Friday, April 25, 2014

Accuracy of administrative diagnostic data for pathologically confirmed cases of Creutzfeldt-Jakob disease in Massachusetts, 2000-2008

Article in Press

 

Accuracy of administrative diagnostic data for pathologically confirmed cases of Creutzfeldt-Jakob disease in Massachusetts, 2000-2008

 

Jed A. Barash, MD Affiliations Department of Medicine, Yale University School of Medicine, Robert Wood Johnson Foundation Clinical Scholars Program, New Haven, CT Department of Neurology, Veterans Affairs Medical Center, West Haven, CT Corresponding Author InformationAddress correspondence to Jed A. Barash, MD, Lahey Clinic, Department of Neurology, 41 Mall Rd, Burlington, MA 01805. email address, James K. West, PhD Affiliations Bureau of Infectious Diseases, Massachusetts Department of Public Health, Boston, MA , Alfred DeMaria Jr., MD Affiliations Bureau of Health Statistics, Research, and Evaluation, Massachusetts Department of Public Health, Jamaica Plain, MA published online 10 April 2014. Corrected Proof

 

Abstract

 

Background Creutzfeldt-Jakob disease (CJD) is a transmissible disorder that is monitored by public health authorities at the state and national levels in the United States. Little is known about the current accuracy and concurrence of CJD diagnoses across national and state sources of surveillance data.

 

Methods Using multiple sources, including the National Prion Disease Pathology Surveillance Center (NPDPSC) registry, we sought to identify all deceased Massachusetts patients with pathologically diagnosed CJD between 2000 and 2008. Pathologically verified CJD cases were then matched to their respective records in the Massachusetts hospital discharge and death certificate datasets. Using these data, we also aimed to estimate the sensitivity and specificity of death certificate diagnoses.

 

Results Death certificate and hospital discharge dataset diagnoses of CJD combined accounted for 80% (35 of 44) of pathologically confirmed cases. The estimated sensitivity and specificity for death certificate diagnoses alone were 71% (27 of 38) and 75% (9 of 12), respectively.

 

Conclusions Death certificate diagnoses were less sensitive for pathologically confirmed CJD than reported previously. Increasing reliance on autopsy over biopsy and an expanding spectrum of health care delivery may be responsible for this discrepancy. The findings reported here underscore the value of using multiple mechanisms in national CJD surveillance.

 

Key Words: Prion diseases, Surveillance, Death certificate

 


 

 

J Neurol Neurosurg Psychiatry published online August 21, 2013

 

Genevieve M J A Klug, Handan Wand, Marion Simpson, et al.

 

Intensity of human prion disease surveillance predicts observed disease incidence

 

ABSTRACT

 

Background Prospective national screening and surveillance programmes serve a range of public health functions. Objectively determining their adequacy and impact on disease may be problematic for rare disorders. We undertook to assess whether objective measures of disease surveillance intensity could be developed for the rare disorder sporadic Creutzfeldt–Jakob disease (CJD) and whether such measures correlate with disease incidence.

 

Method From 10 countries with national human prion disease surveillance centres, the annual number of suspected prion disease cases notified to each national unit (n=17 610), referrals for cerebrospinal fluid (CSF) 14-3-3 protein diagnostic testing (n=28 780) and the number of suspect cases undergoing diagnostic neuropathological examination (n=4885) from 1993 to 2006 were collected. Age and survey year adjusted incidence rate ratios with 95% CIs were estimated using Poisson regression models to assess risk factors for sporadic, non-sporadic and all prion disease cases. Results Age and survey year adjusted analysis showed all three surveillance intensity measures (suspected human prion disease notifications, 14-3-3 protein diagnostic test referrals and neuropathological examinations of suspect cases) significantly predicted the incidence of sporadic CJD, non-sporadic CJD and all prion disease.

 

Conclusions Routine national surveillance methods adjusted as population rates allow objective determination of surveillance intensity, which correlates positively with reported incidence for human prion disease, especially sporadic CJD, largely independent of national context. The predictive relationship between surveillance intensity and disease incidence should facilitate more rapid delineation of aberrations in disease occurrence and assessment of the adequacy of disease monitoring by national registries.

 

snip...

 

COMMENT

 

This is the first study to directly address and verify previous suggestive findings17 and prevailing assumptions that greater scrutiny of a population may lead to higher rates of human prion disease detection and thereby reported disease incidence. Integral to the more objective assessment approach described in our study is the adjustment of surveillance detection methods as population interrogation rates. Employing this method, we have shown that relatively simple, accessible measures (clinical case recognition with notification made to a national surveillance centre combined with a routine diagnostic test like CSF 14-3-3 protein detection and neuropathological examination) can be adjusted to generate metrics of surveillance intensity, which correlate sufficiently with sporadic CJD incidence to be predictive. The broad multinational context, very large number of cases included and the extended time period of the study all add support for the robustness of the findings. As such, our observations provide important insight into factors that contribute to variations in reported prion disease incidence, particularly for sporadic CJD.9 Nevertheless, in the absence of universal autopsy, some uncertainty inevitably persists regarding the ascertainment of all human prion disease cases and the absolute incidence of CJD.

 

The observed predictive relationship between surveillance intensity and sporadic CJD incidence was present despite the recognised clinical profile variations across the sporadic CJD subtypes,11 18 suggesting that national surveillance can be achieved for a disease through primarily relying on clinical detection even when there is a somewhat diverse phenotypic spectrum. It is also of interest that advanced age, well beyond that more typically associated with sporadic CJD, does not appear to impede clinical recognition, with previous studies suggesting that increased incidence appears to correlate with increased referrals of suspect cases in the very elderly.17 19

 

The epidemiological history of human prion diseases, especially acquired forms such as those related to the therapeutic use of cadaveric dura mater explants and pituitary hormones20 as well as variant CJD21 and ongoing concerns regarding transmission risks posed by routine surgery, including nonneurosurgery, 22 23 should serve as a sobering precaution against any public health complacency in relation to this group of diseases. The key objectives of prospective national surveillance programmes are to ensure adequate detection of the disease and accurate depiction of the epidemiological profile so that significant departures in disease incidence or demographic characteristics can be recognised.24 Our findings should subserve both of these objectives. As described for variant CJD,21 an altered phenotype can indicate important epidemiological changes with respect to disease aetiology. Notwithstanding this influence, a more accurately defined and predictive relationship between population surveillance intensity and disease recognition rates (with 95% CIs) should facilitate more rapid and confident delineation of significant deviations in national disease incidence for a given surveillance intensity and serve to prompt more detailed evaluation of why this change has occurred, possibly leading to more expeditious deployment of public health responses.

 

Our study revealed major variations, approximately two orders of magnitude, in annual crude notification rates of persons with suspected prion disease across the study period in the countries assessed. Although some of this variation may be a natural finding based on variable population sizes, it demonstrates the likely underappreciation of true differences when only drawing comparisons of unadjusted, average disease incidence rates from countries with varied population sizes. Over the study timeframe, CJD awareness and recognition increased markedly both nationally and globally due to factors including the bovine spongiform encephalopathy (BSE) epidemic, improved surveillance systems and advances in diagnostic capabilities, in particular the CSF 14-3-3 diagnostic test. These influences have contributed to improved notification and diagnostic assessment of suspected cases, a feature reflected in the positive temporal trends observed for suspect case and 14-3-3 CSF test referrals and, to a lesser degree, with neuropathological examination in the participant countries. Although temporal variation in predictor and outcome variables was significant between the countries over the study period, the analysis of pooled data, adjusted for time and age, demonstrated that time was independent of the association between surveillance intensity measurements and incidence, further underscoring the strength of this study.

 

Referrals for 14-3-3 CSF analysis in France and Germany were noticeably higher than in other countries. We surmise this may be due to subsidisation of the costs of testing and/or the strong tradition of employing CSF surrogate biomarker detection in the evaluation of dementias, including CJD. In Hungary and the Czech Republic, the lower number of referrals for 14-3-3 testing is due to the later point at which 14-3-3 testing was introduced and adopted into the criteria in comparison with France and Germany. However, despite the higher levels of CSF testing in Germany and France, incidence was not increased in comparison with other countries, suggesting that the correlation with sporadic CJD incidence also relies on referral of suspect cases to a national reference centre, as well as neuropathological examination. Furthermore, this finding argues against a potential misconception from this study that widespread 14-3-3 CSF testing is required for optimal case ascertainment. The negative association observed between CSF referrals and non-sporadic CJD cases may relate in part to modest increases in prion protein gene (PRNP) testing observed over the study timeframe, translating into a reduced likelihood of non-sporadic CJD cases (mainly genetic) undergoing 14-3-3 CSF testing. This is a plausible explanation, however, unverified in this study, with the negative association also possibly related to the fact that CSF 14-3-3 protein detection was primarily developed for sporadic CJD detection.

 

The multi-national context of the present study was an intended and important design feature by which it was ensured relatively minor but ‘real life’ variations in specific mechanisms of national prion disease surveillance were encompassed. Despite this, the findings clearly demonstrate overall support for a positive and predictive correlation between surveillance intensity and sporadic CJD incidence; however, we note that this predictive association was not observed in two of the nine countries. The reason for this is uncertain but may relate to unapparent variations in surveillance methods employed within these countries or a potential saturation point where no new cases are identified despite increasing surveillance intensity.

 

Although the public health and epidemiological context of each disease undergoing national screening or surveillance is relatively unique, and therefore of limited direct comparability, the finding that observed population diagnosis rates can be influenced by testing and resourcing issues is not unique to CJD. HIV infection diagnosis in the UK is estimated at 74% of all infections, while in Australia, the estimate is 85%–90%.25 26 The Australian epidemic remains largely transmitted through male homosexual contact, a well-informed group with a high rate of HIV testing.27 In contrast, the epidemic in the UK is more heterogenous and often associated with migration to the UK from high prevalence countries.28

 

So, in conclusion, our study has confirmed that routine national surveillance methods adjusted as population rates allow objective determination of surveillance intensity, which correlates positively with reported incidence for human prion disease, especially sporadic CJD, largely independent of national context. The predictive relationship between surveillance intensity and disease incidence should facilitate more rapid delineation of aberrations in disease occurrence and permit objective assessment of the adequacy of disease monitoring by national registries. Further, the approach outlined in our study could extend to other rare disorders, and should allow more objective assessment of the adequacy of population scrutiny by extant or potential members of surveillance consortia.

 


 

 

-------- Original Message --------

 

Subject: Challenging the Clinical Utility of the 14-3-3 Protein for the Diagnosis of Sporadic Creutzfeldt-Jakob Disease

 

Date: Mon, 16 Jun 2003 16:38:34 –0500

 

From: "Terry S. Singeltary Sr."

 

To: Bovine Spongiform Encephalopathy

 

CC: CJDvoice , bloodcjd@yahoogroups.com

 

Challenging the Clinical Utility of the 14-3-3 Protein for the Diagnosis of Sporadic Creutzfeldt-Jakob Disease

 

Michael D. Geschwind, MD, PhD; Jennifer Martindale, BS; Deborah Miller, MD; Stephen J. DeArmond, MD, PhD; Jane Uyehara-Lock, MD; David Gaskin, MD; Joel H. Kramer, PhD; Nicholas M. Barbaro, MD; Bruce L. Miller, MD

 

Arch Neurol. 2003;60:813-816.

 

Background Creutzfeldt-Jakob disease (CJD) is a rapidly progressive and fatal neurodegenerative disorder for which there is no noninvasive and disease-specific test for premortem diagnosis. Previous studies have suggested that, in the proper clinical context, the 14-3-3 protein in cerebrospinal fluid is a reliable marker for sporadic CJD.

 

Objective To assess the sensitivity of the cerebrospinal fluid 14-3-3 protein test among patients with definite sporadic CJD.

 

Design and Setting We reviewed cases of sporadic CJD referred to our institution that were ultimately proved by pathological examination and on which cerebrospinal fluid 14-3-3 testing had been performed.

 

Participants Patients with CJD referred to our institution for clinical and/or pathological evaluation (biopsy- or autopsy-confirmed diagnosis) from January 1, 1998, through July 15, 2002, and on whom 14-3-3 testing had been performed. Thirty-two such patients with definite sporadic CJD were identified.

 

Main Outcome Measure The 14-3-3 test results, from various laboratories, in these 32 patients.

 

Results Seventeen of the 32 patients had a positive result for the 14-3-3 test, yielding a sensitivity of only 53%. A positive 14-3-3 result was significantly correlated with a shorter time between disease onset and the lumbar puncture for the 14-3-3 test.

 

Conclusions Testing for the 14-3-3 protein is only modestly sensitive to sporadic CJD, and we caution against ruling out a diagnosis of the disease on the basis of a negative 14-3-3 result.

 

From the Departments of Neurology (Drs Geschwind, D. Miller, Kramer, and B. L. Miller and Ms Martindale), Pathology (Drs DeArmond, Uyehara-Lock, and Gaskin), and Neurosurgery (Dr Barbaro), University of California, San Francisco Medical Center, San Francisco.

 


 

 

> Conclusions Testing for the 14-3-3 protein is only modestly sensitive to sporadic CJD,

 

> and we caution against ruling out a diagnosis of the disease on the basis of a negative > 14-3-3 result.

 

 

but how many were ruled out as having CJD with 14-3-3 ?

 

kinda makes the one-in-a-million myth, just that, a myth...TSS

 

Asante/Collinge et al, 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;

 


 

 

Original Contribution | June 2003

 

Challenging the Clinical Utility of the 14-3-3 Protein for the Diagnosis of Sporadic Creutzfeldt-Jakob Disease

 

FREE Michael D. Geschwind, MD, PhD; Jennifer Martindale, BS; Deborah Miller, MD; Stephen J. DeArmond, MD, PhD; Jane Uyehara-Lock, MD; David Gaskin, MD; Joel H. Kramer, PhD; Nicholas M. Barbaro, MD; Bruce L. Miller, MD [+-] Author Affiliations From the Departments of Neurology (Drs Geschwind, D. Miller, Kramer, and B. L. Miller and Ms Martindale), Pathology (Drs DeArmond, Uyehara-Lock, and Gaskin), and Neurosurgery (Dr Barbaro), University of California, San Francisco Medical Center, San Francisco.

 

 Arch Neurol. 2003;60(6):813-816. doi:10.1001/archneur.60.6.813. Text Size: A A A Published online Article Tables References Comments ABSTRACT ABSTRACT | METHODS | RESULTS | COMMENT | ARTICLE INFORMATION | REFERENCES Background Creutzfeldt-Jakob disease (CJD) is a rapidly progressive and fatal neurodegenerative disorder for which there is no noninvasive and disease-specific test for premortem diagnosis. Previous studies have suggested that, in the proper clinical context, the 14-3-3 protein in cerebrospinal fluid is a reliable marker for sporadic CJD.

 

Objective To assess the sensitivity of the cerebrospinal fluid 14-3-3 protein test among patients with definite sporadic CJD.

 

Design and Setting We reviewed cases of sporadic CJD referred to our institution that were ultimately proved by pathological examination and on which cerebrospinal fluid 14-3-3 testing had been performed.

 

Participants Patients with CJD referred to our institution for clinical and/or pathological evaluation (biopsy- or autopsy-confirmed diagnosis) from January 1, 1998, through July 15, 2002, and on whom 14-3-3 testing had been performed. Thirty-two such patients with definite sporadic CJD were identified.

 

Main Outcome Measure The 14-3-3 test results, from various laboratories, in these 32 patients.

 

Results Seventeen of the 32 patients had a positive result for the 14-3-3 test, yielding a sensitivity of only 53%. A positive 14-3-3 result was significantly correlated with a shorter time between disease onset and the lumbar puncture for the 14-3-3 test.

 

Conclusions Testing for the 14-3-3 protein is only modestly sensitive to sporadic CJD, and we caution against ruling out a diagnosis of the disease on the basis of a negative 14-3-3 result.

 

THE 14-3-3 protein is a normal neuronal protein that is released into cerebrospinal fluid (CSF) in association with acute neuronal injury.1 It has been suggested that the presence of 14-3-3 protein in CSF is a reliable marker for Creutzfeldt-Jakob disease (CJD), with sensitivity and specificity for this protein reported as high as 96% and 93% to 100%, respectively.2- 4 These reports have recently led the World Health Organization to revise its diagnostic criteria for probable sporadic CJD (sCJD) to allow substitution of a positive 14-3-3 test for a positive electroencephalogram, provided the disease has less than a 2-year duration.5 Yet, a series of studies has suggested that both sensitivity and specificity for sCJD are lacking with this test.1,6,7

 

Previous studies that have examined the sensitivity of the 14-3-3 protein for CJD were performed in a single laboratory and did not restrict themselves to pathology-proved cases.4,8,9 In this study, to assess the true sensitivity of the 14-3-3 test, we included only cases that were pathology-proved for sCJD. In addition, because 14-3-3 tests were sent by referring physicians to one or more of several possible laboratories, this study may better reflect typical clinical experience with 14-3-3 in the United States.

 


 

 

Ann Neurol. Author manuscript; available in PMC Aug 1, 2013. Published in final edited form as: Ann Neurol. Aug 2012; 72(2): 278–285. doi: 10.1002/ana.23589 PMCID: PMC3458796 NIHMSID: NIHMS365401

 

Copyright notice and Disclaimer

 

RT-QuIC analysis of cerebrospinal fluid in sporadic Creutzfeldt-Jakob disease

 

Lynne I. McGuire, PhD,1 Alexander H. Peden, PhD,1 Christina D. Orrú, PhD,3 Jason M. Wilham, PhD,3 Nigel E. Appleford, Cbiol,2 Gary Mallinson, PhD,2 Mary Andrews, BSc,1 Mark W. Head, PhD,1 Byron Caughey, PhD,3 Robert G. Will, FRCP,1 Richard S.G. Knight, FRCP,1 and Alison J.E. Green, PhD1 1The National CJD Research & Surveillance Unit, University of Edinburgh, Edinburgh, Scotland, UK 2Bristol Institute for Transfusion Sciences, NHS Blood and Transplant, Bristol, UK 3Laboratory of Persistent Viral Disease, NIAID Rocky Mountain Laboratories, National Institutes of Health, Montana, USA Corresponding author: Dr Alison J.E. Green, The National CJD Research & Surveillance Unit, University of Edinburgh, Western General Hospital, Edinburgh, United Kingdom EH4 2XU, Tel no: + 44 (0)131 537 3075, Fax no: + 44 (0) 131 343 1404, Email: Alison.Green@ed.ac.uk Small right arrow pointing to: The publisher's final edited version of this article is available at Ann Neurol Small right arrow pointing to: See other articles in PMC that cite the published article. Other Sections▼

 

Abstract

 

INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION Supplementary Material References

 

Abstract

 

Objective Current cerebrospinal fluid (CSF) tests for sporadic Creutzfeldt-Jakob disease (sCJD) are based on the detection of surrogate markers of neuronal damage such as CSF 14-3-3 which are not specific for sCJD. A number of prion protein conversion assays have been developed, including real-time quaking induced conversion (RT-QuIC). The objective of this study is to investigate whether CSF RT-QuIC analysis could be used as a diagnostic test in sCJD.

 

Methods An exploratory study was undertaken which analysed 108 CSF samples from patients with neuropathologically confirmed sCJD or from control patients. Of the 108 CSF samples 56 were from sCJD patients (30 female, 26 male, aged 31–84 years; 62.3 ± 13.5 years) and 52 were from control patients (26 female, 26 male, aged 43–84 years; 67.8 ± 10.4 years). A confirmatory group of 118 patients were subsequently examined which consisted of 67 cases of neuropathologically confirmed sCJD (33 female, 34 male, aged 39–82 years; 67.5 ± 9.0 years) and 51 control cases (26 female, 25 male, aged 36–87 years; 63.5 ± 11.6 years).

 

Results The exploratory study showed that RT-QuIC analysis had a sensitivity of 91% and a specificity of 98% for the diagnosis of sCJD. These results were confirmed in the confirmatory study which showed that CSF RT-QuIC analysis had a sensitivity and specificity of 87% and 100% respectively. Interpretation This study shows that CSF RT-QuIC analysis has the potential to be a more specific diagnostic test for sCJD than current CSF tests.

 


 

 

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 Richard Camicioli, MD, FRCPC

 

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). Neurology® 2012;79:1499–1506

 


 

 

Use of 14-3-3 and other brain-specific proteins in CSF in the diagnosis of variant Creutzfeldt-Jakob disease

 

A Green, E Thompson, G Stewart, M Zeidler, J McKenzie, M MacLeod, J Ironside, R Will, and R Knight The National Creutzfeldt-Jakob Disease Surveillance Unit, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, UK. Email: Alison.Green@ed.ac.uk Author information ► Copyright and License information ► Copyright notice This article has been cited by other articles in PMC.

 

Abstract

 

OBJECTIVES—The detection of the protein 14-3-3 in the CSF has been shown to be a reliable and sensitive marker for sporadic Creutzfeldt-Jakob disease (CJD). Other brain-specific proteins such as neuron specific enolase (NSE), S-100b, and tau protein have also been reported to be increased in the CSF of patients with sporadic CJD. In 1996a variant of CJD (vCJD) was described which is likely to be causally linked to the bovine spongiform encephalopathy agent. This study reports and compares the findings of CSF brain specific protein analysis in 45 patients with vCJD and in 34 control patients.

 

METHODS—The CSF from 45 patients with vCJD and 34 controls were investigated for the presence of 14-3-3 by SDS-polyacrylamide gel electrophoresis (SDS-PAGE) and western blotting with chemiluminescent detection. Tau protein, S-100b, and NSE concentrations in CSF were measured using enzyme immunoassays.

 

RESULTS—Protein 14-3-3 was detected in the CSF of 22/45 patients with vCJD and in 3/34 controls. The mean concentrations of NSE, S-100b, and tau protein in CSF were significantly raised in patients with vCJD compared with controls. The positive predictive value of CSF 14-3-3 was 86% and the negative predictive value was 63%. These values are lower than those reported for sporadic CJD. An increased CSF tau had a positive predictive value of 93% and a negative predictive value of 81%. The combination of CSF 14-3-3 and/or increased CSF tau had a positive predictive value of 91% and a negative predictive value of 84%.

 

CONCLUSIONS—CSF protein 14-3-3 is not as useful a marker for vCJD as it is for sporadic CJD. Increased concentration of CSF tau was found to be a sensitive marker of vCJD but as concentrations may be increased in many forms of non-CJD dementia, this may limit its usefulness as a diagnostic test.

 


 

 

Published online 30 January 2011 | Nature | doi:10.1038/news.2011.59

 

News

 

CJD diagnosis just got easier Test for Creutzfeldt–Jakob disease raises hopes of speedier diagnosis.

 

Tiffany O'Callaghan

 

human prionIn prion diseases such as CJD, an isomer of a prion protein takes on an abnormal shape.AP Photo/Professors Stanley Prusiner/Fred Cohen, University of California San Francisco Medical School Invasive biopsy is currently the only sure way to diagnose the degenerative neurological condition Creutzfeldt–Jakob Disease (CJD). But a highly sensitive assay could change that, providing a fast, accurate alternative for early diagnosis of this rare but deadly condition.

 

snip...

 

So Atarashi and his colleagues used a new assay known as a real-time quaking-induced conversion (RT-QUIC) assay. 'Quaking-induced' refers to in vitro shaking, which researchers believe helps to accelerate the reactions, enabling the assay to produce results more quickly.

 

The team tested cerebrospinal fluid samples from 18 people with CJD and 35 people with other neurodegenerative diseases. This pilot group produced no false positives, and CJD was correctly diagnosed more than 83% of the time.

 

The researchers compared these results with those obtained using an existing assay that tests for levels of a protein known as 14-3-3, which is a marker for sporadic CJD. When tested on patient samples, the accuracy of 14-3-3 was 72.2%, whereas the specificity was 85.7%.

 

In a subsequent blind trial on 30 cerebrospinal fluid samples from Australia, RT-QUIC showed 100% specificity, resulting in no false positives among the 14 control samples, and correct diagnoses of 87.5%. 14-3-3 was equally accurate, but the rate of false positives was much higher.

 

"This technique allows definitive ante-mortem confirmation of CJD," says Atarashi, adding that this is currently difficult because it demands the detection of PrPSc in patients' biopsy specimens.

 


 

 

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.

 


 

 

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 ;

 

snip...

 

I would kindly like to add to my initial concerns, something I brought up years ago, and I believe that still hold true today, more so even than when I first stated these concerns in 2003 ;



routine passive mortality CJD surveillance USA ?


THIS has been proven not to be very useful in the U.K.;


THE EPIDEMIOLOGY OF CJD RG WILL 1984 (182 PAGES)

snip...

One reason for this was the _inaccuracy_ in coding of cases correctly certified as CJD Coding is carried out by staff who are not medically qualified and it is not surprising that coding errors occur in the processing of large numbers of certificates. In 1982, 12,000 certificates per week were processed at the office of population censuses and surveys by 15 coders and 6 checkers (Alderson et al., 1983). The occurrence of both inter- and intra-observer coding errors has been described (Curb et al., 1983) and the _inaccuracies_ of BOTH certification and coding discovered in this study _support_ the introduction of a more accurate system of death certificates and a more detailed and specific coding system...

snip...


http://web.archive.org/web/20040521215716/http://www.bseinquiry.gov.uk/files/mb/m26/tab01.pdf

 


Draft Proposal For The Monitoring of Creutzfeldt-Kakob Disease 1989 Dr. R. Will

snip...

IDENTIFICATION OF CASES

Cases of CJD may be identified from death certificates, but this alone is unlikely to provide adequate monitoring. ERRORS are made in certification and diagnosis; in the Oxford study death certificates were obtained on a series of known confirmed cases and CJD was mentioned in only 66% of certificates. In another series of 175 certified cases, 42 patients were judged not to have suffered from CJD after examination of case notes (7)...

full text;


 

 


 

 

snip...see my full text submission here ;

 

 

re-Human Prion Diseases in the United States

 

Posted by flounder on 01 Jan 2010 at 18:11 GMT

 


 

 

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

 


 


Wednesday, December 11, 2013

*** Detection of Infectivity in Blood of Persons with Variant and Sporadic Creutzfeldt-Jakob Disease ***
http://creutzfeldt-jakob-disease.blogspot.com/2013/12/detection-of-infectivity-in-blood-of.html


Creutzfeldt-Jakob Disease CJD cases rising North America updated report August 2013

*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada seeing an extreme increase of 48% between 2008 and 2010 ***
http://creutzfeldt-jakob-disease.blogspot.com/2013/08/creutzfeldt-jakob-disease-cjd-cases.html


Sunday, October 13, 2013

*** CJD TSE Prion Disease Cases in Texas by Year, 2003-2012
http://creutzfeldt-jakob-disease.blogspot.com/2013/10/cjd-tse-prion-disease-cases-in-texas-by.html


Sunday, March 09, 2014

A Creutzfeldt-Jakob Disease (CJD) Lookback Study: Assessing the Risk of Blood Borne Transmission of Classic Forms of Creutzfeldt-Jakob Disease

FDA TSEAC CIRCUS AND TRAVELING ROAD SHOW FOR THE TSE PRION DISEASES
http://creutzfeldt-jakob-disease.blogspot.com/2014/03/a-creutzfeldt-jakob-disease-cjd.html

 

 

Sunday, April 06, 2014

 

SPORADIC CJD and the potential for zoonotic transmission there from, either directly or indirectly via friendly fire iatrogenic mode, evidence to date

 


 

 

Tuesday, April 01, 2014

 

Questions linger in U.S. CJD cases 2005, and still do in 2014

 


 

 

Monday, March 10, 2014

 

Investigators study silent variant of mad cow disease Galveston Daily News March 4, 2014

 


 

 

Thursday, February 27, 2014

 

BEEF, CANCER, PRIONS, AND OTHER DANGEROUS AND DEADLY PATHOGENS, APPARENTLY, IT'S WHAT'S FOR DINNER

 


 

Thursday, March 6, 2014

 

TEXAS RECALL LIST MASSIVE FROM DEAD STOCK DOWNER CANCER COWS OFFAL from Class I Recall 002-2014 and 013-2014 Health Risk: High Jan 13, 2014 and Feb 8, 2014 shipped to Texas, Florida, and Illinois UPDATE FEBRUARY 14, 2014

 


 

Thursday, March 20, 2014

 

JACK IN THE BOX NOW CAUGHT UP IN MASSIVE RANCHO DEAD STOCK DOWNER CANCER COW RECALL

 


 

Friday, March 21, 2014

 

Rancho Dead Stock Cancer Downers Recall Explained FSIS March 20 2014 ?

 

“As of March 20, 2014, FSIS has completed all checks (effectiveness checks and disposition verification checks) for recalls 002-2014 and 013-2014 regarding Rancho Feeding Corporation. FSIS has determined that based on the number of successful checks (see Directive 8080.1, Attachment 1, Table 3) where businesses were notified of the recall and removed affected products from commerce that the recall activities were effective.”

 


 

Monday, March 10, 2014

 

Investigators study silent variant of mad cow disease Galveston Daily News March 4, 2014

 


 

Thursday, February 20, 2014

 

Unnecessary precautions BSE MAD COW DISEASE Dr. William James FSIS VS Dr. Linda Detwiler 2014

 


 

Saturday, November 2, 2013

 

APHIS Finalizes Bovine Import Regulations in Line with International Animal Health Standards while enhancing the spread of BSE TSE prion mad cow type disease around the Globe

 


 

Friday, April 4, 2014

 

China, Australia, Argentina, Brazil, Uruguay, Morocco, Israel, South Africa and Saudi Arabia still retain BSE-related closures

 


 

Monday, March 3, 2014

 

*** Gov. C.L. "Butch" Otter of Idaho signs bill that will force consumers to eat dead stock downers and whatever else the industry decides

 

see updated Rancho CLASS 1 HIGH RISK dead stock cancer downer recall for IDAHO

 


 


 

 

*** Because typical clinical signs of BSE cannot always be observed in nonambulatory disabled cattle, and because evidence has indicated these cattle are more likely to have BSE than apparently healthy cattle, FDA is designating material from nonambulatory disabled cattle as prohibited cattle materials.

 


 


 


 


 

Saturday, April 19, 2014

 

Human prion diseases and the risk of their transmission during anatomical dissection

 


 

Saturday, April 19, 2014

 

Estimation of the Exposure of the UK Population to the Bovine Spongiform Encephalopathy Agent through Dietary Intake During the Period 1980 to 1996

 


 

Sunday, April 06, 2014

 

SPORADIC CJD and the potential for zoonotic transmission there from, either directly or indirectly via friendly fire iatrogenic mode, evidence to date

 


 

Thursday, April 17, 2014

Novant: Three more may have been exposed to disease CJD
http://creutzfeldt-jakob-disease.blogspot.com/2014/04/novant-three-more-may-have-been-exposed.html


 

Sunday, August 09, 2009

CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009
http://creutzfeldt-jakob-disease.blogspot.com/2009/08/cjdstraight-talk-withjames.html


 

 

Subject: Re: Hello Dr. Gibbs...........

 

Date: Wed, 29 Nov 2000 14:14:18 –0500

 

From: "Clarence J. Gibbs, Jr., Ph.D."

 

To: "Terry S. Singeltary Sr." References: <3a254430 .9fb97284="" wt.net="">

 

Hi Terry:

 

326 E Stret N.E., Washington, D. C. 20002.

 

Better shrimp and oysters than cards!!!!

 

Have a happy holiday and thanks for all the information you bring to the screen.

 

Joe Gibbs ==========

 

 

Tuesday, August 18, 2009

* BSE-The Untold Story - joe gibbs and singeltary 1999 - 2009
http://madcowusda.blogspot.com/2009/08/bse-untold-story-joe-gibbs-and.html


 

CJD and Baby foods (the great debate 1999)

 

Subject: Re: Girl, 13, shows CJD symptoms.

 

From: "Terry S. Singeltary Sr."

 

Reply-To: Bovine Spongiform Encephalopathy

 

Date: Wed, 24 Nov 1999 11:35:44 -0600 Content-Type: text/plain Parts/Attachments: text/plain (67 lines)

 


 

Sunday, May 18, 2008

 

MAD COW DISEASE BSE CJD CHILDREN VACCINES

 


 

Sunday, May 18, 2008

 

BSE Inquiry DRAFT FACTUAL ACCOUNTS DFAs

 


 

Monday, May 19, 2008

 

*** SPORADIC CJD IN FARMERS, FARMERS WIVES, FROM FARMS WITH BSE HERD AND ABATTOIRS ***

 


 

 

Saturday, April 19, 2014

 

*** Exploring the zoonotic potential of animal prion diseases: In vivo and in vitro approaches ***

 
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).


 

 

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