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
TSS
posted by Terry S. Singeltary Sr. at
5:43 PM
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