Corrupted Proteins Spread Disease

A protein fragment involved in Alzheimer’s can seed new clusters throughout the brain, pointing to prion-like qualities of the disease.

By | June 18, 2012

image: Corrupted Proteins Spread Disease Amyloid-beta plaques in brain tissueWikimedia Commons, Nephron

Amyloid-beta plaques in brain tissueWIKIMEDIA COMMONS, NEPHRON

Many neurological diseases are caused by misfolded proteins that gather in large, destructive clumps, causing neuronal degeneration. Some of these proteins can also convert normal versions into their own twisted images, thus spreading the disease throughout the brain. The classic examples are prion diseases like mad cow disease and Creutzfeld-Jacob disease (CJD). They are caused by misshapen forms of the PrP protein, which corrupts the shapes of normal PrPs.

Now, new research published today in the Proceedings of the National Academy of Sciences suggests that Alzheimer’s disease might work in a similar way. Its hallmarks include tangled clumps of amyloid-beta, a peptide (protein fragment) that aggregates in large plaques, which according to the new study, can seed more protein clusters, creating a wave of plaques that spreads through the brain.

“While this had been suspected, there was previously no proof,” said Kurt Giles, who studies neurodegenerative diseases at the University of California, San Francisco, and led the new study. “I think it is a really important paper,” added Anne Bertolotti from the MRC Laboratory of Molecular Biology, who also works on misfolded proteins but was not involved in the research. “It strongly supports the idea that the prion phenomenon applies to Alzheimer's disease.”

In 1982, Nobel prize-winner Stanley Prusiner first discovered prions—misfolded proteins that act as infectious agents, spreading the disease within and among individuals. Two years later, he speculated that Alzheimer’s disease might involve a similar spread of malformed proteins, at least within patients. Recent experiments have supported his idea. For example, Lary Walker from Emory University and Mathias Jucker from the University of Tübingen managed to trigger the spread of amyloid-beta plaques in the brains of mice by injecting them with brain extracts already containing clumps of the peptide.

But these extracts always contained other proteins that could have been responsible for the spread of the plaques. Now, Prusiner, along with Jan Stohr and Joel Watts from University of California, San Francisco, have shown that pure amyloid-beta can achieve the same effect on its own.

The researchers injected purified amyloid-beta into mice whose brains were engineered to fluoresce as plaques built up. By measuring the light given off by their brains, the team showed that the purified peptides were enough to induce plaques throughout the brain within 5 to 6 months. Even if the peptides were injected into just one side of the brain, both halves eventually started to glow.

Next, the team created the peptides from scratch “so there could be no doubt about other contaminants,” Giles said, and even these synthetic peptides were enough to create plaques. “It’s the first clear demonstration that amyloid-beta alone can induce amyloid-beta deposition in the living brain,” said Walker.

The synthetic peptides did appear to be somewhat less effective at seeding fresh plaques than the purified versions, however. It may be that only some “strains” of amyloid-beta can cause native proteins to clump together, or that different strains spread at different speeds, Walker said—“not all seeds are equivalent.” Identifying the strains that most accelerate Alzheimer’s disease could provide novel drug targets, Giles added.

It is becoming increasingly clear that the spread of corrupted proteins is a unifying feature in many brain diseases. Clumps of alpha-synuclein, a protein involved in Parkinson’s disease, for example, can spread from one neuron to another, transform local proteins, and gather them into clusters. SOD1, a protein involved in Lou Gehrig’s disease, can do the same.

However, unlike classical prions, it doesn’t appear that the corrupted proteins in involved these diseases can spread infections from one individual to another. “There is still no evidence that Alzheimer’s disease is infectious under everyday circumstances,” said Walker.

J. Stohr et al.. “Purified and synthetic Alzheimer’s amyloid beta (Aß) prions,” Proceedings of the National Academy of Sciences, doi:10.1073/pnas.1206555109, 2012.

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Avatar of: wiz652

wiz652

Posts: 1

June 19, 2012

Interesting article...so what would happen if the Alzheimer plaque material was fed to the mice instead of injection? or even still transfused blood?

Avatar of: Edgehrman

Edgehrman

Posts: 2

June 19, 2012

Prion research is a dead end.  The TSE diseases are all the result of spiroplasma infection.  Anyone interested should read the research of Dr. Frank Bastian.
His latest efforts can be found at
http://www.sciencedirect.com/s...

Prions are the result of infection, not the cause.
Ed Gehrman

Avatar of: Guest

Anonymous

June 19, 2012

It's good to see prions back in the news.

Remember where you first read or heard what I am about to say, please.  On more than one occasion this old retired commenter has asserted something that has drawn much disagreement and even much resentment and anger -- yet, later on, as someone ELSE'S claimed brainstorm, it has taken hold.  A half century ago, this then-young thorn in the side of professors he argued with was accused by a professor of plagiarism, on grounds a paper he wrote was TOO GOOD to have been written by its writer.  I threw down the gauntlet, "Prove it and you won't have to charge me formally, because I'll quit."

Some assertions from that paper mysteriously showed up, a year or so later, in a speech by that professor.

Recently in this forum this bloody-but-unbowed old head drew much objection for saying that the field of bio-evolution theory is being dragged into the 21st Century kicking and screaming.  It's problem, I continue to maintain, is that it places too much emphasis on phenomena that occur at the macro-biological dynamic, and many of its most die-hard apologists continue to cite, in defense of their hypotheses, definitions and phenomena which have been popular since Darwin's day.  I pointed out that my argument is not that those macro-phenomena do not occur, but rather that the mechanisms driving most heritable changes in species will be found over time, not at the macro level, but at the level of smaller and smaller emergent levels-of-size-scale-unique dynamics (ELOSSUD's).

(One example of two different size scale dynamic sets, each with its own "laws," is classical physics versus quantum physics.  An example from biology is macrobiology versus microbiology.  Just as neither Newton nor Leibniz came come up with much that had not been thought of and mentioned by someone else previously,  they made a huge impact on calculation and technical analysis and design, organizing those previously touched-on ideas into a veritable powerhouse mathematical engine.  Similarly, no matter how much Napier developed powerful logarithmic tables applying the number e, it would not be until Bernoulli that its importance and usefulness would be recognized and fully unveiled.  And now I predict that someone will suddenly, perhaps sometime soon, "reveal" the power of focusing upon the differential dynamic systems that emerge at various size scales, and their inter-dynamical relationships.) 
 
But now to the phenomenon of self-propagation or self-driven-self-replication in nature, and prions...

Throughout the study of nature (which sometimes is mistaken for mankind's anthropocentric and egocentric exploitation of nature) one of the recurring themes is what might be termed conglomerations of characteristics which predispose to self-perpetuation, or self-driven-propagation, or self-driven replication.  The common characteristic of "things" that fall into this "class" is that whatever symmetry of characteristics they have, tends one way or another to increase the population of what amounts to copies of itself.  Some cancers metastasize.  Some simple organisms multiply by dividing in two.  Some ideas (now given the name "memes") seem to take on a metaphorical "life of their own," and "multiply" across income levels and cultural level and such.  So, let me repeat for emphasis, somebody, one of these days, is going to focus on they details of the dynamics of self-copying drivers... seeking to know how any two of them differ from one another, and how many (though probably not all) share some particulars in common OTHER THAN merely the characteristic of somehow drawing energy from their milieu and utilizing it to cause, or influence, copies of themselves to be made.

Prions do this.  Some crystals do it.  Bacteria do it.  Viruses (by invading and exploiting cells) do this, and, cancer cells, rather than doing what their hosts own homeostasis would benefit from, rebel and say, in effect, "To heck with you, I'm going to make copies of MYSELF... even if it kills us both."  The birds and the bees do it.  And perhaps it will be not only interesting but also highly useful -- when someone gets around to it -- to make a specialty of studying whether, and if so what, are the COMMON characteristics (I don't mean the macrocharacteristics -- the kind many bio-evo theorists seem to want to use to focus in in pointing out the change HAPPENS) but the subtleties which arise out of the unique dynamic sets of things as they occur as OTHER EMERGENT SIZE-SCALE LEVELS (and the inter-dynamical stimulus-response patterns whereby one such level interfaces with another).

Some minds balk when confronted with anything they are not already programmed to perceive.

That's okay.

Someday someone will toss it out there and, instead of being generally balked against, it will catch on with first one, and than another... will resonate... and will become a meme... will get focused on in a new and different way... and here and there one researcher, and then another and another, will get up the will and the courage to make a specialty of studying it.

Until then, it will be nothing new, and not much worth being talked about.

(:>)

 

Avatar of: Edgehrman

Edgehrman

Posts: 2

June 19, 2012

Basically, for four decades, some researchers have continued to suspect
bacteria or virus to be involved in TSE diseases. However, in the early 1980s
some researchers were frustrated by the inability to specifically identify a
bacterial or viral origin and hence proposed a non-biotic process as creating
these diseases, AKA non- DNA coded prions (proteinaceous infectious particles).
Through very adroit and expert PR manipulation, the theory (initially nixed by
the scientific community) caught on and eventually led to a Nobel Prize for Dr.
Stan Pruisner. Since then, research monies have flowed like water, but the
results have been less than stellar. Prion theory has major flaws, some
seemingly fatal, e.g., multiple strains of disease (21 kinds of sheep scrapie),
animal-to-animal transmission but no detectable transferring agent, a
suppression of the disease by tetracycline (an antibiotic), the presence of
foreign DNA within diseased cells, and so on.

As such, when my own animals contracted CWD (I had 350 elk, 3 of which got
the disease) I watched the disease progression very closely. Using basic
scientific observation skills (I am a geologist-geochemist, a noted elk expert
and national championship level elk antler grower) I tried to better understand
the disease. Then, over the next year I read all I could find from the National
Institute of Health library, and discovered that not everyone believes in
prions. A Tulane University professor had very interesting proofs that TSE may
be caused by bacteria.

The gist of this theory (actually Dr. Bastian's, as he originally proposed it
some 35 years ago) is founded and explained with my disease "symptom chart"
found about two-thirds of the way into the paper. There are twenty-one symptoms
of TSE disease and a bacteria can cause all 21 of them! Every symptom of TSE
disease can be explained by a very peculiar bacteria which is very poorly
understood by most medical personnel. Sprioplasmas were only "discovered" in the
mid-1970s. All my proofs are from independently documented sources. When
presented in the whole (for the first time in my paper) the evidence is, in my
humble opinion, overwhelming. This is the first time anyone will have seen all
this information in one place. This makes a compelling case!
http://www.deer-library.com/ar...

Dr. Bastian's latest research can be found at

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http://www.sciencedirect.com/s...

June 19, 2012

Um, I thought everybody already knew about this --- that prions and "Alzheimer's protein" have this close similarity and can "seed" the unfolding of not-yet-unfolded versions of their own amino acid sequences ...

There are patents out there for detection mechanisms that are based on this fundamental physico-chemical property of both of these proteins ...

Duh.

June 19, 2012

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?
 
http://aaic.scsubmissions.com/...
 
 
 
 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.
 
 
http://onlinelibrary.wiley.com...
 
 

BSE101/1 0136
 
 IN CONFIDENCE

CMO

From: Dr J S Metters DCMO

4 November 1992
 
 TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
 
 
http://collections.europarchiv...
 
 
 
 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
 
 
http://collections.europarchiv...
 
 

Wednesday, January 5, 2011

ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011 Prions

David W. Colby1,* and Stanley B. Prusiner1,2
 
 
http://cshperspectives.cshlp.o...
 
 

http://betaamyloidcjd.blogspot...
 
 

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
 
 
http://www.nature.com/mp/journ...
 
 
see more here ;
 
 

http://betaamyloidcjd.blogspot...
 
 

http://transmissiblespongiform...
 
 

Wednesday, September 21, 2011
 
 
PrioNet Canada researchers in Vancouver confirm prion-like properties in Amyotrophic Lateral Sclerosis (ALS)
 
 

http://transmissiblespongiform...
 
 

http://betaamyloidcjd.blogspot...

 
 

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==========
 
 

http://betaamyloidcjd.blogspot...

TSS

Wednesday, May 16, 2012

Alzheimer’s disease and
Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?

Proposal ID: 29403

http://betaamyloidcjd.blogspot...

June 20, 2012

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

From: Terry S. Singeltary Sr.

Sent: Wednesday, May 16, 2012 3:29 PM

To: CJD-L@LISTS.AEGEE.ORG

Subject: [CJD-L] 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?

http://aaic.scsubmissions.com/...

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.

http://onlinelibrary.wiley.com...

BSE101/1 0136

IN CONFIDENCE

CMO

From: Dr J S Metters DCMO

4 November 1992

TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES

http://collections.europarchiv...

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

http://collections.europarchiv...

Wednesday, January 5, 2011

ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011
Prions

David W. Colby1,* and Stanley B. Prusiner1,2

http://cshperspectives.cshlp.o...

http://betaamyloidcjd.blogspot...

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

http://www.nature.com/mp/journ...

see more here ;

http://betaamyloidcjd.blogspot...

http://transmissiblespongiform...

Wednesday, September 21, 2011

PrioNet Canada researchers in Vancouver confirm prion-like properties in
Amyotrophic Lateral Sclerosis (ALS)

http://transmissiblespongiform...

http://betaamyloidcjd.blogspot...

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==========

http://betaamyloidcjd.blogspot...

Wednesday, May 16, 2012

Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?

Proposal ID: 29403

http://betaamyloidcjd.blogspot...

 

layperson

Terry S. Singeltary Sr.

Avatar of: N K Mishra

N K Mishra

Posts: 1457

June 21, 2012

Misfolding could be due to substitution of amino acid residues or by enzymatic/ non-enzymatic breaks at certain places along the protein chain. Factors that promote Protein-protein aggregation giving rise to plaques have to be looked into.

Avatar of: Zack Mensinger

Zack Mensinger

Posts: 1

June 22, 2012

But it had not been previously shown that synthetic peptide alone could induce that misfolding in vivo.

Avatar of: mistersoft

mistersoft

Posts: 2

June 25, 2012

...but (A)  that's really obvious ...i've worked in the field previously, and I'm gobsmacked that hasn't been done before(!)

and (B) oligomers NOT amyloid fibrillar tangles and plaques have been shown to be the real cytotoxic agents of neuronal damage ...and (I'm nigh on certain, the following has been posited if not proven too..)  that the body might even encourage "partly misfolded protein" (the little devil seeds if you will) to go right down the amyloid/fibrillar path rather than stick at forming stable /quasi-stable oligomers and cause the damage they do...

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