Print

---

Thanks for the Info, Mel.
Extremely informative, and shaking in its implications.

Owen Sant' Angelo
[log in to unmask]

----- Original Message -----
From: <[log in to unmask]>
To: <[log in to unmask]>
Sent: Friday, February 02, 2001 7:02 PM
Subject: Brain Eroding Diseases


> Most of us will now have been made aware by the media of an horrific brain
> eroding disease called Mad Cow or Creutzfeld-Jakob Disease.  The following
> selections of readings provide some interesting insights into the nature
of
> this unique disease.
>
> < http://www.sightings.com/health/madcowinfridge.htm>
>
> Mad Cow Disease causes no antibody response. The damage to the brain is
done
> by infectious prions or rogue proteins which become part of the cell walls
in
> the infected host. When infection enters any animal, the victim's immune
> system shows no sign of fighting the infection as it does with bacteria,
> germs, and viruses.  This means the immune system can neither detect nor
> fight it, nor can scientists use the antibody-search method to see if
someone
> is sick, as we do with AIDS.   CJD (Creutzfeld-Jakob Disease) disease
takes
> 10 months to 50 years to eat away human brain.
>
> Mad Cow, or BSE, (Bovine Spongiform Encephalopathy) causes transmissable
> genetic mutation which means that if you have it,  all your children will
be
> born with it. Sheep and cows pass it to offspring, too, and chickens to
their
> eggs. If it weren't transmissable, why for decades has the FDA demanded
that
> all donors to the blood supply answer the question 'has anyone in your
family
> died of CJD?  That disease is entirely inherited and one drop of blood of
a
> descendant of a CJD victims can infect the rest of your line.  PRION
diseases
> are well known to be genetic in that they bond with with DNA and are
passed
> on.
>
> No scientist can tell if a cow or human is in an incubating phase. Except
for
> brain biopsies, there are no tests, no genetic markers. Prions are not
> reliably found in urine. You can see prions in brain tissue but you cannot
> open the skull of a live mammal to scoop them out. If a cow whose milk you
> are drinking has it, her calf, sent to be a veal chop last Winter, also
had
> it when you ate it.  A long incubation period means that the farmer cannot
> see that the animal is ill.
>
> Consider the link which scientists are now following.  Alzheimer's is
rampant
> in America and yet few people talk about how these scientists think that
it
> could also be a prion or protein-borne disease associated with the
> consumption of tainted meat and dairy products.   This research began in
> earnest when Pittsburgh Veterans hospital autopsied 53 SEQUENTIAL
Alzheimer's
> victims.  Sample A showed 5.5% had died of Mad-Cow; Sample B showed that
6.3
> Percent died of Mad-Cow. Alzheimer's death tolls are doubling and
tripling,
> which is not characteristic of a normal genetic disease.  It appears as if
> some statistics for Mad Cow and CJD are being obscured by Alzheimer’s
> statistics.
>
> Pasteurization or even radiation cannot destroy prions which can tolerate
> these adverse conditions because they are not living infectious agents.
Mad
> Cow prions can't be killed the way we fought the plague or fight cholera
> epidemics, or Ebola, by burning bodies. Prions are, for all practical
> purposes, indestructible. These rogue proteins will only begin to degrade
at
> 800 degrees fahrenheit, way above the temperature that would reduce them
to
> ash! In fact, burning is a bad idea, as prion molecules will rise up in
the
> smoke, become airborne and fall back on the land.
>
> No laboratory will accept a Mad Cow autopsy as the laboratory cannot be
> sterilized afterwards. You canot kill prions with fire or disinfecting
> agents. Those are the facts. Remember, beef and sheep farmers have been
> sending livestock to factories to be made into 'protein powder' for
livestock
> for the last 26 years.   Mad Cow prions could be in every ounce of meat,
> milk, pork, chicken, egg, cheese, or butter you eat today and in gelatin
> caps, animal glandular supplements, and in the glue on every postage
stamp.
> Until all slaughterhouses have brain autopsy labs, until no animal we eat
is
> fed another animal's dead body, under penalty of law, and not just leaving
it
> to farmers' discretion, nobody can feel safe eating meat, butter, eggs or
> drinking milk any longer.
>
> Chickens and turkeys are also high risk because cattle blood is sprayed
onto
> their feed! The FDA recommended a ban on feeding dead cows to live ones,
but
> has said nothing about the practice of using the blood of cattle as food
for
> cattle or any other livestock or poultry. Any good doctor will tell you
that
> the blood is a carrier of virtually all diseases present in a sick animal.
> So, remember the next time you are in line at the fast food restaurant, or
> heading out to your favourite steak house, you might be about to eat your
way
> to a prion eroded brain in a few years' time, especially if the prions are
> found to be the missing link in the Alezheimer’s riddle.
>
> ------------------------------------------------------
>
> Here are some sites with plenty of information on Creutzfeld-Jakob (CJD)
and
> Mad Cow Disease:
>
> <http://www.cjdfoundation.org/CJDInfo.html>
> <http://www.mad-cow.org/>
>
> ----------------------
>
> One of the theories explaining these types of disease maintains that
special
> infectious proteins called "prions" (proteinaceous infectious particle)
cause
> "Mad Cow" disease.  The following websites discuss this topic:
>
> <http://www.sciam.com/askexpert/medicine/medicine14.html>
>
> "The term 'prion' was coined by Stanley B. Prusiner of the University of
> California School of Medicine at San
> Francisco in 1982 to distinguish the infectious agent that causes scrapie
in
> sheep, Creutzfeldt-Jakob disease
> (CJD) in humans and bovine spongiform encephalopathy (BSE) in cattle from
> other, more typical infectious
> agents. The prion hypothesis postulates that these diseases are caused not
by
> a conventional virus or bacterium
> but by a protein that has adopted an abnormal form.
>
> Here is an article by Dr Prusiner himself reporting  in "The Scientific
> American" on the nature of prions:
>
> <http://www.sciam.com/0896issue/prion.html>
>
> "Fifteen years ago I evoked a good deal of skepticism when I proposed that
> the infectious agents causing certain degenerative disorders of the
central
> nervous system in animals and, more rarely, in humans might consist of
> protein and nothing else. At the time, the notion was heretical. Dogma
held
> that the conveyers of transmissible diseases required genetic material,
> composed of nucleic acid (DNA or RNA), in order to establish an infection
in
> a host. Even viruses, among the simplest microbes, rely on such material
to
> direct synthesis of the proteins needed for survival and replication.
>
> Later, many scientists were similarly dubious when my colleagues and I
> suggested that these "proteinaceous infectious particles"-or "prions," as
I
> called the disease-causing agents-could underlie inherited, as well as
> communicable, diseases. Such dual behavior was then unknown to medical
> science. And we met resistance again when we concluded that prions
> (pronounced "pree-ons") multiply in an incredible way; they convert normal
> protein molecules into dangerous ones simply by inducing the benign
molecules
> to change their shape.
>
> Today, however, a wealth of experimental and clinical data has made a
> convincing case that we are correct on all three counts. Prions are indeed
> responsible for transmissible and inherited disorders of protein
> conformation. They can also cause sporadic disease, in which neither
> transmission between individuals nor inheritance is evident. Moreover,
there
> are hints that the prions causing the diseases explored thus far may not
be
> the only ones. Prions made of rather different proteins may contribute to
> other neurodegenerative diseases that are quite prevalent in humans. They
> might even participate in illnesses that attack muscles."
>
> -------------------------------------------
>
> This article discusses potential risks from vaccines and cultures made
from
> cattle:
>
> <http://www.mad-cow.org/00/01jan_news.html>
>
> -------------------------------------------
>
> This article discusses similarities between Mad Cow and Alzheimer's
Proteins
>
> <http://www.cnn.com/2000/HEALTH/08/24/bc.health.madcow.reut/>
>
> WASHINGTON (Reuters) August 24, 2000 -- Proteins linked with Alzheimer's
and
> the human version of mad cow disease have some striking similarities --
and
> thus might be susceptible to similar treatments, a researcher said.  Both
> diseases are marked by a gradual deterioration of the brain and both are
> associated with rogue proteins. Both are always fatal.
>
> Chi Ming Yang, a professor of chemistry at Nankai University in Tianjin,
> China, said he used a computer model to map the prion protein associated
with
> Creutzfeldt-Jakob disease (CJD), the human equivalent of mad cow disease,
and
> the amyloid precursor protein associated with Alzheimer's.
>
> Proteins are made up of amino acids, and Yang told a meeting of the
American
> Chemical Society in Washington that he found a similar pattern of amino
acids
> in the two proteins -- a reductive amino acid followed by three
non-reductive
> amino acids.   "This suggests a common molecular mechanism underlying the
> initiation stages of sporadic Alzheimer's disease and both sporadic and
> genetic prion diseases," he said in a statement.
>
> ------------------------------------------
>
> The Mystery of Mad Cow Disease:
>
> <http://www.msnbc.com/news/439861.asp?cp1=1&cp1=1#BODY>
>
> "THE CULPRIT behind the so-called transmissible spongiform
encephalopathies
> (TSEs), such as mad cow disease or the human version, Creutzfeldt-Jakob
> disease, is thought by many to be a misfolded protein called a prion.
These
> misshapen molecules also have been linked to more common, non-infectious
> brain diseases such as Alzheimer’s, Parkinson’s, Huntington’s and Lou
> Gehrig’s.   If prions truly are the culprits behind these diseases, their
> existence flies in the face of the conventional wisdom that only organisms
> with a genome (such as viruses or bacteria) can spread disease or
perpetuate
> themselves in living cells."
>
> --------------------------------------
>
> What USA Authorities may not be admitting about CJD:
>
> A cover-up style of article citing instances of where CJD was first spread
> among cattle in the USA, and only later to the UK.  You will have to check
> through various references to extract what is fact and what is not:
>
> <http://home.earthlink.net/~astrology/udder.htm>
>
> "....From the Pittsburgh sampling we realize that there are hundreds if
not
> thousands of CJD deaths in America but they are passed off as Alzheimer's.
> BSE (Bovine Spongiform Encephalopathy)  is entrenched in American beef
> regardless of what the US Government wants you to believe, and boy, there
> seems to be an  effort to control what you believe.
>
> Ted Koppel interviewed BSE and CJD expert, Dr. Richard Marsh, on the
> Nightline TV program in 1996.   The interview went like this:
>
> Koppel:   But we (USA) don't feed sheep brains to cows, do we?"
> Dr Marsh blinked. "I don't know where your information comes from, but we
> do."
> He was instantly cut off by a commercial and did not reappear  that night.
> (Capitol Cities which owns ABC was founded by William Casey of the CIA. It
is
> as close to being an official mouthpiece of the oligarchy as exists....
>
> The truth is, Virologist Veteran Marsh knows of what he speaks. All those
BSE
> cow bodies he saw in Wisconsin 1981-1989 had been fed dead  sheep, yet the
> cows became 'feeder cattle' to feed thousands of other cows who have bred
> thousands of animals. Papuan prions have  been spread to herds from Maine
to
> Hawaii. Knowing the genetic mode of transmission of the disease is to all
> offspring, it is reasonable to  suspect that there is sponge brain
infection
> slowly crawling up the brain stem of every cow in America as well as all
the
> humans who have eaten  them as well as all the offspring of both species.
And
> to pigs, chickens who were also fattened with the deadly Soylent Green. As
a
> poultry  farmer told a prion researcher, "rendering salesmen brought us
bags
> of this powder saying it was wonderful stuff and had ever so many uses:
we
> could use it for fertilizer or to feed our chickens."
>
> As so many CJD deaths are misclassified as Alzheimer and private labs
won't
> let CJD tissue in the door to be examined, it is certain the American
public
> will not be informed of the disease that is in our food, our kitchens and
our
> bodies. We are scheduled to be 'downers' and Ted Koppel doesn't want us to
> know it.
>
> Dr. Richard Deandrea, a Los Angeles physician who has studied CJD and BSE
> extensively, tells of his first CJD patient. After her death, which
featured
> frills atypical of Alzheimer's (fingers numb, blindness, slurred speech,
weak
> knees), Deandrea dogged the Center for Disease Control  for a pathologist
> who'd give him an autopsy to see if it might be CJD.  CDC evaded 3 weeks
of
> his calls. Finally, a female CDC staffer told him  that off the record -
> she'd deny it later -"CJD is an issue no pathologist will deal with, a
> virtual death sentence to a lab. A well trained  pathologist knows the
> quarantine would never be lifted. You couldn't sterilize the lab to OSHA
> protocols. It would have to be gutted,  incinerated. Forget it. Your
patient
> died of Alzheimer's." So, there may be CJD deaths but there sure aren't
going
> to be CJD death certificates. ......>
>
> ----------------------------------
>
> Scientific articles on a possible prion role in CJD and Alzheimer's:
>
> <http://www.alzforum.org/members/research/news/index.html#molecularClue>
>
> The process by which a normal prion protein (provoked by an abnormal
prion)
> undergoes a conformational change to the abnormal form, and the
hypothesized
> resulting neuropathology, is of particular interest to researchers of
other
> neurodegenerative diseases that also feature abnormal buildup of toxic
> proteins. Because the presence of abnormal prion alone does not lead to
> neurodegeneration, it is assumed that the protein must work via other
> molecules.  Aguzzi and colleagues in Switzerland and Austria determined
that
> plasminogen - a plasma component that serves as the proenzyme for the
> protease plasmin - binds selectively to the prion protein in its abnormal
> form, probably via lysine residues on the prion. They found this to be
true
> with mouse prion protein, as well as with prion protein from the brains of
> human Creutzfeldt-Jakob disease patients.
>
> Normal Prion Protein Signals With Fyn (14 September 2000).
>
> The intracellular protein Fyn, a suspect in the formation of
neurofibrillary
> tangles because of its associations with tau protein--has now popped up in
> conjunction with prion diseases. Researchers in France report in
tomorrow's
> Science that Fyn couples with the normal form of prion protein, an
> interaction that also involves the protein caveolin-1.
>
> There is still no demonstrated function for the normal form of prion
protein
> (as opposed to the abnormal form thought to cause transmissible spongiform
> encephalopathies such as mad-cow disease and scrapie). The fact that it is
> localized in particularly high concentrations in the cell membranes of
> neurons has led to speculation that it is involved in signal transduction
> across the membrane. The current Science report adds fuel to that idea,
> finding that the normal prion protein is involved in an interactions with
the
> intracellular tyrosine kinase Fyn. Because the two proteins are localized
in
> different compartments, the researchers searched for an intermediate that
> might be able to link the two and found caveolin-1 involved in this
cascade.
> (The protein clathrin, included as a control, also had some effect on the
> interaction, suggesting that it too may be involved.)
>
> The researchers also noted that Fyn was not activated until the cultured
> cells had differentiated into neurons and that the signaling cascade
seemed
> to only involve prion molecules located on neurites, and not on the cell
> body. Implicit in these results is the idea that an extracellular
messenger
> must somehow be involved. (See William Klein's comment below on whether
there
> might be some common factor in signal cascades in prion disease and in
> Alzheimer's.)
>
> ( Mouillet-Richard S, et al. Science. 15 Sept 2000; 289: 1925-8.
>
> Comment by William Klein:
>
> Coupling of cellular prion proteins to Fyn is a real surprise, but maybe
it
> shouldn't be. Fyn keeps popping up. Shirazi and Wood showed that
> tangle-bearing neurons in AD have a hefty overload of Fyn. Gloria
>