Thursday, September 20, 2012

Evidence-based guideline: Diagnostic accuracy of CSF 14-3-3 protein in sporadic Creutzfeldt-Jakob disease

Special Article


Evidence-based guideline: Diagnostic accuracy of CSF 14-3-3 protein in sporadic Creutzfeldt-Jakob disease


Report of the Guideline Development Subcommittee of the American Academy of Neurology


Taim Muayqil, MBBS, FRCPC, Gary Gronseth, MD, FAAN and Richard Camicioli, MD, FRCPC


+ Author Affiliations


From the King Saud University (T.M.), Riyadh, Saudi Arabia; University of Kansas Medical Center (G.G.), Kansas City; and University of Alberta (R.C.), Edmonton, Canada.


Correspondence & reprint requests to American Academy of Neurology: guidelines@aan.com


View Complete Disclosures


Abstract


Objective: To assess the available evidence for the diagnostic accuracy of CSF testing for protein 14-3-3 in patients with suspected sporadic Creutzfeldt-Jakob disease (sCJD).


Methods: The authors performed a systematic review of the available literature from 1995 to January 1, 2011, to identify articles involving patients who were suspected of having sCJD and who had CSF analysis for protein 14-3-3. Studies were rated according to the American Academy of Neurology classification of evidence scheme for diagnostic studies, and recommendations were linked to the strength of the evidence. A pooled estimate of sensitivity and specificity was obtained for all studies rated Class II or higher. The question asked is “Does CSF 14-3-3 protein accurately identify Creutzfeldt-Jakob disease (CJD) in patients with sCJD?”


Results: The analysis was conducted on the basis of samples of 1,849 patients with suspected sCJD from 9 Class II studies. Assays for CSF 14-3-3 protein are probably moderately accurate in diagnosing sCJD: sensitivity 92% (95% confidence interval [CI] 89.8–93.6), specificity 80% (95% CI 77.4–83.0), likelihood ratio of 4.7, and negative likelihood ratio of 0.10.


Recommendation: For patients who have rapidly progressive dementia and are strongly suspected of having sCJD and for whom diagnosis remains uncertain (pretest probability ∼20%–90%), clinicians should order CSF 14-3-3 assays to reduce the uncertainty of the diagnosis (Level B). Received February 21, 2012. Accepted June 22, 2012. Copyright © 2012 by AAN Enterprises, Inc.







 
 
Wednesday, June 27, 2012


First US BSE Case Since 2006 Underscores Need for Vigilance


Neurology Today 21 June 2012







PO-028: Oral transmission of L-type bovine spongiform encephalopathy (L-BSE) in primate model Microcebus murinus


Nadine Mestre-Frances,1 Simon Nicot,2 Sylvie Rouland,1 Anne-Gaëlle Biacabe,2 Isabelle Quadrio,3 Armand Perret-Liaudet,3 Thierry Baron,2 Jean-Michel Verdier1 1IN SER M UM2; Montpellier, France; 2Anses; Lyon, France; 3Hopitaux Civils de Lyon; Lyon, France


An atypical form of bovine spongiform encephalopathy has been identified in cattle in Europe, North America and Japan and was designed as L-type BSE (L-BSE) due to the lower apparent molecular mass of the unglycosylated, protease-resistant prion protein (PrPres) detected by western blot compared with classical BSE. Experimental evidences from studies in transgenic mice expressing human PrP and in primate models suggest a higher risk of transmission to humans of the L-BSE form than for classical BSE agent. However, a major unresolved issue concerns the potential transmissibility of the L-BSE agent by oral route. To address this question, we infected mouse lemurs (Microcebus murinus), a non-human primate model, with L-BSE by intracerebral or oral route.


Four adult lemurs were intracerebrally (IC) inoculated with 5mg of L-BSE infected brain homogenate of an atypical French BSE case (02-2528). Four young and four adult animals were fed with 5 mg or 50 mg of infected brain. After sacrifice, the brain tissues were biochemically and immunocytochemically investigated for PrPres.


The 4 animals IC inoculated died at 19 and 22 months postinoculation (mpi). They developed blindness, tremor, abnormal posture, incoordinated movements, balance loss. Symptoms get worse according to the disease progression, until severe ataxia. Severe spongiosis was evidenced into the thalamus, the striatum, the mesencephalon, and the brainstem, whereas into the cortex the vacuolisation was weaker. Strong deposits of PrPres were detected into the thalamus, the striatum, and the hippocampus whereas in the cerebral cortex, PrPres was prominently accumulated in plaques.


The orally inoculated animals showed similar clinical symptoms occurring between 27 and 34 mpi. Disease was characterized by progressive prostration, loss of appetite and poor appearance of the fur. Only one adult animal showed disequilibrium. PrPres was strongly accumulated only in the striatum and thalamus and weakly into the cortex. No plaques were evidenced. Two animals that were orally challenged at the age of two years are still alive and healthy 34 months after inoculation. The western blot analysis showed uniform molecular profiles, irrespective of the route or dose of infection, and included notably a PrPres form with low apparent molecular mass (~19 kDa) similar to the PrPres in the original cattle brain. However, the PrPres profile in lemurs was characterized by a higher proportion of di- and mono-glycosylated species (up to 95% of the total signal) than in the bovine L-BSE inoculum (~80%). In addition, small amounts of PrPres were detected by western blotting in the spleen of three animals (one intra-cerebrally inoculated and two fed with 5 mg of cattle brain).


Here, we demonstrate that the L-BSE agent can be transmitted by oral route from cattle to young and adult mouse lemurs. In comparison to IC inoculated animals, orally challenged lemurs were characterized by longer survival periods as expected with this route of infection.








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...











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








Wednesday, August 01, 2012


Behavioural and Psychiatric Features of the Human Prion Diseases: Experience in 368 Prospectively Studied Patients









Monday, August 06, 2012


Atypical neuropathological sCJD-MM phenotype with abundant white matter Kuru-type plaques sparing the cerebellar cortex








 
Monday, August 20, 2012



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










Tuesday, June 26, 2012


Creutzfeldt Jakob Disease Human TSE report update North America, Canada, Mexico, and USDA PRION UNIT as of May 18, 2012


type determination pending Creutzfeldt Jakob Disease (tdpCJD), is on the rise in Canada and the USA








Monday, August 6, 2012


TAFS BSE in USA August 6, 2012


BSE in USA









Saturday, May 26, 2012


Are USDA assurances on mad cow case 'gross oversimplification'?


SNIP...


What irks many scientists is the USDA’s April 25 statement that the rare disease is “not generally associated with an animal consuming infected feed.”


The USDA’s conclusion is a “gross oversimplification,” said Dr. Paul Brown, one of the world’s experts on this type of disease who retired recently from the National Institutes of Health. "(The agency) has no foundation on which to base that statement.”


“We can’t say it’s not feed related,” agreed Dr. Linda Detwiler, an official with the USDA during the Clinton Administration now at Mississippi State.


In the May 1 email to me, USDA’s Cole backed off a bit. “No one knows the origins of atypical cases of BSE,” she said


The argument about feed is critical because if feed is the cause, not a spontaneous mutation, the California cow could be part of a larger outbreak.


SNIP...






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


Saturday, August 4, 2012


Final Feed Investigation Summary - California BSE Case - July 2012




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


SUMMARY REPORT CALIFORNIA BOVINE SPONGIFORM ENCEPHALOPATHY CASE INVESTIGATION JULY 2012


Summary Report BSE 2012


Executive Summary




Saturday, August 4, 2012


Update from APHIS Regarding Release of the Final Report on the BSE Epidemiological Investigation






Sunday, August 26, 2012


Detection of PrPSc in peripheral tissues of clinically affected cattle after oral challenge with BSE






2011 Monday, September 26, 2011


L-BSE BASE prion and atypical sporadic CJD






 
 
Public release date: 24-Sep-2012
 
 
 
Contact: Jason Bardi jason.bardi@ucsf.edu 415-502-4608 JAMA and Archives Journals
 
 
 
Study examines delayed, misdiagnosis of sporadic Jakob-Creutzfeldt disease

 
CHICAGO – A medical record review study of 97 patients with the fatal, degenerative brain disorder sporadic Jakob-Creutzfeldt disease (sCJD) suggests that a correct diagnosis of the disease was often delayed by a variety of misdiagnoses, according to a report published Online First by Archives of Neurology, a JAMA Network publication.

 
The disease is often misdiagnosed because of a variability of early symptoms and signs, a variability in disease duration and a lack of recognition of the condition in the medical community. Often, sCJD is mistaken for other neurodegenerative conditions such as Alzheimer disease and dementia with Lewy bodies, according to the study background.

 
Ross W. Paterson, M.R.C.P., and colleagues from the University of California, San Francisco, retrospectively reviewed all cases referred to the UCSF Memory and Aging Center rapidly progressing dementia and CJD clinical research program between August 2001 and February 2007. They identified 97 patients with pathology-proven sCJD for whom they had sufficient medical records (40 women and 57 men who ranged in age from 26 to 83 years).

 
The 97 patients had received a combined total of 373 alternative diagnoses prior to their diagnosis of likely CJD, with an average of 3.8 misdiagnoses per patient. The physicians who most commonly made the misdiagnoses were primary care physicians and neurologists. In the 18 percent of patients (17 patients) who were correctly diagnosed at their first assessment, the diagnosis was almost always made by a neurologist. The average time from onset to diagnosis was almost eight months, an average of two-thirds the way through the disease course, according to the study results.
 
 
 
"In any patient with a rapidly progressive dementia who has been given multiple potential diagnoses, sCJD must be considered," the authors comment.
 
 
 
Researchers note that "early and accurate" diagnosis of sCJD is valuable for public health reasons and to allow for potential treatments to be tested as early as possible in the disease course.
 
 
 
"It would therefore be valuable to improve early and accurate diagnosis of sCJD premortem to identify at-risk persons, allowing for public health measures that would prevent transmission to healthy individuals through blood donation, infected surgical equipment and or other medical procedures," the authors conclude.

 
###
 
 
 
(Arch Neurol. Published online September 24, 2012. doi:10.1001/2013.jamaneurol.79. Available pre-embargo to the media at http://media.jamanetwork.com.)

 
Editor's Note: An author made financial disclosures. The study was supported by the National Institute on Aging, the National Institutes of Health National Institute of Neurological Disorders and Stroke, the Michael J. Homer Family Fund, the National Institutes of Health National Center for Research Resources University of California, San Francisco Clinical and Translational Science Institute and the John Douglas French Alzheimer's Foundation. Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.
 
 
 
Editorial: (Mis)diagnosis of Disease

 
In an editorial, Richard J. Caselli, M.D., of the Mayo Clinic Arizona, Scottsdale, writes: "Unquestionably, when confronted with the syndrome of rapidly progressive dementia, our first concern must be the search for reversible causes, a point that Paterson et al discuss in this issue of Archives, but their main point is to illustrate the diagnostic journey patients with CJD travel on their way to a final and very unfortunate diagnosis."

 
"There is also a societal dimension to the timely diagnosis of CJD. At this time of global economic crisis, national health care reform, escalating medical expenditures and an aging population (creating projections of accelerating health care-driven financial gloom and doom), the financial burden posed by prolonged and duplicative testing that results from diagnostically ambiguous cases of rapidly progressive dementia must also be considered," Caselli continues.
 
 
 
"As we attempt to rein in health care costs while sacrificing no degree of medical accuracy or compassion, we owe it to our patients and to society to have the necessary knowledge to consider the diagnosis, establish the diagnosis as efficiently as possible, and then work with patients, families and palliative care providers to maximize the quality of life for our dying patients," Caselli concludes.
 
 
 
(Arch Neurol. Published online September 24, 2012. doi:10.1001/2013.jamaneurol.1. Available pre-embargo to the media at http://media.jamanetwork.com.)
 
 
 
Editor's Note: Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.

 
To contact corresponding author Michael D. Geschwind, M.D., Ph.D., call Jason Bardi at 415-502-4608 or email jason.bardi@ucsf.edu. To contact editorial author Richard J. Caselli, M.D., call Jim McVeigh at 480-301-4222 or email mcveigh.jim@mayo.edu.
 
 
 
 
 
 
 
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
 
 
 
 
 
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***
 
 
 
 
 
 
 
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.
 
 
 
 
 
 
re-Diagnosis and treatment of rapidly progressive dementias
 
 
 
 
 
 
Greetings Dr. Geschwind, UCSF, Neurology et al,
Thank You for putting out this study to bring forth the challenges with all the dementias, and diagnosis there from. Not having access to your full text study, not knowing if the TSE prion disease was mentioned further into your article, I wish to send the following information and submissions of this very concern you bring forward.
My Mom died from the hvCJD ‘confirmed’, my Mema (her Mom) died with moderate dementia or Alzheimer’s, and just got a call that my uncle Bo (my Moms brother from Mema), was admitted again to the mental ward for aggression toward his wife, he has severe dementia or Alzheimer’s, and my half brother from my Mom died with severe mental retardation. he had been institutionalized for decades. so, I am very much aware of the challenges that exist when trying to properly diagnose an individual with rapid progressive dementia or Alzheimer’s or a Transmissible Spongiform Encephalopathy TSE prion disease, like with my Mom i.e. the Heidenhain Variant of Creutzfeldt Jakob disease, which was very, very rapid from onset of first clinical symptoms to death, of about 3 months. we just never could catch up with it.
What is Alzheimer’s anyway?
Alzheimer’s disease, Iatrogenic TSE, what if ???
snip...
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
 
 
 
 
 
 
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
snip...
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
flounder9@verizon.net
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==========
 
 
snip...full submission with references ;
 
 
 
 
 
Wednesday, May 16, 2012
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?

 
Proposal ID: 29403

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

 
 
 
 
*********************
 
Monday, August 20, 2012
 
 
CASE REPORTS CREUTZFELDT-JAKOB DISEASE: AN UNDER-RECOGNIZED CAUSE OF DEMENTIA
 
 
 
 
*********************
 
 
Wednesday, June 27, 2012
 
 
First US BSE Case Since 2006 Underscores Need for Vigilance
 
Neurology Today 21 June 2012
 

 
 
 



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