Brain Researchers Create Synthetic Prion

Infectious Proteins Cause Many Brain-Wasting Diseases

Prion research is still unfolding, but researchers have successfully created a synthetic version, which could help solve some riddles.

Neurodegenerative disease , including Alzheimer’s disease, is the fastest-growing cause of death in the world. Autism also continues to surge. Some parts of the world are impacted more than others.

A variety of factors can trigger neurodegenerative disease, including genetics, head trauma and neurotoxins. Exposure to deadly proteins, however, could be the greatest threat to your brain.

Brain-wasting diseases are a terrifying prospect, made all the more distressing because of the lack of effective treatments. While we know that such disorders, like Creutzfeldt-Jakob disease (CJD), mad cow disease and chronic wasting disease (deer) are caused by infectious proteins called prions, experts have struggled to decode these proteins. However, we know that they migrate, mutate, multiply and kill. We know that they aren’t alive, therefore, we can’t kill them. Neutralizing them with complete confidence in all conditions, including in vivo, is virtually impossible. So far, prion diseases are always incurable and fatal. They also are highly transmissible.

Dr. Stanley Prusiner, an American neuroscientist from the University of California at San Francisco, earned a Nobel Prize in 1997 for discovering and characterizing prions (PREE-ons) and prion disease, also known as transmissible spongiform encephalopathy (TSE). The operative word is “transmissible.”

Prion disease and Alzheimer's disease

President Obama awarded Prusiner the National Medal of Science in 2010 to recognize the importance of his research. Unfortunately, Prusiner’s science is being ignored.

Prions are a deadly and unstoppable form of protein that migrates, mutates, multiplies and kills with unparalleled efficiency.

TSE is a spectrum disease. The spectrum includes Alzheimer’s disease, Parkinson’s disease and an extremely aggressive version known as Creutzfeldt-Jakob disease. Prusiner claims that all forms of TSE are caused by infectious prions. The prion spectrum varies in severity. It also varies depending on which region of the brain is impacted first. When the presenting symptom is memory loss, the diagnoses flow along the following chart.

prion disease spectrum

Prions cause fatal neurodegenerative diseases in humans and animals by converting the cellular version of prion protein into a toxic form that builds up in the brain.

Scientists at Case Western Reserve University School of Medicine (CWRU) have synthesized the world’s first artificial human brain prion in a lab. Case Western is a global leader on prion research. It hopes that its new development will help us better understand how these deadly, infectious proteins misfold, spread and kill mammals–and possibly other species.

“This accomplishment represents a watershed event,” said Jiri G. Safar, the study’s lead author. “Until now our understanding of prions in the brain has been limited. Being able to generate synthetic human prions in a test tube, as we have done, will enable us to achieve a much richer understanding of prion structure and replication.

“This is crucial for developing inhibitors of their replication and propagation throughout the brain, which is essential for halting prion-based brain disease.”

The better we understand prions, the closer we get to developing treatments. What we already know is that prions are proteins that have folded incorrectly, which can cause neighboring proteins to continue the deadly sequence until the neurodegeneration carves holes throughout the entire brain. Upon death, the brain looks like a sponge.

In Nature Communications, scientists describe an essential contributory cause of prion disease – a process known as ganglioside GM1. This process helps prions convert other proteins into a new mutation of prions.

We know that each mutation becomes more aggressive and lethal. There are likely thousands of mutations floating through the man-made and natural worlds. Prions shed from humans are the deadliest, since humans are at the top of the food chain, which makes us prion collectors, condensers and distributors.

The researchers also traced the infection of prions to an area on the molecule’s structure known as the C terminal domain.

“Our findings explain, at the structural level, the emergence of new human prions and provide a basis for understanding how seemingly subtle differences in misfolded protein structure and modifications affect their transmissibility, cellular targeting, and thus manifestation in humans,” said Safar.

Non-human prions have previously been synthesized, with studies carried out on mice and hamsters, but the research from CWRU is the first to involve an aggressive and “highly destructive” artificial human prion. They made the artificial prion from a human prion protein expressed in E. coli bacteria (yes, you should be concerned about all of the food-borne illnesses. Sewage is getting into the food chain and our water supplies. Sewage is a prion super-highway. If E.coli, listeria and other poisons are making it into grocery stores and restaurants, so are prions).

The results of the study could alter how we think about degenerative disorders. Sincee Parkinson’s and Alzheimer’s disease spread through the brain much like CJD spreads, the researchers hope to develop better treatments for these diseases.

Unfortunately, there is a growing stack of evidence that Alzheimer’s disease is a transmissible disease—prion disease. For example, millions of these people have the severe form of Alzheimer’s disease, which is Creutzfeldt-Jakob disease (CJD). CJD is clearly a prion disease. Prion disease is highly contagious, incurable and fatal. Victims should be quarantined, but they are not.

According to neuroscientists Dr. Laura Manuelidis, at least 25 percent of Alzheimer’s diagnoses are not Alzheimer’s disease. These misdiagnoses are actually CJD, which is further up the prion spectrum. CJD, without dispute, is extremely infectious to caregivers and loved ones, but it has not been declared a reportable disease in the U.S. and many other nations. Millions of cases of deadly CJD are being misdiagnosed as Alzheimer’s disease. Millions of patients and caregivers are being misinformed, misguided and exposed to an aggressive disease. Millions of people with prion disease have exposed us all to their infectious waste thanks to misinformation and mismanagement.

Prions are in the urine, feces, blood, saliva, mucus, skin and cell tissue of all victims–all human byproducts that are washed, dumped, or flushed down sinks and toilets. One can assume that the waste is extra infectious when it comes from funeral homes, nursing homes, hospitals, dental offices, veterinarians, slaughterhouses and some laboratories.

land application sewage sludge and biosolids

Wastewater treatment plants can’t detect or stop prions. Therefore, they ignore them. So does the EPA. So do various other government agencies around the world. Wastewater reclamation and reuse spreads prions back into our world, our watersheds and our food supplies. Applying sewage sludge to open land is insane. It’s time to stop growing our food in this toxic soup of carcinogens, nerve agents and endocrine disruptors. Allowing rains and runoff to rinse these toxins into our rivers, streams, lakes and oceans is taking its toll on public health and marine life. Ironically, this public health disaster began when global leaders realized that dumping sewage in our oceans killed entire underwater ecosystems and spoiled our beaches. Now, we’re being told that sewage sludge should be reclassified as biosolids and sold as fertilizer. Good thinking.

Suffice it to say, prion science is still unfolding. However, we know enough to say that prion pathways and prion diseases are being mismanaged.

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Wastewater Treatment Plants Spreading Brain Disease

Alzheimer’s Disease An Infectious Disease

Neurodegenerative diseases are the fastest-growing causes of death around the world. The mismanagement of infectious waste is contributing to the epidemic.

Dr. Stanley Prusiner earned a Nobel Prize in 1997 for his pioneering research on deadly prions—an infectious form of protein that connects a deadly spectrum disease called transmissible spongiform encephalopathy (TSE). The operative word is “transmissible.” TSEs include Alzheimer’s disease, Parkinson’s disease, Creutzfeldt-Jakob disease, mad cow disease and chronic wasting disease in deer, elk, moose and reindeer. TSE is also killing dolphins, whales, camels and many other species of mammals. It’s the environmental equivalent of Pandora’s Box. Actually, it’s Pandora’s Lunchbox.

Prions and Alzheimer's disease

President Obama awarded Prusiner the National Medal of Science in 2010 to recognize the importance of his work. Unfortunately, this groundbreaking research is being ignored. This negligence is fueling a public health disaster around the world, as critical pathways are being ignored and mismanaged. The mismanagement also is contributing to the global surge in autism.

In June 2012, Prusiner confirmed that Alzheimer’s, Parkinson’s, Huntington’s and even ALS are prion diseases similar, if not identical, to Creutzfeldt-Jakob disease. The primary difference being which part of the brain the disease attacks first. The other variable is that there are now an unknown number of prion mutations. Mutations of these deadly prions are the common denominator between all forms of TSEs. Most of the carnage is being swept under the rug as the problem escalates.

“There is now real evidence of the potential transmissibility of Alzheimer’s,” says Thomas Wiesniewski M.D. a prion and Alzheimer’s researcher at New York University School of Medicine. “In fact, this ability to transmit an abnormal conformation is probably a universal property of amyloid-forming proteins.”

Although there are many causes contributing to prion disease, many people and animals are contracting it from environmental exposure (food, water and soil) and then contaminating the environment even more with their own bodily fluids. Victims of prion disease are walking time bombs. Creutzfeldt-Jakob disease (CJD) is the most deadly form of prion disease in humans. Without dispute, it is a very contagious disease that kills rapidly. There is no cure for CJD, Alzheimer’s and other forms of prion disease.

Alzheimer’s and CJD are often indistinguishable to neurologists and general practitioners. Misdiagnoses are common. It appears that CJD is caused by a more aggressive mutation of prion than Alzheimer’s, but a deadly prion is a deadly prion. There is no reason to believe that some prions behave differently than others in disease transmission and progression. There should be no difference in disease management.

Unfortunately, as more people contract these brain diseases, the more deadly wastewater streams become. Meanwhile, wastewater reuse is surging around the world in response to growing populations and dwindling water resources. Other by-products from the wastewater stream known as biosolids (sewage sludge) also are being used to fertilize crops, pastures for livestock, golf courses, playgrounds and gardens. Millions of people, including your family, are in harm’s way because wastewater treatment plants can’t stop prions.

joel pedersen prion research

Prion researcher Dr. Joel Pedersen, from the University of Wisconsin, found that prions become 680 times more infectious in certain soils. Pedersen also found that sewage treatment does not inactivate prions. Therefore, prions are lethal, mutating, migrating and multiplying everywhere sewage is dumped.

“Our results suggest that if prions enter municipal wastewater treatment systems, most of the agent would bond to sewage sludge, survive anaerobic digestion, and be present in treated biosolids,” Pedersen said. “Land application of biosolids containing prions represents a route for their unintentional introduction into the environment. Our results emphasize the importance of keeping prions out of municipal wastewater treatment systems.

Prions could end up in sewage treatment plants via slaughterhouses, hospitals, dental offices and mortuaries just to name a few of the pathways. The disposal of sludge represents the greatest risk of spreading prion contamination in the environment. Plus, we know that sewage sludge pathogens, pharmaceutical residue and chemical pollutants are absorbed by plants and vegetables grown in sewage sludge.”

Regulators and industry are playing dumb as the body count keeps rising. It’s a deadly circle enabled by an outdated risk assessment. Modern science is being ignored.

The largest prion pathway in the world is wastewater (infectious waste) from homes, hospitals, nursing homes, slaughterhouses, dental offices and other high-risk sources. The problem is that prions are in all bodily fluids and cell tissue of millions of victims who often go undiagnosed. Their mucus, saliva, feces, and urine are flushed down millions of toilets and rinsed down sinks every day. Once inside the wastewater system, prions proceed to migrate, mutate and multiply. Reckless risk assessments enable wastewater treatment plants to spread these deadly agents far and wide. Deadly prions are building up and incubating in wastewater treatment plants and then dumped openly on land. They are swept into the air by the wind. Now, water contaminated by prions is migrating into our rivers, lakes and oceans. It’s being injected into groundwater and it’s being recycled as tap water.

biosolids land application sewage sludge

I used to support wastewater reclamation and reuse projects until I realized that the risk assessments were prepared decades ago—before Dr. Prusiner characterized prions and prion disease. These microscopic protein particles have converted sewage and its by-products a public health disaster.

Read The Full Story About Prion Disease and Alzheimer’s Disease At

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Prion Science Putting Dementia In Perspective

Alzheimer’s, Creutzfeldt-Jakobs, Parkinson’s Disease All Part Of Prion Spectrum

Editor’s Note: On September 9, 2015 additional research adds to the evidence that suggests that Alzheimer’s disease is a transmissible disease. Scientists have shown that tissues can transmit symptoms of the disease between animals. A new study published in the journal Nature raises additional concern about the transmissibility of Alzheimer’s disease between people and between species.

A scientific truth triumphs not by convincing its opponents but because its opponents eventually die, said influential physicist Max Planck. For Nobel prize-winning neurologist Stanley Prusiner, the quotation is “so mean” that he doesn’t like to use it. “But it is absolutely true,” he says.

Prions and Alzheimer's disease

Prusiner won the Nobel prize in 1997 for his discovery of prions – infectious proteins that cause fatal neurodegenerative diseases in people and animals, the most famous of which is BSE or mad cow disease and its human form, variant CJD. But his claim to have found an entirely new type of disease-causing agent, which he first termed a prion in 1982, was treated as heretical by many of his peers and the media for years. Bacteria, viruses, fungi and parasites are the only known infectious agents – a mere protein, with its lack of genetic material, is not alive so can’t transmit disease – so an army of naysayers maintained. Even his Nobel prize in physiology or medicine, for which he was the sole winner, didn’t silence all the critics.

“I understood the skepticism,” says Prusiner. “When there is a really new idea in science, most of the time it’s wrong, so for scientists to be skeptical is perfectly reasonable…[But] it didn’t make it any easier.”

Madness and Memory by Stanley Prusiner

Prusiner tells the story of his discovery in a new autobiographical book, Madness and Memory. He wrote the book, he says, both to ensure that the story was recorded in his own words and the science was properly described.

Prusiner was born in Des Moines, Iowa, in 1942. As a youngster, he had no interest in science and was happy to get Bs in school with little effort. When, later, he wanted to take advanced chemistry, a subject he liked because he didn’t have to memorize anything, the school said he wouldn’t be able to comprehend the science. He took a lower course, but went on to major in the subject at the University of Pennsylvania, following it up with a medical doctorate received in 1968.

Alzheimer's disease transmission

It was during his chemistry degree that he got his first taste of research – a summer project to help boost his application to medical school. He found the project, studying hypothermia in rats, fascinating and by the end of medical school had become excited about the possibility of pursuing biomedical research as a career.

After completing a grueling internship in medicine that was required for the post, he took a research job at the US National Institutes of Health. He remained at the NIH for three years, studying enzymes in bacteria, before deciding it was time to move on and build his own laboratory.

Prusiner found his scientific destiny after an encounter with a patient with a rare brain disorder in San Francisco in 1972. He had recently begun a clinical residency in neurology at the University of California, San Francisco (UCSF), with the goal of identifying a big problem to investigate, when a patient dying of Creutzfeldt-Jakob disease (CJD) was placed under his care.

The disease was thought to be caused by a “slow virus” that took many months or years to produce symptoms and, intrigued, Prusiner began reading up. “The more I read, the more fascinated I became,” he says.

Kuru disease

Other seemingly related slow virus diseases included scrapie (which occurs in sheep) and kuru (found in the Fore people of Papua New Guinea and spread by cannibalism), all three causing a spongy degeneration of the brain and being transmissible to similar species via injection of infected brain tissue. Yet no actual viruses had ever been isolated and previous work by British scientists on the scrapie agent had even found it had some strange properties, including being resistant to killing by radiation.

They had raised the controversial prospect that it may not even contain DNA or RNA. Prusiner had his problem: he would isolate and characterize the elusive infectious agent responsible for scrapie, which could be studied with rodents, and in so doing shed light on these so-called slow virus diseases.

He began work in 1974 having accepted an academic position at UCSF and despite colleges’ warnings that the problem would be too difficult to crack. It was tough going. He lacked funds to pay for the upkeep of the thousands of laboratory animals he needed and the work was slow because the disease took so long to manifest (he found crucial private funding and sped up the work by moving from mice to hamsters and redesigning his measurement method). “I could now do in one year what would have taken me 80,” he says.

As experimental data began to accumulate, Prusiner grew puzzled. He had anticipated that the scrapie agent he was enriching and purifying from brain material would turn out to be a different and interesting virus. Yet his preparations lacked any genetic material that would indicate one. All he found was a protein. He summarized the work in a journal article in Science in 1982, introducing the term “prion” to denote such a particle.

“I just thought it was really counterproductive to keep calling it a virus when it wasn’t,” says Prusiner. “If you call it that and you believe it at some level, then you miss the next set of experiments.”

The word came from Prusiner’s pondering how “protein” and “infectious” might fit together. When “proin” didn’t sound quite right, he flipped two letters. “What else was I going to do?” he laughs. “I couldn’t come up with some clever Greek words because I don’t know any Greek.” (He pronounces it “pree-on“.)

The word and the concept elicited what he describes as a “firestorm” of criticism and skeptics began staking careers on hunting down the scrapie virus (it has never been found). One particularly low moment he recalls was a 1986 article in the science magazine Discover, which accused him of being more interested in fame than science. He adopted a policy, which he maintained for years, of not speaking to the press.

Prusiner’s answer to his scientific doubters was to keep producing data. Among his contributions, he characterized the scrapie prion and added CJD and other diseases to the list caused by prions. He also showed how prions replicate. They come in two forms, he found, with different shapes: a normal uninfectious form that all animals and people have that is particularly abundant in the brain (it is encoded by a prion protein gene) and a more stable disease-causing form. The disease-causing form can act like a template to guide the normal form to refold into the disease-causing one.

In the late 1980s, as scientific data converged, the tide began to turn on the acceptance of the work. He was elected to various professional bodies and began winning awards. Soon afterwards, so-called knockout mouse studies (which abolished the prion gene in mice making them resistant to prion infection) added further evidence.

mad cow disease


Then, in 1996, the first cases in Britain of the human form of mad cow disease were reported and prions were implicated. Variant CJD, it was suspected, had arisen from the consumption of beef infected with BSE, which had been identified as a prion disease using Prusiner’s methods after it was first reported in Britain a decade earlier. A year later, Prusiner won the Nobel prize.

Did the spotlight on prions influence the Nobel committee’s decision?

“It didn’t hurt,” he says.

At the press conference that followed, he faced incredulous journalists still insisting prions were an impossibility. “A Nobel prize doesn’t wipe the scepticism away for some people,” he says.

Prusiner attributes his tenacity in the face of years of doubt to the nature of the problem itself. He would have quit, he says, except there was no alternative that excited or captivated him more. But good scientist, he adds, also stay focused on the problem, going deeper and deeper trying to understand it. That is where the “real opportunity to discover something lies”, he says.

Prusiner is now looking for ways to stop prion diseases (which he believes includes Alzheimer’s and Parkinson’s – though the science of this is not yet settled). For despite all that has been revealed about the strange world of prions, they remain a death sentence to those infected. “We don’t have a single therapy,” he says.

Alzheimer’s Disease Is Transmissible, Mismanaged

Alzheimer’s Disease Has Many Causes

It’s estimated that more than 44 million people around the world today are in the grasp of dementia and its deadly spiral. That number is expected to triple or more within 25 years. The medical world knows very little about this family of neurodegenerative diseases, which includes Alzheimer’s disease, Huntington’s, Parkinson’s and the most feared of all–Creutzfeldt-Jakob disease.

Alzheimer's disease treatment

We know that these diseases are fatal (other than Parkinson’s) and that there is not a cure in sight. We know that these diseases are essentially identical and that diagnosis is not an art or science. Doctors basically determine what the patient doesn’t have and the process of elimination reveals that (voila) the patient must have dementia. Then doctors basically flip a four-sided coin to see what name to give it–Alzheimer’s, CJD, Huntington’s or Parkinson’s.

“It must be Alzheimer’s,” says the doctor.”But we aren’t absolutely sure.”

I recently heard of two cases where the Mayo Clinic diagnosed people with Parkinson’s in less than half of an hour, gave them a prescription and sent them home. One of those people has been falling down, drools and exhibits alarming behavior. I just don’t believe that a 30-minute observation really determined:

A. That it’s a complex prion disease.

B. Which prion disease has a hold on the man.

What if these people really have the very aggressive mutation–CJD? Shouldn’t families be given more than just a guess? Should they be told to take some precautions to avoid prion transmission?

That’s what an Alzheimer’s or Parkinson’s diagnosis looks like today. It’s far from scientific and full of risk for caregivers and family members as I explain below (and in the e-Book). I’m alarmed at what seems to be a general sense of dismissal at many levels in terms of diagnosis, treatment, precautions and regulations. We share an even more horrifying CJD diagnosis and progression in the book.

Again, world health officials are predicting that the number of Alzheimer’s victims around the world will triple by 2050, if not sooner. When you consider that the death rates from all other major causes of death, including cancer and heart disease, are on the decline, the spike in prion diseases (including Alzheimer’s) demands even more attention.

Now, let’s inject some science into that equation and see where facts can explain the Alzheimer’s contribution to a global prion epidemic. Deadly prions (pronounced PREE-on) are contagious and unstoppable. Prions migrate, mutate, multiply and kill with incredible efficiency.

Prions and Alzheimer's disease

“The (human) brain diseases caused by prions includes Alzheimer’s, Parkinson’s, Huntington’s, amyotrophic lateral sclerosis (Lou Gehrig’s disease), and other disorders known as frontotemporal dementias,” said Nobel Laureate Stanley Prusiner, who earned a Nobel Prize in Physiology in 1997 for discovering deadly prions.

U.S. President Barack Obama awarded Prusiner the National Medal of Science in 2010 for his vital work. Prions are not science fiction. They have the attention of the entire scientific community and world leaders alike. Prions are a deadly form of protein that triggers the nervous system to consume itself, while attacking nerves throughout the body (including in muscle tissue of animals).

Prion disease is not limited to humans. The deadly prion epidemic is already taking its toll in nature. Deer, elk and moose populations in the United States and Canada, for example are being decimated by prion disease. In these species, the disease isn’t called by the human names, it’s been labeled as “chronic wasting disease” or CWD. The Canadian government recently announced that prion disease among wildlife is unstoppable. They are right. It’s unstoppable in people and all mammals, including livestock and ocean mammals, such as whales and dolphins. The species barrier is a myth. We can give it to animals and animals can give it to people. The scientific name for prion disease is Transmissible Spongiform Encephalopathy (TSE). It’s important to emphasize the word “transmissible.”

Once thought to be just age-related diseases among humans and even a genetic disease, we now know that prion disease also is an environmental nightmare. As more people and animals contract prion disease (regardless of source), the victims proceed to add to the environmental contamination, which adds momentum to an already established epidemic.

Alzheimer's disease infectious disease

Alzheimer’s Is Now An Environmental Disease

People and animals who contract prion disease can carry the disease for months and even years before they exhibit clinical signs of the disease and start their downward spiral. During this time, their body releases deadly prions through bodily discharges, including blood, mucus, saliva, sweat, milk, urine and feces. In essence, everything that an Alzheimer’s or CJD victim touches becomes contaminated. What makes this even more alarming is that it’s impossible to sterilize something once it has been contaminated by a person or animal with prion disease.

We now have a situation where the disease in people can infect wildlife and livestock. We now have a situation where infected wildlife and livestock can transmit the disease to humans just because of the contamination that they add to land (urine, feces, mucus and blood), which runs off into streams, ponds, lakes, groundwater and oceans–likely exposing food and drinking water supplies.

biosolids land application sewage sludge

Even sophisticated healthcare systems have failed to grasp the severity and infectivity of prion disease and its ability to spread. For example, hospitals around the world have been sued successfully for spreading CJD to innocent patients. So far, these lawsuits have been limited to the use of contaminated surgical instruments. In these cases, surgeons use the devises on a person with undiagnosed prion disease. Unknowing to the hospital, the surgical equipment and the surgery room become permanently contaminated by the prions in the patient. Subsequently, the tools undergo an ineffective sterilization and are then used again and again in surgeries. Later, the prion patient is diagnosed and the trail of contamination is already in place. (Just Google it for the most recent examples. It’s still happening every day.) Dental offices represent the same risk. So does blood and organ donation.

Most health care systems are still misinformed and under-informed about the dangers that CJD patients pose to others. Therefore, these care facilities are exposing others and contributing to a global mismanagement problem. So are nursing homes, coroners and funeral homes.

Want more proof? Most coroners refuse to touch the body of someone who likely died of CJD. All dementia patients and their bodies demand special handling and burial to avoid infecting others. Call your local coroner and ask. Just Google “coroners and CJD protocol.”

If coroners and other insiders in the medical industry won’t take the risk, why aren’t caretakers being warned? Why aren’t other precautions being taken (see the link on the menu bar above about Sewage).

Alzheimer’s and Creutzfeldt-Jakob disease are indistinguishable. They are essentially the same disease. CJD is caused by a more aggressive mutation of prion than Alzheimer’s, but medical professionals cannot tell the difference. Only time will tell the difference (if there is one).

For the skeptics in the crowd, let’s dissect the issue from another angle. There is absolutely no question that CJD is highly transmissible and very aggressive. Doctors have no ironclad way to distinguish between Alzheimer’s and CJD (let’s assume that there is a difference between the two diseases other than the speed of mental decay). Since the medical industry now admits that 15-20 percent of Alzheimer’s cases are misdiagnosed and should have been classified as CJD, around 20 percent of “Alzheimer’s” patients are walking biohazards with CJD. These victims are absolutely exposing care facilities, caretakers, family and beyond (not to mention the contamination that they spread before the diagnosis).

Summary: Alzheimer’s is a deadly prion disease. There is no cure for prion disease in any animal. Prion diseases are transmissible. Prion disease is spreading via many pathways, including genetics. The pathways are expanding and uncontrollable. We have a global epidemic that is escalating. We have a global epidemic that is being mismanaged. Some populations and regions of the world are at a higher risk than others of Alzheimer’s and other forms of prion disease.

Alzheimer’s and Mad-Cow Disease Share Same Pathogen

Prion Disease Impacts Most Mammals

Not surprisingly, Mad-Cow disease, the medical term Bovine Spongiform Encephalopathy (BSE), has been rampant in the U.S. for decades.  The human form of Mad Cow is Creutzfeldt-Jakob disease (CJD).  The USDA and FDA have done a very good job of keeping this under wraps, as well as displaying a healthy disregard for human life by their neglect as well as their silence. The testing on cattle raised for food in the U.S. is ‘careless’ and ‘irresponsible’ according to The World Health Organization (WHO).

chronic wasting disease

Testing one cow out of every 2,000 cows is seriously negligent. Because of this fact, no one knows how many infected cattle enter the human food chain; however it is certain it leads to CJD and Alzheimer’s.

WHO has issued a warning stating that the U.S. is violating the guidelines set forth for the prevention of BSE or Mad-Cow disease making its way into the human population. WHO states that the U.S. is inadequately testing the brains of human dementia victims and is likely missing hundreds of human cases of Creutzfeldt Jakob Disease (CJD), caused by none other than Mad-Cow disease.

mad cow disease

The warning goes on to state that the feeding of infected animals to other animals must be ceased immediately. The feeding of slaughterhouse waste, including blood, feathers and excrement, to other farmed animals is causing major health risks to all who eat beef, or any other farmed animal. Deer, elk, sheep, pigs and chickens can all carry this disease in different forms.

Prions and Alzheimer's disease

CJD and Alzheimer’s disease are caused by an infectious prion, which is not a virus. A prion is a protein, but a mutated protein that is somewhat different in shape. These prions fold into an abnormal pattern, at which time they begin killing off brain cells by the millions.

Steven Strittmatter, Professor of Neurology at Yale University, comments, “It’s too bizarre that these two diseases would share this common protein.”

Further, a well-known physician said, “The most frequent misdiagnosis of CJD among the elderly is Alzheimer’s disease. Neither CJD nor Alzheimer’s can be conclusively diagnosed without a brain biopsy, and the symptoms and pathology of both diseases overlap.” Michael Greger, M.D.

The gestation period for this prion can be years or even decades. The problem with this is that many people infected will not even show signs of the disease for years, and the final death toll may not show up until it’s too late to actually do something about the rest of the population. Also, since CJD is often mis-diagnosed, getting the true picture will be difficult.

Regrettably, the National Institute of Neurological Disorders indicates that there is not one single diagnostic test for detecting CJD. The only way to confirm a diagnosis of CJD is by brain biopsy or autopsy. The biopsy is a dangerous procedure because it means removing a part of a person’s brain, and getting the part that is infected is not likely.   And, when testing in either autopsy or biopsy, surgeons performing the test have to take extreme care to be certain they don’t become infected themselves. Strict surgical and disinfection procedures must be followed to perform this kind of test.

I’d venture to say that most doctors would do just about anything BUT this, in order to avoid the risks involved, as well as the time and expense; hence – misdiagnosis.