Alzheimergate? When miscommunication met sensationalism
On Sept 5, The Lancet was alerted by a UK Government source to the
impending publication of a Nature paper allegedly about the possible
transmission of Alzheimer’s disease. The source was anxious about the likely
media coverage and the potential for a public health scare. Although the UK’s
Science Media Centre was involved in helping to communicate the findings
reported in the paper accurately, our source urged us to consider what we might
do to reduce further the risk of a scare. We wrote to the Science Media Centre,
explaining our understanding of the potential alarm and asking if we could help
in some way. The Science Media Centre did not think the paper by John Collinge
and Sebastian Brandner was unduly alarmist. It noted that several highly
experienced press officers were working hard on the communication of the
research findings to prevent any possibility of a scare. They added that if
there were alarmist headlines, it would not be for the want of trying to prevent
them.
On Sept 10, the UK newspapers took a very different angle than predicted,
or hoped for, by our colleagues at the Science Media Centre. Ranging from
“Alzheimer’s may be a transmissible infection” in The Independent to “You can
catch Alzheimer’s” in The Daily Mirror or “Alzheimer’s bombshell” in The Daily
Express, the general tone of the headlines was indeed deeply alarmist. Some news
sources tried to redress the harm done. The BBC ran a story on its website
saying there was “No evidence to support the headlines”. Meanwhile, in many
other countries, the story was either not covered at all, or news headlines at
least included a question mark.
Question marks were wise and judicious additions, if one reads what the
published study actually showed (and did not show). The title promises “Evidence
for human transmission of amyloid-β pathology and cerebral amyloid angiopathy”.
But the study does not provide evidence of human transmission, as the authors
acknowledge themselves in their fi nal paragraph—”there is no suggestion that
Alzheimer’s disease is a contagious disease and no supportive evidence from
epidemiological studies that Alzheimer’s disease is transmissible.” What John
Collinge and Sebastian Brandner’s elegant autopsy study of eight patients shows
is that some patients treated with cadaveric human growth hormone who
subsequently developed iatrogenic Creutzfeldt-Jakob disease also showed evidence
of amyloid β deposition in their pituitary glands. The study does not show
whether these patients would have actually developed Alzheimer’s disease had
they lived longer (they died from Creutzfeldt-Jakob disease and they had no sign
of tau protein pathology characteristic of Alzheimer’s disease). The study does
not demonstrate that these patients’ amyloid β deposits were caused by growth
hormone contaminated with “amyloid β seeds”. As the authors state in the paper,
“Analysis of any residual archival batches of c-hGH [cadaveric-derived human
growth hormone] for both prions and Aβ [amyloid β] seeds might be informative in
this regard”—informative, and actually crucial to support their hypothesis.
Controlled experiments injecting cadaveric human growth hormone into animals to
discover whether amyloid deposits develop as a consequence are also needed to
support their theory.
The much overused phrase “paradigm shift” was quoted in some news reports.
But the fi ndings, although certainly interesting, were a long way from a true
“paradigm shift”. The use of this phrase likely heightened the interest and
attention of journalists—and headline writers. Was “Evidence for human
transmission” an appropriate title for this paper? The report does not describe
human transmission of amyloid pathology. Rather, it reports amyloid pathology in
patients with iatrogenic Creutzfeldt-Jakob disease. Therefore, such a strong
statement in a title also seems misleading and potentially alarmist.
Neuropathology experts, including those selected by the Science Media Centre,
were left with the difficult task of balancing plausible explanations against
tenuous extrapolations. The public ended up being warned about “Alzheimer’s link
to blood transfusions” or “You can catch Alzheimer’s”, thereby generating
unnecessary anxiety and potentially diminishing years of effort against
patients’ stigmatisation.
Taking these events together, this episode of scientific reporting was
handled poorly. One senior protagonist in this affair felt “upset and
bewildered” by the outcome. Despite the best efforts of some, the system in
place to assist science journalists broke down through a mix of inattention and
perhaps even complacency. Preventive actions by the UK’s public health
authorities were too weak and too late. The lesson that might be learned from
this episode is that goodwill and hope are insufficient to prevent a public
health scare. The Lancet
For the Nature paper see http://www.nature.com/nature/journal/v525/n7568/full/nature15369.html
www.thelancet.com Vol 386 September 19, 2015 1109
Wednesday, September 23, 2015
Science Government’s top doctor tried to discredit claims Alzheimer's
might be infectious Dame Sally Davies
Science Government’s top doctor tried to discredit claims Alzheimer's
might be infectious
Dame Sally Davies approached the editor of a rival scientific journal to
discredit the study in the eyes of the public, the Independent understands Steve
Connor | @SteveAConnor | Wednesday 23 September 2015 18:03 BST| 0 comments |
The study suggests the seeds of Alzheimer’s disease may be transmitted
from one person to another during certain medical procedures The study suggests
the 'seeds' of Alzheimer’s disease may be transmitted from one person to another
during certain medical procedures Corbis
A senior government adviser attempted to undermine a controversial study
suggesting that Alzheimer’s is a transmissible disease before it was published
in the journal Nature.
Dame Sally Davies, the chief medical officer at the Department of Health,
approached the editor of a rival scientific journal, The Lancet, to discredit
the study in the eyes of the public, The Independent understands.
Dame Sally told Richard Horton, the editor of The Lancet, that the study
on Alzheimer’s was likely to result in a public scare and asked him for advice
on how to handle the media reaction before it came out in Nature.
The study, published earlier this month, suggested that the “seeds” of
Alzheimer’s disease may be transmitted from one person to another during certain
medical procedures.
It was based on the brain autopsies of eight people aged between 36 and 51
who had died of Creutzfeldt-Jakob disease (CJD) after receiving injections of
human growth hormone derived from the pituitary glands of dead people.
Seven of the eight has signs of a brain protein linked with Alzheimer’s,
although they had no genetic predisposition to the disease and were too young to
have developed it naturally – strongly suggesting transmission via contaminated
hormone injections.
Dame Sally, a haematologist by training, contacted Dr Horton on the
weekend before Nature intended to publish the study having received confidential
information under the strict embargo terms of the journal, which prohibit any
approaches to third parties unless it is “solely for soliciting informed
comment”.
8-Sally-Davies-Get.jpg Dame Sally Davies, chief medical officer at the
Department of Health (Getty)
In an unsigned editorial in The Lancet this week, Dr Horton writes that an
unnamed government source informed him on the study’s impending publication and
urged him to consider what he might do to reduce further the risk of a scare.
Dr Horton then wrote to the Science Media Centre in London, which was
coordinating expert reaction to the study with the help of University College
London and the Medical Research Council, which funded the work by Professor John
Collinge, a world authority on transmissible brain diseases.
Although The Lancet’s source is not identified, The Independent
understands that it was Dame Sally, who knows Dr Horton personally and has
shared several conference platforms with The Lancet’s outspoken editor.
A spokesman for the Department of Health said last night that the identity
of The Lancet’s source is the subject of a freedom of information request and
cannot therefore comment.
It is highly unusual for a government science adviser to approach a
medical journal for help in media management relating to a controversial study
published in a rival journal with its own distinguished track-record of handling
contentious research findings.
hell, this is old news, the government has been trying to cover up that
fact since the late 80s, early 90s.
cover up, cover up, cover up at all cost, including human and animal
health $$$
AND WE ALL KNEW THIS WAS THE CASE $$$
Self-Propagative Replication of Ab Oligomers Suggests Potential
Transmissibility in Alzheimer Disease
Received July 24, 2014; Accepted September 16, 2014; Published November 3,
2014
*** IN STRICT CONFIDENCE ***
Singeltary comment ;
Singeltary comment reply to above ‘’Self-Propagative Replication of Ab
Oligomers Suggests Potential Transmissibility in Alzheimer Disease’’
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
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
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.
CJD1/9 0185 Ref: 1M51A
IN STRICT CONFIDENCE
Dr McGovern 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
1. CMO will wish to be aware that a meeting was held at DH yesterday, 4
January, to discuss the above findings. It was chaired by Professor Murray
(Chairman of the MRC Co-ordinating Committee on Research in the Spongiform
Encephalopathies in Man), and attended by relevant experts in the fields of
Neurology, Neuropathology, molecular biology, amyloid biochemistry, and the
spongiform encephalopathies, and by representatives of the MRC and AFRC. 2.
Briefly, the meeting agreed that:
i) Dr Ridley et als findings of experimental induction of p amyloid in
primates were valid, interesting and a significant advance in the understanding
of neurodegenerative disorders;
ii) there were no immediate implications for the public health, and no
further safeguards were thought to be necessary at present; and
iii) additional research was desirable, both epidemiological and at the
molecular level. Possible avenues are being followed up by DH and the MRC, but
the details will require further discussion. 93/01.05/4.1
BSE101/1 0136
IN CONFIDENCE
5 NOV 1992 CMO From: Dr J S Metters DCMO 4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC
have recognized the public sensitivity of these findings and intend to report
them in their proper context. This hopefully will avoid misunderstanding and
possible distortion by the media to portray the results as having more greater
significance than the findings so far justify.
2. Using a highly unusual route of transmission (intra-cerebral injection)
the researchers have demonstrated the transmission of a pathological process
from two cases one of severe Alzheimer's disease the other of
Gerstmann-Straussler disease to marmosets. However they have not demonstrated
the transmission of either clinical condition as the "animals were behaving
normally when killed'. As the report emphasizes the unanswered question is
whether the disease condition would have revealed itself if the marmosets had
lived longer. They are planning further research to see if the conditions, as
opposed to the partial pathological process, is transmissible. What are the
implications for public health?
3. The route of transmission is very specific and in the natural state of
things highly unusual. However it could be argued that the results reveal a
potential risk, in that brain tissue from these two patients has been shown to
transmit a pathological process. Should therefore brain tissue from such cases
be regarded as potentially infective? Pathologists, morticians, neuro surgeons
and those assisting at neuro surgical procedures and others coming into contact
with "raw" human brain tissue could in theory be at risk. However, on a priori
grounds given the highly specific route of transmission in these experiments
that risk must be negligible if the usual precautions for handling brain tissue
are observed.
92/11.4/1-1 BSE101/1 0137
4. The other dimension to consider is the public reaction. To some extent
the GSS case demonstrates little more than the transmission of BSE to a pig by
intra-cerebral injection. If other prion diseases can be transmitted in this way
it is little surprise that some pathological findings observed in GSS were also
transmissible to a marmoset. But the transmission of features of Alzheimer's
pathology is a different matter, given the much greater frequency of this
disease and raises the unanswered question whether some cases are the result of
a transmissible prion. The only tenable public line will be that "more research
is required" before that hypothesis could be evaluated. The possibility on a
transmissible prion remains open. In the meantime MRC needs carefully to
consider the range and sequence of studies needed to follow through from the
preliminary observations in these two cases. Not a particularly comfortable
message, but until we know more about the causation of Alzheimer's disease the
total reassurance is not practical.
JS METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH
832 121/YdeS 92/11.4/1.2
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
Tuesday, November 26, 2013
Transmission of multiple system atrophy prions to transgenic mice
‘’Our results provide compelling evidence that α-synuclein aggregates
formed in the brains of MSA patients are transmissible and, as such, are
prions.’’
Transmission of a neurodegenerative disorder from humans to mice
The findings suggest that the α-synuclein deposits that form in the brains
of patients with MSA behave like prions and are transmissible under certain
circumstances, according to the authors. — N.Z.
α-Synuclein deposits in the brainstems of inoculated mice.
kind regards, terry
No competing interests declared.
*** Singeltary comment ***
Self-Propagative Replication of Ab Oligomers Suggests Potential
Transmissibility in Alzheimer Disease
Received July 24, 2014; Accepted September 16, 2014; Published November 3,
2014
*** IN STRICT CONFIDENCE ***
Singeltary comment ;
*** NOW PLEASE READ THIS SHORT ABSTRACT FROM DECADES AGO, THE LATE GREAT
DR. GIBBS, PLEASE READ THIS 3 TIMES AND THEN PROCEED***
Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes
contaminated during neurosurgery.
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD
20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of
a middle aged woman with progressive dementia were previously implicated in the
accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger
patients. The diagnoses of CJD have been confirmed for all three cases. More
than two years after their last use in humans, after three cleanings and
repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were
implanted in the cortex of a chimpanzee. Eighteen months later the animal became
ill with CJD. This finding serves to re-emphasise the potential danger posed by
reuse of instruments contaminated with the agents of spongiform
encephalopathies, even after scrupulous attempts to clean them.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract
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
SEE FULL TEXT AND SOURCE REFERENCES ;
Wednesday, May 16, 2012
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Proposal ID: 29403
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==========
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 feed 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.
Wednesday, September 9, 2015
*** Evidence for human transmission of amyloid-β pathology and cerebral
amyloid angiopathy
Wednesday, September 2, 2015
Clinically Unsuspected Prion Disease Among Patients With Dementia
Diagnoses in an Alzheimer’s Disease Database
Tuesday, September 1, 2015
Evidence for α-synuclein prions causing multiple system atrophy in humans
with parkinsonism
Thursday, August 13, 2015
Iatrogenic CJD due to pituitary-derived growth hormone with genetically
determined incubation times of up to 40 years
Friday, January 10, 2014
vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial
type prion disease, what it ???
Tuesday, May 26, 2015
*** Minimise transmission risk of CJD and vCJD in healthcare settings ***
Last updated 15 May 2015
Monday, August 17, 2015
FDA Says Endoscope Makers Failed to Report Superbug Problems OLYMPUS
I told Olympus 15 years ago about these risk factors from endoscopy
equipment, disinfection, even spoke with the Doctor at Olympus, this was back in
1999. I tried to tell them that they were exposing patients to dangerous
pathogens such as the CJD TSE prion, because they could not properly clean them.
even presented my concern to a peer review journal GUT, that was going to
publish, but then it was pulled by Professor Michael Farthing et al... see ;
IBNC Tauopathy or TSE Prion disease, it appears, no one is sure
Singeltary et al
Posted by flounder on 03 Jul 2015 at 16:53 GMT
Tuesday, September 1, 2015
Evidence for α-synuclein prions causing multiple system atrophy in humans
with parkinsonism
Wednesday, January 28, 2015
Another new prion disease: relationship with central and peripheral
amyloidoses
here we go again...
Alzheimer's, iatrogenic, transmissible, tse, prion, what if ?
Wednesday, September 9, 2015
*** Evidence for human transmission of amyloid-β pathology and cerebral
amyloid angiopathy
Wednesday, September 2, 2015
*** Clinically Unsuspected Prion Disease Among Patients With Dementia
Diagnoses in an Alzheimer’s Disease Database
Tuesday, September 1, 2015
*** Evidence for α-synuclein prions causing multiple system atrophy in
humans with parkinsonism
Thursday, September 10, 2015
25th Meeting of the Transmissible Spongiform Encephalopathies Advisory
Committee Food and Drug Administration Silver Spring, Maryland June 1, 2015
Wednesday, September 23, 2015
NIH Availability for Licensing AGENCY: [FR Doc. 2015–24117 Filed 9–22–15;
8:45 am] Detection and Discrimination of Classical and Atypical L-Type BSE
Strains by RT-QuIC
SAVE THE INDUSTRIES AT ALL COST, INCLUDING HUMAN AND ANIMAL HEALTH $$$
that’s why we are in this mess...
Wednesday, September 23, 2015
Science Government’s top doctor tried to discredit claims Alzheimer's might
be infectious Dame Sally Davies
Tracking spongiform encephalopathies in North America
Terry S. Singeltary Sr.
UPDATED DECEMBER 10, 2015
UPDATED DECEMBER 10, 2015
Evidence for human transmission of amyloid-B pathology and cerebral amyloid
angiopathy, Singeltary Submission to Nature
2015-12-07 02:27 AM
