENARIO 4: ‘WE HAD OUR CHANCE AND WE BLEW IT’






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.









Wednesday, May 16, 2012


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


Proposal ID: 29403







Terry S. Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis













full text with source references ;







14th ICID International Scientific Exchange Brochure - 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 fed 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.











Friday, October 05, 2012




Differential Diagnosis of Jakob-Creutzfeldt Disease










Monday, August 20, 2012



CASE REPORTS CREUTZFELDT-JAKOB DISEASE: AN UNDER-RECOGNIZED CAUSE OF DEMENTIA








see the Duke, Pa, Yale, and Mexican study here, showing the misdiagnosis of CJD TSE prion disease as Alzheimers ;








Letters| February 14, 2001


Diagnosis and Reporting of Creutzfeldt-Jakob Disease


Terry S. Singeltary, Sr


JAMA. 2001;285(6):733-734. doi:10-1001/pubs.JAMA-ISSN-0098-7484-285-6-jlt0214. Text Size: AA A Published online Article References



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.










TSS

Sunday, November 18, 2012

For Alzheimer’s, Detection Advances Outpace Treatment Options

For Alzheimer’s, Detection Advances Outpace Treatment Options



Awilda Jimenez got a scan for Alzheimer’s after she started forgetting things. It was positive.



By GINA KOLATA Published: November 15, 2012





When Awilda Jimenez started forgetting things last year, her husband, Edwin, felt a shiver of dread. Her mother had developed Alzheimer’s in her 50s. Could his wife, 61, have it, too?



He learned there was a new brain scan to diagnose the disease and nervously agreed to get her one, secretly hoping it would lay his fears to rest. In June, his wife became what her doctor says is the first private patient in Arizona to have the test.




“The scan was floridly positive,” said her doctor, Adam S. Fleisher, director of brain imaging at the Banner Alzheimer’s Institute in Phoenix.




The Jimenezes have struggled ever since to deal with this devastating news. They are confronting a problem of the new era of Alzheimer’s research: The ability to detect the disease has leapt far ahead of treatments. There are none that can stop or even significantly slow the inexorable progression to dementia and death.




Families like the Jimenezes, with no good options, can only ask: Should they live their lives differently, get their affairs in order, join a clinical trial of an experimental drug?




“I was hoping the scan would be negative,” Mr. Jimenez said. “When I found out it was positive, my heart sank.”




The new brain scan technology, which went on the market in June, is spreading fast. There are already more than 300 hospitals and imaging centers, located in most major metropolitan areas, that are ready to perform the scans, according to Eli Lilly, which sells the tracer used to mark plaque for the scan.




The scans show plaques in the brain — barnaclelike clumps of protein, beta amyloid — that, together with dementia, are the defining feature of Alzheimer’s disease. Those who have dementia but do not have excessive plaques do not have Alzheimer’s. It is no longer necessary to wait until the person dies and has an autopsy to learn if the brain was studded with plaques.




Many insurers, including Medicare, will not yet pay for the new scans, which cost several thousand dollars. And getting one comes with serious risks. While federal law prevents insurers and employers from discriminating based on genetic tests, it does not apply to scans. People with brain plaques can be denied long-term care insurance.




The Food and Drug Administration, worried about interpretations of the scans, has required something new: Doctors must take a test showing they can read them accurately before they begin doing them. So far, 700 doctors have qualified, according to Eli Lilly. Other kinds of diagnostic scans have no such requirement.




In another unusual feature, the F.D.A. requires that radiologists not be told anything about the patient. They are generally trained to incorporate clinical information into their interpretation of other types of scans, said Dr. R. Dwaine Rieves, director of the drug agency’s Division of Medical Imaging Products.




But in this case, clinical information may lead radiologists to inadvertently shade their reports to coincide with what doctors suspect is the underlying disease. With Alzheimer’s, Dr. Rieves said, “clinical impressions have been misleading.”




“This is a big change in the world of image interpretation,” he said.




Like some other Alzheimer’s experts, Dr. Fleisher used the amyloid scan for several years as part of a research study that led to its F.D.A. approval. Subjects were not told what the scans showed. Now, with the scan on the market, the rules have changed.


Dr. Fleisher’s first patient was Mrs. Jimenez. Her husband, the family breadwinner, had lost his job as a computer consultant when the couple moved from New York to Arizona to take care of Mrs. Jimenez’s mother. Paying several thousand dollars for a scan was out of the question. But Dr. Fleisher found a radiologist, Dr. Mantej Singh Sra of Sun Radiology, who was so eager to get into the business that he agreed to do Mrs. Jimenez’s scan free. His plan was to be the first in Arizona to do a scan, and advertise it.




After Dr. Sra did the scan, the Jimenezes returned to Dr. Fleisher to learn the result.




Dr. Fleisher, sad to see so much plaque in Mrs. Jimenez’s brain, referred her to a psychiatrist to help with anxiety and suggested she enter clinical trials of experimental drugs.


But Mr. Jimenez did not like that idea. He worried about unexpected side effects.


“Tempting as it is, where do you draw the line?” he asks. “At what point do you take a risk with a loved one?”


At Mount Sinai Medical Center in New York, Dr. Samuel E. Gandy found that his patients — mostly affluent — were unfazed by the medical center’s $3,750 price for the scan. He has been ordering at least one a week for people with symptoms ambiguous enough to suggest the possibility of brain plaques.


Most of his patients want their names kept confidential, fearing an inability to get long-term care insurance, or just wanting privacy.








(Page 2 of 2)




A woman from New Zealand was told by one doctor that she had Alzheimer’s and by another that she had frontotemporal dementia, a rare brain disease that strikes people at younger ages than Alzheimer’s and progresses faster. She had a scan. The result was clear — no significant accumulation of plaques. She had frontotemporal dementia. Unfortunately, Dr. Gandy said, there was nothing he could offer her, not even a clinical drug trial.



A man given a diagnosis of Parkinson’s disease was totally immobile and demented. Could he have had Alzheimer’s all along?



A scan showed he did.




Dr. Gandy’s first patient, Alexander Dreyfoos, an 80-year-old electronics engineer and businessman, was one of the very few willing to be open about his experience. He is independently wealthy and was not worried about privacy or insurance.




But he was very worried about Alzheimer’s. His mother, who died at age 79, had it. “I watched her deteriorate to the point where she couldn’t even recognize me,” Mr. Dreyfoos said. And he had begun seeing signs that his memory was slipping.




“A few years ago, I realized I wasn’t at the top of my game,” he said.




Mr. Dreyfoos had his DNA sequenced by a commercial company and learned that he had a gene, ApoE4, that increases the risk of Alzheimer’s. At Massachusetts General Hospital, he learned he had shrinkage of his brain — typical of Alzheimer’s. After doctors tested his memory and reasoning, he said, they told him he was right to worry.




Finally, Mr. Dreyfoos went to Dr. Gandy at Mount Sinai, looking for an experimental treatment for the Alzheimer’s he was sure he had. Dr. Gandy also suspected he had the disease, but suggested a scan.


The scan did not show an abnormal accumulation of amyloid. As far as Dr. Gandy is concerned, Mr. Dreyfoos does not have Alzheimer’s.




Mr. Dreyfoos was surprised, “wonderfully so,” he said.




Dr. Gandy said that as many as 30 percent of people who seem to have Alzheimer’s turn out not to have it when they get the scan. But those who get bad news struggle to cope.




Desperate to slow the progression of his wife’s disease, Mr. Jimenez is now giving her turmeric, coenzyme Q10, astaxanthin, krill oil, ginkgo biloba and coconut oil — remedies he found on the Internet. There is no good evidence they work, and each costs about $5 to $15 a month. But, Mr. Jimenez says: “What am I going to do? People feel so helpless with this disease that they are willing to try anything.”




He worries about the future and how they will survive financially. He wonders if it might have been better not to know the diagnosis.




“It is financially, emotionally and spiritually draining,” Mr. Jimenez said. “Everything hangs by a thread.”










>>> While federal law prevents insurers and employers from discriminating based on genetic tests, it does not apply to scans.




>>> People with brain plaques can be denied long-term care insurance.






THIS IS WRONG !





Review



On the issue of transmissibility of Alzheimer disease: A critical review



November/December 2012


Keywords: Alzheimer, dementia, epidemiology, prion, transmissibility


Authors: Christian Schmidt, André Karch, Carsten Korth and Inga Zerr


Christian Schmidt


Corresponding author: schmidt102@gmail.com


Clinical Dementia Center; Department of Neurology; Georg-August University; Goettingen, Germany


André Karch


Clinical Dementia Center; Department of Neurology; Georg-August University; Goettingen, Germany


Carsten Korth


Department of Neuropathology; Heinrich-Heine University; Duesseldorf, Germany


Inga Zerr


Clinical Dementia Center; Department of Neurology; Georg-August University; Goettingen, Germany



Abstract:


Results from recent experiments with rodents imply that Alzheimer disease might be inducible by seeding Aβ peptides into recipient animals. In respect to this new experimental data, public health aspects as well as epidemiological data have to be reevaluated. In this article, the available experimental and epidemiological data are reviewed.



snip...



In summary, epidemiological evidence is extremely difficult to assess in this context. This is especially true, since case definitions and case detection rates have changed over time. Given the fact that a potential way of transmission is not only unknown but that no way of transmission can be excluded yet, careful assessment is imperative.



Public health implications



In the epidemic of non-communicable diseases AD plays an important role for morbidity and mortality as well as the associated costs. To date, AD is the 6th leading cause of death in the US and the projected costs in the US by 2050 are $1.1 trillion.66



Knowledge about transmissibility is essential in all kinds of epidemics for prevention, diagnosis and treatment. If AD featured transmission patterns comparable with those of prion diseases, iatrogenic induction/transmission would play a major role for public health. Prevention would be first priority and might include measures such as extended sterilization methods for surgical instruments as well as identification of patients potentially posing a risk as well as patients at risk. From a public health perspective also alternate ways of transmission not evaluated yet must be considered. For prevention to work, biomarkers for early disease detection must be validated, independently of the ways of possible induction since the disease itself starts well before clinical onset. As Sigurdsson stated correctly almost 10 years ago, future research on therapies might also be limited as long as there is no convincing evidence against transmissibility of AD.8 This is especially true for vaccination studies and clinical trials using parts of β-amyloid.



Conclusion



In conclusion, with this short review, we want to encourage a broader discussion and modern epidemiological research in this context. Well-designed epidemiologic studies have to be initiated. Methodologically these studies must be constructed to address the epidemiologically challenging aspects of Alzheimer disease such as dissociation between first neuropathological alterations and clinical onset, uncertainties in early diagnosis as well as AD heterogeneity.



This work was supported by a Bundesministerium für Bildung und Forschung grant within the German Network for Degenerative Dementia (KNDD-2, 2012-2015, determinants for disease progression in AD, grant no. 01GI1010C), as well as JPND, EU-FP7 PRIORITY.Authors’ contributions: C.S. was responsible for the initiation of the project, general conception and the composition of the final manuscript. A.K. provided parts of the section on epidemiology. C.K. provided parts of the section on experimental clues regarding AD transmissibility/inducibility. I.Z. was responsible for the initiation of the project, the critical review for contentual errors and writing parts of the conclusion. All authors contributed to the revision of the manuscript. The authors declare no conflicts of interest.







Wednesday, May 16, 2012


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


Proposal ID: 29403






Wednesday, May 16, 2012


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


Proposal ID: 29403


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 disease, and it’s variants, in many cases are merely names of the people that first discovered them. 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 than the TSE prion disease. Symptoms are very similar, and pathology is very similar. 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. today, there is enough documented science (some confidential), that shows that indeed Alzheimer’s is transmissible. The risk factor for friendly fire, and or the pass-it-forward mode i.e. Iatrogenic transmission is a real threat, and one that needs to be addressed immediately.


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


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. TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit. you cannot cook the TSE prion disease out of meat. you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE. Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well. the TSE prion agent also survives Simulated Wastewater Treatment Processes. IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades. you can bury it and it will not go away. TSE prion agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area. it’s not your ordinary pathogen you can just cook it out and be done with. that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.


Conclusions


There should be a Global Congressional Science round table event (one of scientist and doctors et al only, NO CORPORATE, POLITICIANS ALLOWED) 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 let 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. what’s the use of science progressing human life to the century mark, if your brain does not work?







combined cannot exceed 350 Words



shortened to proper word count ;




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




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


source references


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


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







Wednesday, January 5, 2011


ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011 Prions


David W. Colby1,* and Stanley B. Prusiner1,2










Tuesday, October 4, 2011


Molecular Psychiatry


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


De novo induction of amyloid-ß deposition in vivo


Our results suggest that some of the typical brain abnormalities associated with AD can be induced by a prion-like mechanism of disease transmission through propagation of protein misfolding. These findings may have broad implications for understanding the molecular mechanisms responsible for the initiation of AD, and may contribute to the development of new strategies for disease prevention and intervention. Keywords: amyloid; prion; protein misfolding; disease transmission






see more here ;










Wednesday, September 21, 2011


PrioNet Canada researchers in Vancouver confirm prion-like properties in Amyotrophic Lateral Sclerosis (ALS)









snip...end




Thank You for accepting my submission



# 29403, Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ? and the opportunity to present it, at the Alzheimer’s Association International Conference 2012 (AAIC), as a poster presentation. However, with great sadness, I must regretfully decline the invitation due to a medical reasons, and traveling to Canada, of which is not possible. ...


Thank You,



With Kindest Regards,


I am sincerely,


Terry S. Singeltary Sr.


P.O. Box 42


Bacliff, Texas USA 77518






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==========






TSS





UPDATE JUNE 28, 2012



Scottish TSE Network November Symposium Announcement Event: 12 November 2012


Chair: Prof Hugh Perry, University of Southampton, Southampton UK


Location: The Roslin Institute Building Auditorium


If you would like to book a place at this event, please let Gila Holliman know.


Cost: £125.


Title: Is Alzheimer’s Disease a transmissible disease?


Speakers:


Session 1:


Prof Bob Will, National CJD Surveillance Unit, Edinburgh UK


Prof James Ironside, National CJD Surveillance Unit, Edinburgh UK


Prof Lary Walker, Emory School of Medicine, Atlanta USA


Session 2:


Prof Mathias Jucker, Hertie Institute for Clinical Brain Research, Stuttgart Germany


Prof William Van Nostrand, Stony Brook University, Stony Brook USA


Dr Claudio Soto, University of Texas Medical School, Houston USA


Session 3:


Dr Fabrizio Tagliavini, Instituto Neurologico Carlo Besta, Milan Italy


Prof Pedro Piccardo, Food and Drug Administration, Washington DC USA


Dr Bruce Chesebro, National Institutes of Health, Missoula USA








see ;



Wednesday, May 16, 2012



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



Proposal ID: 29403








14th ICID International Scientific Exchange Brochure -


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 fed 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.








Friday, October 05, 2012


Differential Diagnosis of Jakob-Creutzfeldt Disease






Monday, August 20, 2012


CASE REPORTS CREUTZFELDT-JAKOB DISEASE: AN UNDER-RECOGNIZED CAUSE OF DEMENTIA






see the Duke, Pa, Yale, and Mexican study here, showing the misdiagnosis of CJD TSE prion disease as Alzheimers ;






Terry S. Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis










full text with source references ;






re-Human Prion Diseases in the United States Posted by flounder on 01 Jan 2010 at 18:11 GMT


I kindly disagree with your synopsis for the following reasons ;






Tuesday, November 08, 2011


Can Mortality Data Provide Reliable Indicators for Creutzfeldt-Jakob Disease Surveillance? A Study in France from 2000 to 2008 Vol. 37, No. 3-4, 2011 Original Paper


Conclusions:These findings raise doubt about the possibility of a reliable CJD surveillance only based on mortality data.






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?






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








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.






Saturday, January 2, 2010


Human Prion Diseases in the United States January 1, 2010 ***FINAL***







Monday, March 29, 2010


CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER URGENT, PLEASE NOTE ;



>>> Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. <<<




Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010 in Mesquite Texas.


She left 6 Kids and a Husband.The Purpose of this web is to give information in Spanish to the Hispanic community, and to all the community who want's information about this terrible disease.- Physician Discharge Summary, Parkland Hospital, Dallas Texas Admit Date: 12/29/2009 Discharge Date: 1/20/2010 Attending Provider: Greenberg, Benjamin Morris; General Neurology Team: General Neurology Team Linda was a Hispanic female with no past medical history presents with 14 months of incresing/progressive altered mental status, generalized weakness, inability to walk, loss of appetite, inability to speak, tremor and bowel/blader incontinence. She was, in her usual state of health up until February, 2009, when her husbans notes that she began forgetting things like names and short term memories. He also noticed mild/vague personality changes such as increased aggression. In March, she was involved in a hit and run MVA,although she was not injured. The police tracked her down and ticketed her. At that time, her son deployed to Iraq with the Army and her husband assumed her mentation changes were due to stress over these two events. Also in March, she began to have weakness in her legs, making it difficult to walk. Over the next few months, her mentation and personality changes worsened, getting to a point where she could no longer recognized her children. She was eating less and less. She was losing more weight. In the last 2-3 months, she reached the point where she could not walk without an assist, then 1 month ago, she stopped talking, only making grunting/aggressive sounds when anyone came near her. She also became both bowel and bladder incontinent, having to wear diapers. Her '"tremor'" and body jerks worsened and her hands assumed a sort of permanent grip position, leading her family to put tennis balls in her hands to protect her fingers. The husband says that they have lived in Nebraska for the past 21 years. They had seen a doctor there during the summer time who prescribed her Seroquel and Lexapro, Thinking these were sx of a mood disorder. However, the medications did not help and she continued to deteriorate clinically. Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. The husband says that he does not know any fellow workers with a similar illness. He also says that she did not have any preceeding illness or travel.








Friday, August 24, 2012


Iatrogenic prion diseases in humans: an update






Thursday, April 12, 2012


Health professions and risk of sporadic Creutzfeldt–Jakob disease, 1965 to 2010


Eurosurveillance, Volume 17, Issue 15, 12 April 2012


Research articles


snip...


In 2009, a pathologist with sporadic Creutzfeldt–Jakob Disease (sCJD) was reported to the Spanish registry. This case prompted a request for information on health-related occupation in sCJD cases from countries participating in the European Creutzfeldt Jakob Disease Surveillance network (EuroCJD). Responses from registries in 21 countries revealed that of 8,321 registered cases, 65 physicians or dentists, two of whom were pathologists, and another 137 healthcare workers had been identified with sCJD. Five countries reported 15 physicians and 68 other health professionals among 2,968 controls or non-cases, suggesting no relative excess of sCJD among healthcare professionals. A literature review revealed: (i) 12 case or small case-series reports of 66 health professionals with sCJD, and (ii) five analytical studies on health-related occupation and sCJD, where statistically significant findings were solely observed for persons working at physicians' offices (odds ratio: 4.6 (95 CI: 1.2–17.6)). We conclude that a wide spectrum of medical specialities and health professions are represented in sCJD cases and that the data analysed do not support any overall increased occupational risk for health professionals. Nevertheless, there may be a specific risk in some professions associated with direct contact with high human-infectivity tissue.


snip...







Friday, August 10, 2012


Incidents of Potential iatrogenic Creutzfeldt-Jakob disease (CJD) biannual update (July 2012)






Wednesday, January 5, 2011


ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011


Prions


David W. Colby1,* and Stanley B. Prusiner1,2






Monday, March 26, 2012


CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE


OR-09 15:10 - 15:25


CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE






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



*** Saturday, October 6, 2012


*** TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES 2011 Annual Report






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


MOM DOD 12/14/97 hvCJD confirmed, Uncle Bo DOD today 10/13/12 RIP with severe and rapid last two weeks Alzheimer’s, he was fishing off pier two weeks ago, hospice 3 days ago, to DOD TODAY (no brain autopsy)?, Mema passed with moderate to slow dementia type Alzheimer’s, wonder what kind of dementia I will get ?


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








Saturday, October 13, 2012


On the issue of transmissibility of Alzheimer disease: A critical review








A VERY IMPORTANT FACTOR that must be weighed in on, HEALTH INSURANCE COMPANIES. IF there is not a provision, clause, that stipulates that being placed AT RISK OF CREUTZFELDT JAKOB DISEASE, would NOT blackball you i.e. MARK you, that NOT in any way can discriminate against you because of the disease, that NOT in any way would jeopardize or enhance cost for health insurance for anyone being placed 'AT RISK'.







Subject: Lord Lucas asked Her Majesty's Government about insurance company's and CJD???

Date: Thu, 6 Apr 2000 09:49:14 -0700

From: "Terry S. Singeltary Sr."

Reply-To: Bovine Spongiform Encephalopathy

To: BSE-L@uni-karlsruhe.de


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



Greetings Everyone,  



I am deeply concerned about the answer given to Lord Lucas on CJD and
insurance company's. In Her Majesty's reply, the reason given for
insurance company's _not_ being able to require candidates for life
insurance to be tested for incipient nvCJD or any human TSE, was because there is no test to date, that would allow them to test.



My question to Her Majesty's Court would have been;
when such a test is available, will the insurance company's be allowed
to test for human TSE's?



It seems Lord Lucas question was not answered fully, it seems Her
Majesty's Court just went around the question.



If in fact, the insurance company's are allowed to do this, once again
the people would have been deceived by their government, for the sake
of money, greed, and corporate industry$$$ This would be devastating
to the people, not only have they been murdered by corporate greed,
but they then would be sold out, for corporate greed. It's a no-win
situation for public consumers...



kind regards,
 

Terry S. Singeltary Sr., Bacliff, Texas USA





April 4, 2000

Lord Lucas asked Her Majesty's Government:


Whether they will permit insurance companies to require that candidates for life insurance be tested for incipient
new-variant CJD.[HL1661]




Lord Hunt of Kings Heath: Insurance companies would be unable to
introduce such a step, as no acceptable test currently exists for the demonstration of infection before the onset of clinical
symptoms.







Subject: Re: re-Lord Lucas U.K. Government sells out CJD victims (and others)'again' / U.K. Government O.K.'s Genetic testing for Insurers, looking for hereditary illnesses


Date: Fri, 13 Oct 2000 09:37:22 -0700

From: "Terry S. Singeltary Sr."


Reply-To: Bovine Spongiform Encephalopathy


To: BSE-L@uni-karlsruhe.de

References: 1



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



first Huntington's, then CJD, then another, and so on.
what needs to take place, is everyone drop their insurance.
once you give these people an opening, it's like a hole in
a dam, there is no closing it, and it just gets bigger and
bigger. This is a serious breach of human ethics, all for the
almighty dollar$$$




kind regards,

Terry




 
DEPARTMENT OF HEALTH 2000/0580 Friday 13th October 2000 COMMITTEE ANNOUNCES DECISION ON USE OF GENETIC TEST
RESULTS FOR HUNTINGTON'S DISEASE BY INSURERS




The Genetics and Insurance Committee (GAIC) has today announced that
the reliability and relevance of the genetic test for Huntington's
Disease is sufficient for insurance companies to use the result when
assessing applications for life insurance.




Professor John Durant, Chairman of GAIC said:  

"Genetic test results are already used in certain circumstances by
insurers and the Committee was asked to look at the reliability and
accuracy of the genetic test for Huntington's Disease. We have
considered carefully the application received from the Association of
British Insurers for approval of the use of these tests.
The evidence presented demonstrates that the two tests for the
Huntington's gene are reliable and that an abnormal result is
associated with significant clinical effects and with an increased
probability of a claim on a life insurance policy. This decision
will mean that those with a negative test result will not be asked to
pay more for life insurance because of their family history of
HuntingtonÆs disease.



"This decision does not mean that individuals will be asked to have a
genetic test for Huntington's Disease before obtaining insurance but,
where individuals have already been tested as part of their medical
care, then there is nothing to prevent insurance companies asking for
that information.



"Many who have a family history of a genetic disorder such as
Huntington's Disease have difficulty in obtaining insurance because
of their family history. The approval of the two tests for
Huntington's Disease will allow insurance to be provided at normal
rates to those who have a normal test result."



A significant amount of data has been collected concerning the
effects of Huntington's Disease on life expectancy and on mortality
risk as part of the process of reviewing this application. The
Committee hopes that the insurance industry will use this information
to look at the problems of those who have an abnormal genetic test
result and of those who have chosen not to have a genetic test (who
have a 50 % chance of carrying the abnormal gene if they have an
affected parent).



The GAIC was asked to examine the actuarial evidence for using
individual genetic tests. The insurance industry, through the main
trade body the Association of British Insurers, has agreed to abide
by GAIC decisions. If GAIC decides that the evidence on the
reliability and relevance of a particular test is insufficient to
justify its use, the Association have agreed to stop using them and
retrospectively reassess affected individual insurance premiums. The
broader social and ethical issues surrounding the use of genetic
tests in insurance and employment have been referred to the new Human
Genetics Commission.



An application for approval of two genetic tests for Huntington's
Disease was submitted to GAIC by the Association of British Insurers
(ABI) in July 2000. The application was sent to a clinical
geneticist and an independent actuary for expert review and also to
support groups for Huntington's Disease and to the Genetic Interest
Group (GIG) for their comments. At their meeting on 28 September,
GAIC considered the application, in the presence of observers from
the ABI, GIG and Huntington's Disease Association. Their decision is
announced today.



The committee recognises that this complex subject is an important
issue to the public, industry and government alike. GAIC will work
closely with the new Human Genetics Commission when they begin their
inquiry into the use of genetic data including in insurance and
employment later this year.



Notes to Editors:   A summary of the decision and further details about GAIC and the
application process are available on the Department of Health web
site at www.doh.gov.uk/genetics/gaic.htm




The establishment of the Genetics and Insurance Committee (GAIC) on
12 April 1999 fulfilled the Government's commitment to establish an
independent review body, to evaluate the scientific and actuarial
evidence presented in support of the use of specific genetic tests
for insurance products. This was made in response to the Human
Genetics Advisory Commission (HGAC) report on the Implications of
Genetic Testing for the Insurance Industry, issued in December 1998.

GAIC is a non-statutory Advisory Committee and has a UK-wide remit.
Its terms of reference are:




- to develop and publish criteria for the evaluation of specific
genetic tests, their application to particular conditions and their
reliability and relevance to particular types of insurance;
- to evaluate
particular tests against those criteria and promulgate
its findings;




- to report to Health, Treasury and Department of Trade and Industry
Ministers on proposals received by GAIC from insurance providers and
the subsequent level of compliance by the industry with the
recommendations of GAIC.




The core membership of GAIC is:   Professor John Durant, Chief Executive of At-Bristol as Chairman, appointed from amongst the members of Advisory Committee on Genetic Testing;



Professor Sandy Raeburn, a geneticist nominated by the Association of
British Insurers (ABI);




Professor Dian Donnai a geneticist nominated by CMO (England); Dr David Muiry, an Actuary nominated by the Faculty and Institute of
Actuaries;




Mr Anthony OÆLeary, an Insurance Practitioner nominated by the ABI; Mrs Susan Watkin and Mrs Barbara Carmichael, members of Patient
Support Organisations nominated by the Genetic Interest Group;
Professor Tim Bishop, an academic with a background in epidemiology
and genetics nominated by the Director of Research, Department of
Health.




GAIC has published evaluation criteria covering the details of the
genetic condition being tested for, the accuracy and reliability of
the tests used to detect it and the relevance of the test results to
decisions about insurance underwriting. GAIC expects that
applications will be for genetic conditions caused by changes in a
single gene, that are very likely to lead to serious ill health or
disability and that are therefore most relevant to the setting of
premiums for life and health insurance.




Over the next few months, GAIC will consider applications relating to
the conditions currently covered by the Association for British
Insurers' Code of Practice on Genetic Testing. These include
Huntington's Disease, myotonic dystrophy, the early-onset form of
Alzheimer's disease and rare inherited cancers. The intention is to
complete review these applications by June 2001.




The Human Genetics Commission, chaired by Baroness Helena Kennedy,
was created in 1999 to provide the Government with strategic advice
on the wider implications of human genetics. It replaces three former
committees and is responsible for making links between all the other
relevant bodies in the advisory and regulatory framework. Further
information can be found at www.hgc.gov.uk




HGC has been formulating a public consultation exercise on the
storage, protection and use of personal genetic information which
will include the use of genetic data for insurance purposes. The
issues are due to be discussed at a public consultative meeting at
the Centre for Life, Newcastle-upon-Tyne in November 2000.




"Terry S. Singeltary Sr." wrote:

 

>
> ######### Bovine Spongiform Encephalopathy #########
>
> Greetings List,
>
> Talk about something that really stinks, this does. First
> the U.K. Government allows the Industry's involved to continue
> to murder (God only knows how many). Then they don't support them,
> and to top it off, they then allow the only hope one has to
> get any kind of medical care, they allow the insurers to bail
> out on victims of this man-made blunder. I thought Lord Lucas
> asked this question to Her Majesty's Court, and Her Majesty's
> Court said;
>
> ######### Bovine Spongiform Encephalopathy
> #########
>
> They replied that as there was no test they could not test, so the
> question did not arise!
>
> Ralph
>
> > Did I miss something or have they not yet responded to this one?
> >
> > Question 20: Whether they will permit insurance companies to require > that
> > customers be tested for incipient nvCJD.
>
> Dear Lord Lucas,
>
> the question has arised again, and should be confronted.
> may i suggest that you ask this question again. it would seem,
> with a test so close to come about for the testing of TSE's,
> one would think, they are just preparing for the worse, and
> covering their butts, at the same time.
>
> Politics as usual, but my God, have not these people suffered
> enough, without the Governments completely stripping them
> from any help at all. Hell, you should just take them out back
> and shoot them........
>
> kind regards,
> Terry S. Singeltary Sr., Bacliff, Texas USA
> ===========================================
>
> Thursday, 12 October, 2000, 11:28 GMT 12:28
> UK Genetic test first for UK
>
> Genetic tests can predict future illness
> Insurers in the UK are to be allowed to use
> genetic test results to identify people with
> hereditary illnesses.
>
> The government will announce on Friday that
> insurers will be able to use those results to
> refuse cover or to push up premiums for those
> born with genes that could lead to fatal
> conditions.
>
> The decision makes Britain the first country to
> approve the commercial use of gene
> technology in this way.
>
> The Genetics and
> Insurance Committee,
> an advisory body
> reporting to the
> Department of Health,
> has decided that a test
> used to identify a
> hereditary risk of
> contracting the disease
> Huntington's chorea is
> technically reliable.
>
> Tests covering several other conditions,
> including hereditary breast cancer and
> Alzheimer's disease, are also awaiting approval.
>
> Two years ago another advisory body, the
> Human Genetics Advisory Commission,
> recommended a moratorium on the use of
> information from such tests.
>
> However, that advice was rejected by the
> government, which decided insurers should be
> able to use such information, subject to the
> Genetics and Insurance Committee agreeing a
> test's technical reliability.
>
> The announcement is likely to fuel the ethical
> debate over the use of genetic information.
>
> Critics fear that vulnerable groups could find it
> difficult to get a mortgage or life insurance, or
> face higher premiums.
>
> But the insurance industry dismissed that
> suggestion.
>
> No compulsion
>
> Professor John Durant, chairman of the
> Genetics and Insurance Committee, told the
> BBC that nobody would be asked to take a
> genetic test by an insurance company.
>
> Rather they would be
> expected to disclose
> the results of any
> genetic test for
> Huntington's disease
> they had taken in the
> past.
>
> Professor Durant said
> this would not be a
> legal obligation, but
> insurance companies
> would have the right to
> refuse to offer
> insurance if a customer
> refused to reveal details.
>
> He said: "It is not a punitive step. This will
> actually benefit very many people seeking
> insurance.
>
> "The only people who are likely to have taken
> a test for Huntington's disease are people with
> a family history of this disease.
>
> "Many of those people will actually have had
> results which show that they are fortunate
> enough not to have inherited the gene, so
> those people will be able to get insurance, at
> the moment they may well find it difficult."
>
> Mary Francis, the Director-General of the
> Association of British Insurers, said that
> companies already asked potential customers
> about family history of disease.
>
> She said: "This is really an extension of what
> already does happen."
>
> Sue Watkin, chair of
> the Huntington's
> Disease Association,
> also said insurance
> companies were already
> using genetic test
> results to calculate or
> refuse premiums.
>
> She said: "Our main concern is that people at
> risk of late onset genetic disorders should be
> able to get insurance of some kind up to a
> certain level.
>
> "At present, many people are made offers they
> just cannot afford."
>
> Ms Watkin said that a person at 50% risk of
> developing Huntington's often found their
> insurance premium loaded by as much as
> 300%.
>
> She called on the government to establish a
> fund to be used to provide insurance for
> people at risk.
>
> The National Consumers' Council is concerned
> people will be put off having tests because
> they feared that the results might count
> against them - with a possible knock-on effect
> on their health.
>
> A spokeswoman said: "A person might think if I
> take a test I will know information that I don't
> know now, and maybe ignorance is bliss.
>
> "If you don't know the information you can't
> put it on the form."
>
> The Human Genetics Commission, another
> government advisory body overseeing
> developments in the use of genetic
> technology, said that it would launch shortly a
> major public consultation exercise about the
> use and protection of genetic information,
> which would include insurance issues.
>
> The exercise would eventually result in the
> Commission making recommendations to
> ministers.
>
> http://news.bbc.co.uk/hi/english/health/newsid_968000/968443.stm
>



END...TSS



Subject: Re: CJD $ BLOOD $ Schmerr test$$$
 

Date: Wed, 18 Oct 2000 11:01:01 -0700

From: "Terry S. Singeltary Sr."

Reply-To: Bovine Spongiform Encephalopathy

To: BSE-L@uni-karlsruhe.de


References: 1


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


Greetings again List Members,  



it just hit me about the blood testing. bought knocked me out of the
chair. could it be, the reason they have stalled the blood testing, they
are waiting for the genetic testing to be perfected for the insurance
company's. once perfected and implemented, and no risk of any type
medical insurance coverage for TSE patients, then they will be allowed
to go ahead with the blood tests for human TSE's. pretty smart huh, they
don't pay all these Gov. Officials just to cram BSE tainted hamburgers
down the throat of their daughters, or just for nothing. They pay a good
portion of them to think up schemes, to get them out of man-made
environmental death sentences. I would love to know, who thought
up the scheme, to brain-wash everyone into believing the 'CHOSEN ONES'
are the only ones tied to this man-made death sentence?
Probably the
same one to think up the genetic testing for insurance companies.
Oh, well, this pretty much does it for me today. Probably already
over-loaded myself today. Now i know why Mr. Schmitt only allows 4
messages.



kind regards,

Terry S. Singeltary Sr., Bacliff, Texas USA


Department of Health Statement - Genetic Testing and Insurance




http://213.38.88.195/coi/coipress.nsf/70e1fa6684c1d3f380256735005750fb/0a8f8fa3eddd8a4b8025697700505ead?OpenDocument




http://213.38.88.195/coi/coipress.nsf/70e1fa6684c1d3f380256735005750fb/80c7e476e82c542680256977003adf9e?OpenDocument





kind regards,

 

Terry S. Singeltary Sr., Bacliff, Texas USA





"Terry S. Singeltary Sr." wrote:


 

>
> ######### Bovine Spongiform Encephalopathy #########
>
> Greetings again list members,
>
> Has anyone heard of any further development of the Schmerr test???
> I knew of powers within, that were trying to inhibit the progress
> of this testing (from a _most_ reliable source), but did not think they
> actually would stop the research.
>
> hmmmm, who knows???
>
> Here are a few links some may find informative;
>
> Opinion On
> Update of the Opinion given by the Scientific Committee on Medicinal
> Products and Medical Devices on The Risk Quantification For CJD
> Transmission Via Substances of Human Origin;
>
> 2. Screening assays
>
> It is assumed that although there is no proven or even probable case of
> transmission by blood or blood products the identification and exclusion
> of donors in the preclinical phase of CJD or vCJD would contribute to an
> increase in the safety margin and, probably, an increase in the
> confidence in blood and blood products by potential recipients.
> Therefore, the SCMPMD in its Opinion of October 1998 emphasised the need
> for "the development of a simple readily available ex vivo diagnostic
> test for preclinical nvCJD/CJD". In addition it stated: "When a
> validated test for TSE infectivity in donor blood becomes available, it
> should be implemented in routine donor screening as soon as possible and
> donors found to be positive should be excluded from donation. Member
> Statos should, in the interest of public health, warrant availability of
> TSE tests for blood screening in collaboration with possible patent
> holders."
>
> During the "WHO Consultation on Diagnostic Procedures for Transmissible
> Spongiform Encephalopathies: Need for Reference Reagents and Reference
> Panels" held in Geneva on March 22 and 23, 1999, M.J. Schmerr presented
> results of a new assay that may be able to detect the pathological fbrm
> of ption protein in blood of animals in the clinical as well as in the
> preclinical phase of TSE (serapie in sheep and chronic wasting disease
> in deer, Schmerr 1999, Schmerr et al. 1999). The basic reaction is the
> competition of the proteinase K treated sample with a labelled peptide
> derived from the sequence of prion protein binding to an antibody mised
> against this peptide (Schmerr et al. 1998). The test material is
> extracted from buff), coat prepreed from a sample of peripheral blood.
> >From the relation between ti'ee and bound peptide as determined by
> capillary electropheresis the amount of corn?ting protein i.e. protease
> resistant prion protein, is calculated.
>
> In contrast to other tests used for the detection of TSE infected
> animals or lbr confirmation of CJD/vCJD in humans the assay proposed by
> Schmerr uses for the first time as test material a body fluid, namely
> blood, which is eaqily availahl,~ In thi~ respect, this assay fulfils a
> prerequisite for a screening assay which could be used in the blood
> donation setting. However, it has to be stressed that this assay is far
> from ir~ing vaildated tidier in animals or in humans. On the contrary,
> preliminary tests with haman material performed in several laboratories
> have not yet validated this test.
>
> There is no doubt that the assay has the potential to be developed into
> a screening assay, but this developmere will need a number of carefully
> designed studies. Use in donor screening will not be possible until
> there is more information on the sensitivity, specificity and validity
> of the assay.
>
> The SCMPMD repeats its recommendation to support efforts in the
> development of easily applicable screening tests for CJD/vCJD.
>
> The SCMPMD would also like to draw the attention to an ethical aspect of
> the expected introduction of a screening assay for CJD/vCJD. The
> information of a positive test result would confront the individual with
> the diagnosis of an inevitably fatal disease without any reliable
> prediction of the duration of the preclinical phase. Such information
> could cause severe psychological stress and would demand careful
> counselling. In such a situation, it would not be surprising if donors
> would stop donating il' such a test for CJD/vCJD were introduced. If the
> number of those dollors is high the introduction of a screening assay
> would lead to a significant loss of donors who would have to be replaced
> by first time donors who are at higher risk of well known blood borne
> infections. This situation should be considered well in advance.
>
> 3. Exclusion of donors at risk for TSE infection by ruminant derived
> material
>
> Until the end of 1998 vCJD cases were observed only in the United
> Kingdom (UK), with one single exception. Therefore, residency in UK was
> described as one of the known risk factors for vCJD (the others being
> young age (i.e. below 53 years) and homozygosity of methionine at codon
> 129 of the prion protein gene). The exclusion of donors who resided for
> some time in the UK could, therefore, be considered as contributing to
> minimising the theoretical risk of vCJD transmission by blood and blood
> products.
>
> The first recommendation of this kind was given by the Ottawa based
> Bayer Advisory Council on Bioethics which stated in his working paper
> "Creutzfeldt-Jakob disease, blood and blood products: A bioethics
> framework" (1998):
> "The differences between classical CJD on the one hand and nvCJD on the
> other creme differences in the quality of the hypothetical risk. As
> discussed earlier, the new variant form appears to have crossed the
> species barrier from cattle. It has an earlier age at onset, and the los
> of pathological ptiohs is much greater than in classical forms of the
> disease. The anatomical distribution of nvCJD infectivity is also
> different, which raises the plausible possibility that it is more likely
> to have infectivity in the blood. Therefore, nvCJD is the wild card that
> warrants special vigilance. The disease appears to be isolated, at
> present, to parts of Europe. The number of people in affected countries
> who are currently incubating the disease is ankhown. The Council
> therefore recommends:
>
> 20. That persons who, at any time since 1980, have resided in a
> geographic area with a significant incidence of BSE or nvCJD not be
> permitted to contraute blood or plasma until the hypothetical risk of
> accepting donations from such persons can be evaluated."
>
> http://europa.eu.int/comm/food/fs/sc/scmp/out28_en.pdf
>
> also, for those interested, here are more documents on this and
> other issues;
>
> http://europa.eu.int/comm/food/fs/sc/scmp/out12_en.pdf
> http://europa.eu.int/comm/food/fs/sc/scmp/out20_en.html
> http://europa.eu.int/comm/food/fs/sc/scmp/out25_en.html
> http://europa.eu.int/comm/food/fs/sc/scmp/out29_en.pdf
>
> kind regards,
> Terry S. Singeltary Sr., Bacliff, Texas USA





2011




According to advisers to the British government, though the test is undoubtedly a significant step towards eliminating the incurable disease and preventing it from becoming endemic in society, it could result in a reduction in the number of blood donors and there are also fears it could increase insurance premiums.



Experts suspect that donors will be reluctant to give blood if they risk being told that they have the possibility of developing the disease which causes a horrible and agonising death.




Dr. John Forsythe, chair of the Advisory Committee on the Safety of Blood Tissues and Organs (SABTO) and a transplant surgeon at the Royal Infirmary of Edinburgh says the test does have significant downsides, despite concerns that the disease could become widespread in the UK.






http://vcjdblood.blogspot.com/2008/11/sabto-summary-of-1st-public-meeting.html



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