Review
On the issue of transmissibility of Alzheimer disease: A critical review
November/December 2012
Keywords: Alzheimer, dementia, epidemiology, prion, transmissibility
Authors: Christian Schmidt, André Karch, Carsten Korth and Inga Zerr
Christian Schmidt
Corresponding author: schmidt102@gmail.com
Clinical Dementia Center; Department of Neurology; Georg-August University;
Goettingen, Germany
André Karch
Clinical Dementia Center; Department of Neurology; Georg-August University;
Goettingen, Germany
Carsten Korth
Department of Neuropathology; Heinrich-Heine University; Duesseldorf,
Germany
Inga Zerr
Clinical Dementia Center; Department of Neurology; Georg-August University;
Goettingen, Germany
Abstract:
Results from recent experiments with rodents imply that Alzheimer disease
might be inducible by seeding Aβ peptides into recipient animals. In respect to
this new experimental data, public health aspects as well as epidemiological
data have to be reevaluated. In this article, the available experimental and
epidemiological data are reviewed.
snip...
In summary, epidemiological evidence is extremely difficult to assess in
this context. This is especially true, since case definitions and case detection
rates have changed over time. Given the fact that a potential way of
transmission is not only unknown but that no way of transmission can be excluded
yet, careful assessment is imperative.
Public health implications
In the epidemic of non-communicable diseases AD plays an important role for
morbidity and mortality as well as the associated costs. To date, AD is the 6th
leading cause of death in the US and the projected costs in the US by 2050 are
$1.1 trillion.66
Knowledge about transmissibility is essential in all kinds of epidemics for
prevention, diagnosis and treatment. If AD featured transmission patterns
comparable with those of prion diseases, iatrogenic induction/transmission would
play a major role for public health. Prevention would be first priority and
might include measures such as extended sterilization methods for surgical
instruments as well as identification of patients potentially posing a risk as
well as patients at risk. From a public health perspective also alternate ways
of transmission not evaluated yet must be considered. For prevention to work,
biomarkers for early disease detection must be validated, independently of the
ways of possible induction since the disease itself starts well before clinical
onset. As Sigurdsson stated correctly almost 10 years ago, future research on
therapies might also be limited as long as there is no convincing evidence
against transmissibility of AD.8 This is especially true for vaccination studies
and clinical trials using parts of β-amyloid.
Conclusion
In conclusion, with this short review, we want to encourage a broader
discussion and modern epidemiological research in this context. Well-designed
epidemiologic studies have to be initiated. Methodologically these studies must
be constructed to address the epidemiologically challenging aspects of Alzheimer
disease such as dissociation between first neuropathological alterations and
clinical onset, uncertainties in early diagnosis as well as AD
heterogeneity.
This work was supported by a Bundesministerium für Bildung und Forschung
grant within the German Network for Degenerative Dementia (KNDD-2, 2012-2015,
determinants for disease progression in AD, grant no. 01GI1010C), as well as
JPND, EU-FP7 PRIORITY.Authors’ contributions: C.S. was responsible for the
initiation of the project, general conception and the composition of the final
manuscript. A.K. provided parts of the section on epidemiology. C.K. provided
parts of the section on experimental clues regarding AD
transmissibility/inducibility. I.Z. was responsible for the initiation of the
project, the critical review for contentual errors and writing parts of the
conclusion. All authors contributed to the revision of the manuscript. The
authors declare no conflicts of interest.
Wednesday, May 16, 2012
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Proposal ID: 29403
Wednesday, May 16, 2012
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Proposal ID: 29403
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Background
Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease
have both been around a long time, and was discovered in or around the same time
frame, early 1900’s. Both disease, and it’s variants, in many cases are merely
names of the people that first discovered them. Both diseases are incurable and
debilitating brain disease, that are in the end, 100% fatal, with the
incubation/clinical period of the Alzheimer’s disease being longer than the TSE
prion disease. Symptoms are very similar, and pathology is very similar. I
propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation
disease, and that Alzheimer’s is Transmissible, and is a threat to the public
via the many Iatrogenic routes and sources. It was said long ago that the only
thing that disputes this, is Alzheimer’s disease transmissibility, or the lack
of. today, there is enough documented science (some confidential), that shows
that indeed Alzheimer’s is transmissible. The risk factor for friendly fire, and
or the pass-it-forward mode i.e. Iatrogenic transmission is a real threat, and
one that needs to be addressed immediately.
Methods
Through years of research, as a layperson, of peer review journals,
transmission studies, and observations of loved ones and friends that have died
from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant
Creutzfelt Jakob Disease CJD.
Results
The likelihood of many victims of Alzheimer’s disease from the many
different Iatrogenic routes and modes of transmission as with the TSE prion
disease. TSE prion disease survives ashing to 600 degrees celsius, that’s around
1112 degrees farenheit. you cannot cook the TSE prion disease out of meat. you
can take the ash and mix it with saline and inject that ash into a mouse, and
the mouse will go down with TSE. Prion Infected Meat-and-Bone Meal Is Still
Infectious after Biodiesel Production as well. the TSE prion agent also survives
Simulated Wastewater Treatment Processes. IN fact, you should also know that the
TSE Prion agent will survive in the environment for years, if not decades. you
can bury it and it will not go away. TSE prion agent is capable of infected your
water table i.e. Detection of protease-resistant cervid prion protein in water
from a CWD-endemic area. it’s not your ordinary pathogen you can just cook it
out and be done with. that’s what’s so worrisome about Iatrogenic mode of
transmission, a simple autoclave will not kill this TSE prion agent.
Conclusions
There should be a Global Congressional Science round table event (one of
scientist and doctors et al only, NO CORPORATE, POLITICIANS ALLOWED) set up
immediately to address these concerns from the many potential routes and sources
of the TSE prion disease, including Alzheimer’s disease, and a emergency global
doctrine put into effect to help combat the spread of Alzheimer’s disease via
the medical, surgical, dental, tissue, and blood arena’s. All human and animal
TSE prion disease, including Alzheimer’s should be made reportable in every
state, and Internationally, WITH NO age restrictions. Until a proven method of
decontamination and autoclaving is proven, and put forth in use universally, in
all hospitals and medical, surgical arena’s, or the TSE prion agent will
continue to spread. IF we wait until science and corporate politicians wait
until politics let science _prove_ this once and for all, and set forth
regulations there from, we will all be exposed to the TSE Prion agents, if that
has not happened already. what’s the use of science progressing human life to
the century mark, if your brain does not work?
combined cannot exceed 350 Words
shortened to proper word count ;
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Background
Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease
have both been around a long time, and was discovered in or around the same time
frame, early 1900’s. Both diseases are incurable and debilitating brain disease,
that are in the end, 100% fatal, with the incubation/clinical period of the
Alzheimer’s disease being longer (most of the time) than the TSE prion disease.
Symptoms are very similar, and pathology is very similar.
Methods
Through years of research, as a layperson, of peer review journals,
transmission studies, and observations of loved ones and friends that have died
from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant
Creutzfelt Jakob Disease CJD.
Results
I propose that Alzheimer’s is a TSE disease of low dose, slow, and long
incubation disease, and that Alzheimer’s is Transmissible, and is a threat to
the public via the many Iatrogenic routes and sources. It was said long ago that
the only thing that disputes this, is Alzheimer’s disease transmissibility, or
the lack of. The likelihood of many victims of Alzheimer’s disease from the many
different Iatrogenic routes and modes of transmission as with the TSE prion
disease.
Conclusions
There should be a Global Congressional Science round table event set up
immediately to address these concerns from the many potential routes and sources
of the TSE prion disease, including Alzheimer’s disease, and a emergency global
doctrine put into effect to help combat the spread of Alzheimer’s disease via
the medical, surgical, dental, tissue, and blood arena’s. All human and animal
TSE prion disease, including Alzheimer’s should be made reportable in every
state, and Internationally, WITH NO age restrictions. Until a proven method of
decontamination and autoclaving is proven, and put forth in use universally, in
all hospitals and medical, surgical arena’s, or the TSE prion agent will
continue to spread. IF we wait until science and corporate politicians wait
until politics lets science _prove_ this once and for all, and set forth
regulations there from, we will all be exposed to the TSE Prion agents, if that
has not happened already.
end...tss
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
source references
Ann N Y Acad Sci. 1982;396:131-43.
Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob
disease).
Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.
Abstract
Ample justification exists on clinical, pathologic, and biologic grounds
for considering a similar pathogenesis for AD and the spongiform virus
encephalopathies. However, the crux of the comparison rests squarely on results
of attempts to transmit AD to experimental animals, and these results have not
as yet validated a common etiology. Investigations of the biologic similarities
between AD and the spongiform virus encephalopathies proceed in several
laboratories, and our own observation of inoculated animals will be continued in
the hope that incubation periods for AD may be even longer than those of CJD.
BSE101/1 0136
IN CONFIDENCE
CMO
From: Dr J S Metters DCMO
4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
CJD1/9 0185
Ref: 1M51A
IN STRICT CONFIDENCE
From: Dr. A Wight Date: 5 January 1993
Copies:
Dr Metters
Dr Skinner
Dr Pickles
Dr Morris
Mr Murray
TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES
Wednesday, January 5, 2011
ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011 Prions
David W. Colby1,* and Stanley B. Prusiner1,2
Tuesday, October 4, 2011
Molecular Psychiatry
advance online publication 4 October 2011; doi: 10.1038/mp.2011.120
De novo induction of amyloid-ß deposition in vivo
Our results suggest that some of the typical brain abnormalities associated
with AD can be induced by a prion-like mechanism of disease transmission through
propagation of protein misfolding. These findings may have broad implications
for understanding the molecular mechanisms responsible for the initiation of AD,
and may contribute to the development of new strategies for disease prevention
and intervention. Keywords: amyloid; prion; protein misfolding; disease
transmission
see more here ;
Wednesday, September 21, 2011
PrioNet Canada researchers in Vancouver confirm prion-like properties in
Amyotrophic Lateral Sclerosis (ALS)
snip...end
Thank You for accepting my submission
# 29403, Alzheimer’s disease and Transmissible Spongiform Encephalopathy
prion disease, Iatrogenic, what if ? and the opportunity to present it, at the
Alzheimer’s Association International Conference 2012 (AAIC), as a poster
presentation. However, with great sadness, I must regretfully decline the
invitation due to a medical reasons, and traveling to Canada, of which is not
possible. ...
Thank You,
With Kindest Regards,
I am sincerely,
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
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==========
UPDATE JUNE 28, 2012
Scottish TSE Network November Symposium Announcement Event: 12 November
2012
Chair: Prof Hugh Perry, University of Southampton, Southampton UK
Location: The Roslin Institute Building Auditorium
If you would like to book a place at this event, please let Gila Holliman
know.
Cost: £125.
Title: Is Alzheimer’s Disease a transmissible disease?
Speakers:
Session 1:
Prof Bob Will, National CJD Surveillance Unit, Edinburgh UK
Prof James Ironside, National CJD Surveillance Unit, Edinburgh UK
Prof Lary Walker, Emory School of Medicine, Atlanta USA
Session 2:
Prof Mathias Jucker, Hertie Institute for Clinical Brain Research,
Stuttgart Germany
Prof William Van Nostrand, Stony Brook University, Stony Brook USA
Dr Claudio Soto, University of Texas Medical School, Houston USA
Session 3:
Dr Fabrizio Tagliavini, Instituto Neurologico Carlo Besta, Milan Italy
Prof Pedro Piccardo, Food and Drug Administration, Washington DC USA
Dr Bruce Chesebro, National Institutes of Health, Missoula USA
see ;
Wednesday, May 16, 2012
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Proposal ID: 29403
14th ICID International Scientific Exchange Brochure -
Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North
America update October 2009
T. Singeltary
Bacliff, TX, USA
Background:
An update on atypical BSE and other TSE in North America. Please remember,
the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been
documented in North America, along with the typical scrapie's, and atypical
Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these
TSE in different species have been rendered and fed to food producing animals
for humans and animals in North America (TSE in cats and dogs ?), and that the
trading of these TSEs via animals and products via the USA and Canada has been
immense over the years, decades.
Methods:
12 years independent research of available data
Results:
I propose that the current diagnostic criteria for human TSEs only enhances
and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD
only theory in 2009. With all the science to date refuting it, to continue to
validate this old myth, will only spread this TSE agent through a multitude of
potential routes and sources i.e. consumption, medical i.e., surgical, blood,
dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion:
I would like to submit a review of past CJD surveillance in the USA, and
the urgent need to make all human TSE in the USA a reportable disease, in every
state, of every age group, and to make this mandatory immediately without
further delay. The ramifications of not doing so will only allow this agent to
spread further in the medical, dental, surgical arena's. Restricting the
reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO
age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge,
Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al
and many more, that the world of TSE Transmissible Spongiform Encephalopathy is
far from an exact science, but there is enough proven science to date that this
myth should be put to rest once and for all, and that we move forward with a new
classification for human and animal TSE that would properly identify the
infected species, the source species, and then the route.
Friday, October 05, 2012
Differential Diagnosis of Jakob-Creutzfeldt Disease
Monday, August 20, 2012
CASE REPORTS CREUTZFELDT-JAKOB DISEASE: AN UNDER-RECOGNIZED CAUSE OF
DEMENTIA
see the Duke, Pa, Yale, and Mexican study here, showing the misdiagnosis of
CJD TSE prion disease as Alzheimers ;
Terry S. Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health
Crisis
full text with source references ;
re-Human Prion Diseases in the United States Posted by flounder on 01 Jan
2010 at 18:11 GMT
I kindly disagree with your synopsis for the following reasons ;
Tuesday, November 08, 2011
Can Mortality Data Provide Reliable Indicators for Creutzfeldt-Jakob
Disease Surveillance? A Study in France from 2000 to 2008 Vol. 37, No. 3-4, 2011
Original Paper
Conclusions:These findings raise doubt about the possibility of a reliable
CJD surveillance only based on mortality data.
Views & Reviews
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in
the United States
Ermias D. Belay, MD, Ryan A. Maddox, MPH, Pierluigi Gambetti, MD and
Lawrence B. Schonberger, MD
+ Author Affiliations
From the Division of Viral and Rickettsial Diseases (Drs. Belay and
Schonberger and R.A. Maddox), National Center for Infectious Diseases, Centers
for Disease Control and Prevention, Atlanta, GA; and National Prion Disease
Pathology Surveillance Center (Dr. Gambetti), Division of Neuropathology,
Institute of Pathology, Case Western Reserve University, Cleveland, OH.
Address correspondence and reprint requests to Dr. Ermias D. Belay, 1600
Clifton Road, Mailstop A-39, Atlanta, GA 30333.
26 March 2003
Terry S. Singeltary, retired (medically) CJD WATCH
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment
on the CDC's attempts to monitor the occurrence of emerging forms of CJD.
Asante, Collinge et al [1] have reported that BSE transmission to the
129-methionine genotype can lead to an alternate phenotype that is
indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD
and all human TSEs are not reportable nationally. CJD and all human TSEs must be
made reportable in every state and internationally. I hope that the CDC does not
continue to expect us to still believe that the 85%+ of all CJD cases which are
sporadic are all spontaneous, without route/source. We have many TSEs in the USA
in both animal and man. CWD in deer/elk is spreading rapidly and CWD does
transmit to mink, ferret, cattle, and squirrel monkey by intracerebral
inoculation. With the known incubation periods in other TSEs, oral transmission
studies of CWD may take much longer. Every victim/family of CJD/TSEs should be
asked about route and source of this agent. To prolong this will only spread the
agent and needlessly expose others. In light of the findings of Asante and
Collinge et al, there should be drastic measures to safeguard the medical and
surgical arena from sporadic CJDs and all human TSEs. I only ponder how many
sporadic CJDs in the USA are type 2 PrPSc?
Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al.
JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1
reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD)
has been stable since 1985. These estimates, however, are based only on reported
cases, and do not include misdiagnosed or preclinical cases. It seems to me that
misdiagnosis alone would drastically change these figures. An unknown number of
persons with a diagnosis of Alzheimer disease in fact may have CJD, although
only a small number of these patients receive the postmortem examination
necessary to make this diagnosis. Furthermore, only a few states have made CJD
reportable. Human and animal transmissible spongiform encephalopathies should be
reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob
disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. FREE FULL
TEXT
The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003
doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI
Tracking spongiform encephalopathies in North America
Original
Xavier Bosch
“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my
mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever
since. What I have found is that we have not been told the truth. CWD in deer
and elk is a small portion of a much bigger problem.” 49-year—old Singeltary is
one of a number of people who have remained largely unsatisfied after being told
that a close relative died from a rapidly progressive dementia compatible with
spontaneous Creutzfeldt—Jakob ...
2 January 2000
British Medical Journal
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well
15 November 1999
British Medical Journal
vCJD in the USA * BSE in U.S.
Saturday, January 2, 2010
Human Prion Diseases in the United States January 1, 2010 ***FINAL***
Monday, March 29, 2010
CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN
AND SPINAL CORD MATTER URGENT, PLEASE NOTE ;
>>> Up until about 6 years ago, the pt worked at Tyson foods where
she worked on the assembly line, slaughtering cattle and preparing them for
packaging. She was exposed to brain and spinal cord matter when she would
euthanize the cattle. <<<
Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010
in Mesquite Texas.
She left 6 Kids and a Husband.The Purpose of this web is to give
information in Spanish to the Hispanic community, and to all the community who
want's information about this terrible disease.- Physician Discharge Summary,
Parkland Hospital, Dallas Texas Admit Date: 12/29/2009 Discharge Date: 1/20/2010
Attending Provider: Greenberg, Benjamin Morris; General Neurology Team: General
Neurology Team Linda was a Hispanic female with no past medical history presents
with 14 months of incresing/progressive altered mental status, generalized
weakness, inability to walk, loss of appetite, inability to speak, tremor and
bowel/blader incontinence. She was, in her usual state of health up until
February, 2009, when her husbans notes that she began forgetting things like
names and short term memories. He also noticed mild/vague personality changes
such as increased aggression. In March, she was involved in a hit and run
MVA,although she was not injured. The police tracked her down and ticketed her.
At that time, her son deployed to Iraq with the Army and her husband assumed her
mentation changes were due to stress over these two events. Also in March, she
began to have weakness in her legs, making it difficult to walk. Over the next
few months, her mentation and personality changes worsened, getting to a point
where she could no longer recognized her children. She was eating less and less.
She was losing more weight. In the last 2-3 months, she reached the point where
she could not walk without an assist, then 1 month ago, she stopped talking,
only making grunting/aggressive sounds when anyone came near her. She also
became both bowel and bladder incontinent, having to wear diapers. Her
'"tremor'" and body jerks worsened and her hands assumed a sort of permanent
grip position, leading her family to put tennis balls in her hands to protect
her fingers. The husband says that they have lived in Nebraska for the past 21
years. They had seen a doctor there during the summer time who prescribed her
Seroquel and Lexapro, Thinking these were sx of a mood disorder. However, the
medications did not help and she continued to deteriorate clinically. Up until
about 6 years ago, the pt worked at Tyson foods where she worked on the assembly
line, slaughtering cattle and preparing them for packaging. She was exposed to
brain and spinal cord matter when she would euthanize the cattle. The husband
says that he does not know any fellow workers with a similar illness. He also
says that she did not have any preceeding illness or travel.
Friday, August 24, 2012
Iatrogenic prion diseases in humans: an update
Thursday, April 12, 2012
Health professions and risk of sporadic Creutzfeldt–Jakob disease, 1965 to
2010
Eurosurveillance, Volume 17, Issue 15, 12 April 2012
Research articles
snip...
In 2009, a pathologist with sporadic Creutzfeldt–Jakob Disease (sCJD) was
reported to the Spanish registry. This case prompted a request for information
on health-related occupation in sCJD cases from countries participating in the
European Creutzfeldt Jakob Disease Surveillance network (EuroCJD). Responses
from registries in 21 countries revealed that of 8,321 registered cases, 65
physicians or dentists, two of whom were pathologists, and another 137
healthcare workers had been identified with sCJD. Five countries reported 15
physicians and 68 other health professionals among 2,968 controls or non-cases,
suggesting no relative excess of sCJD among healthcare professionals. A
literature review revealed: (i) 12 case or small case-series reports of 66
health professionals with sCJD, and (ii) five analytical studies on
health-related occupation and sCJD, where statistically significant findings
were solely observed for persons working at physicians' offices (odds ratio: 4.6
(95 CI: 1.2–17.6)). We conclude that a wide spectrum of medical specialities and
health professions are represented in sCJD cases and that the data analysed do
not support any overall increased occupational risk for health professionals.
Nevertheless, there may be a specific risk in some professions associated with
direct contact with high human-infectivity tissue.
snip...
Friday, August 10, 2012
Incidents of Potential iatrogenic Creutzfeldt-Jakob disease (CJD) biannual
update (July 2012)
Wednesday, January 5, 2011
ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011
Prions
David W. Colby1,* and Stanley B. Prusiner1,2
Monday, March 26, 2012
CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE
OR-09 15:10 - 15:25
CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE
======================
*** Saturday, October 6, 2012
*** TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE
SPONGIFORM ENCEPHALOPATHIES 2011 Annual Report
======================
MOM DOD 12/14/97 hvCJD confirmed, Uncle Bo DOD today 10/13/12 RIP with severe
and rapid last two weeks Alzheimer’s, he was fishing off pier two weeks ago,
hospice 3 days ago, to DOD TODAY (no brain autopsy)?, Mema passed with moderate
to slow dementia type Alzheimer’s, wonder what kind of dementia I will get ?
======================
TSS
