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Deadly Proteins Spark Onset Of Alzheimer’s Disease

Researchers Identify Tau Proteins As Prions

Neurodegenerative disease is the fastest-growing cause of death in the world. There are more questions than answers surrounding this global epidemic, but researchers are connecting the dots to deadly proteins that are killing many mammals, including humans.

The destructive progression of Alzheimer’s disease follows the growth and spread of toxic protein clumps in the brain.

When doctors perform autopsies to look at the brain tissue of people with Alzheimer’s disease, they find toxic buildups of certain proteins – in particular, a protein called tau – in structures called ‘aggregates’. People with more severe dementia have more tau aggregates in their brain. Aggregates form when individual proteins stick together in repetitive patterns, much like the way a single Lego block might attach to another identical one.

Now, a team of researchers from University of Texas Southwestern Medical Center, University of Delaware and Washington University in St. Louis have identified a single protein “seed” that begins the harmful chain of events in this and other tau protein disorders (tauopathies).

Like all proteins, tau is built from a string of amino acids that folds into a specific shape. Normally folded tau proteins do not form aggregates. It was not clear that an individual tau protein had two distinct forms—structures associated with health (“good”) or disease (“bad”). The research appeared in the open-access journal eLife.

Alzheimers disease treatment

Around 5.7 million Americans live with Alzheimer’s disease (AD), and experts expect the number to rise as the population ages. The disease causes neurodegeneration in part due to the accumulation of tau protein clumps called tangles or aggregates.

Previously, researchers thought tau aggregates would build up where tau proteins were abundant. Like salt crystals grown in a briny solution, they simply needed another tau clump to act as a seed.

Scientists thought these seeds, or templates, themselves comprised large clumps of tau. They also thought such a clump could act as a mobile point of origin, or nidus, for other clumps to build on.

“Somehow, these seeds may actually even move from one cell to another and, when they get into a new cell, they promote new formations in that cell,” said Dr. Marc Diamond, who directs the Center for Alzheimer’s and Neurodegenerative Diseases at University of Texas Southwestern Medical Center.

To test these and other hypotheses, the team set out to find the initial molecular trigger that prompts tau proteins to begin forming toxic clumps.

“What is the first, kind of, molecular event where you’re normal and then something happens, and then you start to develop this disease? And what we’re saying is, you can trace that back to a single protein changing its shape,” said Diamond.

Alzheimer's disease treatment

To their surprise, he and his colleagues discovered that a single tau protein could seed an aggregation. That’s because tau proteins exists in two distinct, stable forms: an inert, harmless version and a type that promotes clumping.

What’s more, the harmless shape can change into the damaging one, whose more open structure exposes key amino acids that promote aggregation. Like a wad of one-sided tape uncurled to expose its sticky side, these “bad” tau proteins more readily assemble into toxic aggregates.

The process resembles the one followed by prions, the infections proteins that cause neurodegenerative diseases such as Creutzfeldt-Jakob disease, fatal familial insomnia and mad cow disease. In fact, Diamond’s lab began calling tau proteins prions in 2014, although the prion hypothesis remains controversial.

Identifying how tau proteins go bad could help doctors develop new treatments, earlier diagnostics tests and, someday, perhaps even a vaccine. A better understanding of tau pathologies could contribute to treatments for roughly 25 rarer tau disorders as well.

Tau proteins can convert from an inert shape to a misfolded shape that seeds the growth of fibers that contribute to the pathology of Alzheimer’s disease. Most of the time, proteins fold into a single stable shape to perform their role in the body, but occasionally they can adopt a different conformation. These ‘misfolded’ proteins can be associated with a range of degenerative conditions known as amyloid disorders, which includes the transthyretin amyloidoses as well as Alzheimer’s and Parkinson’s diseases.

Tau forms amyloids that underlie neurodegeneration in a variety of neuropathological syndromes, collectively termed tauopathies. Amyloids are ordered protein assemblies that underlie multiple disorders such as Alzheimer’s disease. Amyloid-forming proteins include tau, synuclein, and expanded polyglutamine proteins such as huntingtin, among many others.

A variety of factors can trigger neurodegenerative disease, including genetics, head trauma and neurotoxins. Deadly, self-replicating tau proteins (prions) appear to be one of those neurotoxins. Unfortunately, these deadly proteins migrate, mutate, multiply and kill with unparallelled efficiency.

Prions (PREE-ons) are a deadly and unstoppable form of protein that migrates, mutates, multiplies and kills with unparalleled efficiency. Dr. Stanley Prusiner, an American neuroscientist from the University of California at San Francisco, coined the term as a contraction of proteinaceous infectious particle. The operative word is “infectious.”

Prion disease research

Prions cause fatal neurodegenerative disease in humans and other animals by converting the cellular version of prion protein into a toxic form that erodes the brain and body. Prions migrate, mutate and multiply. They get stronger as they move up the food chain. At the top of the food chain, humans are highly vulnerable to prion disease. The prions shed from humans are the deadliest and most aggressive. Mismanaging human prions is a big mistake.

Dr. Prusiner earned a Nobel Prize in 1997 for discovering and characterizing prions and prion 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 and we all are facing a public health disaster because of the negligence and reckless disregard for public health.

Prions are a formidable threat to public health. When the U.S. government enacted the Bioterrorism Preparedness and Response Act of 2002, it included a provision to halt research on infectious prions in all but two laboratories. It classified prions as select agents that pose an extreme risk to food, water and health systems. Unfortunately, the Center For Disease Control quietly took prions off the list about two years ago because the classification criminalized multi-billion dollar industries and many industry practices.

PR firm and public health

Crossbow is an award-winning and record-setting communications firm that influences public opinion, public policy and business decisions around the world. We’re helping stakeholders tackle some of the most urgent issues of our time, including Alzheimer’s disease, Creutzfeldt-Jakob disease and autism.

 

Neurodegenerative Disease A Public Health Disaster

Reforms Can Save Lives

Neurodegenerative disease and autism have been surging around the world for the past 30 years. A man-made environmental disaster is creating a public health disaster that’s still unfolding in many ways in most nations.

Neurotoxins are driving the epidemic more than age–in some countries more than others. Teenagers are now dying of Creutzfeldt-Jakob disease–the most severe form of brain wasting disease. Children are contracting autism at an escalating rate and at an uneven rate. The pattern reflects human exposure to environmental toxins. There also is a pattern of mismanagement and denial around the world.

Alzheimer’s disease alone is taking the lives of 50-100 million people around the world now. As millions die, even more will be diagnosed. Millions more are suffering in silence with a misdiagnosis or no diagnosis. Misinformation and mismanagement are fanning the flames. Compounding the problem, the Alzheimer’s Association found that doctors have withheld millions of additional diagnoses. Coroners are keeping diagnoses off of millions of death certificates. Epidemiologists can only guess at the true size of the epidemic.

Despite millions of deaths, experts suggest that the prevalence of the disease will quadruple by 2050, if not sooner. Unfortunately, there is a growing stack of evidence that Alzheimer’s disease, Parkinson’s disease and other brain diseases are transmissible. There is zero evidence to the contrary. Victims also are being misdiagnosed and undiagnosed at an alarming rate.

Prions

A variety of factors can trigger neurodegenerative disease, including genetics, head trauma and neurotoxins. Deadly, self-replicating proteins appear to be one of those neurotoxins.

Prions (PREE-ons) are a deadly and unstoppable form of protein that migrates, mutates, multiplies and kills with unparalleled efficiency. Dr. Stanley Prusiner, an American neuroscientist from the University of California at San Francisco, coined the term as a contraction of proteinaceous infectious particle. The operative word is “infectious.”

Prion disease research

Prions cause fatal neurodegenerative disease in humans and other animals by converting the cellular version of prion protein into a toxic form that erodes the brain and body. Prions migrate, mutate and multiply. They get stronger as they move up the food chain. At the top of the food chain, humans are highly vulnerable to prion disease. The prions shed from humans are the deadliest and most aggressive. Mismanaging human prions is a big mistake.

Dr. Prusiner earned a Nobel Prize in 1997 for discovering and characterizing prions and prion 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 and we all are facing a public health disaster because of the negligence and reckless disregard for public health.

Prions are a formidable threat. When the U.S. government enacted the Bioterrorism Preparedness and Response Act of 2002, it included a provision to halt research on infectious prions in all but two laboratories. It classified prions as select agents that pose an extreme risk to food, water and health systems. Unfortunately, the Center For Disease Control quietly took prions off the list about two years ago because the classification criminalized multi-billion dollar industries and many industry practices.

Prion Disease

Prion disease also is known as transmissible spongiform encephalopathy (TSE). The operative word is “transmissible.” Prusiner claims that all forms of TSE are caused by infectious prions. Prion disease often is described as a wasting disease that causes a loss of body mass and brain mass.

TSE is a spectrum disease that varies in severity and symptoms. It depends on which region of the brain is impacted first and by what prion mutation. Few cases are identical in terms of symptoms and diagnoses. When the presenting symptom is memory loss, the diagnoses flow along the following chart.

prion disease spectrum

In humans, the prion spectrum includes Alzheimer’s disease, Parkinson’s disease and an extremely aggressive version known as Creutzfeldt-Jakob disease. The difference between these diseases is very slight and often indistinguishable to neurologists. For example, millions of people have been told that they have Alzheimer’s disease, when, in reality, it’s CJD–where it’s clearly infectious.

“It is well known that CJD is transmissible via surgical or medical procedures involving prion-infected brain tissue. Our finding of infectious prions in skin is important since it not only raises concerns about the potential for disease transmission via common surgeries not involving the brain, but also suggests that skin biopsies and autopsies may enhance pre-mortem and post-mortem CJD diagnosis,” said Wenquan Zou, Associate Professor of Pathology and Neurology and Associate Director of the National Prion Disease Pathology Surveillance Center at Case Western Reserve School of Medicine. “The level of prion infectivity detected in CJD skin was surprisingly significant, but still much lower than that in CJD brains. Further investigation is necessary to determine whether extra precautions should be taken during non-neurosurgeries of CJD patients, especially when surgical instruments will be reused.”

Prion infectivity is highly concentrated in brain tissue, but it’s also in all bodily fluids and tissue. CJD transmission has occurred after patients were exposed to surgical tools previously contaminated by CJD victims. It’s also happening due to many other pathways.

According to neuroscientists Dr. Laura Manuelidis, at least 25 percent of Alzheimer’s disease diagnoses are actually CJD.

CJD, without dispute, is extremely infectious to caregivers and loved ones, but it has not been declared a reportable disease across 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 prion disease.

Alzheimer's disease caregivers

Prion disease is highly contagious, incurable and fatal. Despite all of the smoke and mirrors, prion disease is prion disease. It’s killing more and more mammals, including humans, every year. The hype about species barriers is ridiculous, reckless and irresponsible. Failure to quarantine CJD patients is negligent at best. Millions of people with prion disease have exposed us all to their infectious waste thanks to misinformation, mismanagement and negligence.

Meanwhile, chronic traumatic encephalopathy (CTE) is likely a form of transmissible spongiform encephalopathy—prion disease. In most of these cases, the trauma was the change agent that caused prions to misfold and become toxic. Once the neurodegeneration of CTE begins, are these victims shedding infectious prions? Hopefully, prion researchers will fill in this very important blank. Again, families and caregivers need to know if they are dealing with a TSE.

Misinformed caregivers, family members, healthcare workers and others are caught in the crossfire of a deadly form of protein. In fact, few family members are warned about the infectious nature of CJD. Meanwhile, hospitals throw out surgical instruments used on such patients. Neurologists prefer not to touch or even be in the same room as a patient with CJD. The CJD Foundation and other advocacy organizations also remain mum on the risk of transmission. The CDC remains silent. Is this cone of silence at all levels incompetence, negligence or criminal misconduct?

Abnormal proteins also are associated with autism. In fact, it appears that age is the biggest difference between the neurodegenerative disease spectrum and autism spectrum disorders. Both spectrums share common environmental causes and pathologies. Plus, CJD is taking the lives of more and more young adults and adolescents.

In humans, most diagnoses are a process of elimination. The key difference is which region of the brain is attacked first and by which mutation of prion. Some prions now kill within weeks of showing clinical symptoms. Prions shed from humans are the most aggressive.

After eliminating all other possibilities, the medical guesswork begins:

  • If the patient has a memory disorder, it’s diagnosed as Alzheimer’s disease;
  • If they have a movement disorder, it’s diagnosed as Parkinson’s disease;
  • If the patient shows both symptoms, doctors flip a coin;
  • If the patient ever had a concussion, it’s now ruled as CTE;
  • If the person is incapacitated, it’s Creutzfeldt-Jakob disease (CJD) and very transmissible;
  • If the victim is in the deer family, it’s chronic wasting disease instead of prion disease;
  • If the victim is a beef or dairy cow, it’s called mad cow disease instead of prion disease;
  • In other mammals, it’s called different things, but prion disease has been found in dolphins, elephants, mink, cats and many other species. The suggestion of a reliable species barrier against thousands, if not millions of mutations is ludicrous.

Prion disease causes memory loss, impaired coordination, and abnormal movements. Prion disease is incurable and fatal.

Prion Pathways

There are many sources and pathways for deadly prions. However, we can’t ignore the biggest pathways. The cruel irony of prion disease is that victims become part of the greater problem. As stated earlier, studies confirm that people and animals dying of prion disease contaminate the environment around them. Infectious prions are in the urine, feces, blood, skin, tissue, mucus and saliva of each victim. Infectious bodily fluids and tissue are contributing to the rapid spread of Alzheimer’s disease and other mutations of prion disease.

“There has been a resurgence of this sort of thinking, because 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 (prions).”

A study published in the journal Nature adds to the evidence about the transmissibility of Alzheimer’s disease between people. A second study by the same scientist in early 2016 supports the claim. Meanwhile, there is absolutely no evidence to the contrary. Even wildlife and sea mammals are contracting brain disease from people because of the dumping of infectious waste on farms, ranches and forests. Yes, research has found that plants/crops grown in infectious prions uptake those prions and become infectious.

Spouses of those with Alzheimer’s disease are 600 percent more likely to contract the disease, which is further evidence that the TSE spectrum is transmissible. Caregivers, family members and others are in harm’s way.

Surgical instruments infected with prions, for example, are impossible to sterilize and hospitals throw them away. Meanwhile, caregivers and family members are not warned. CJD victims are not quarantined. They are sent home to die in many cases. Reckless.

land application sewage sludge and biosolids

Many factors are contributing to the epidemic. Prions are now the X factor. Industry and governments are not accounting for prions or regulating them. They are ignoring the threat completely, which violates the Bioterrorism Preparedness and Response Act of 2002 in the United States. Other nations also are ignoring laws developed to protect food, air and water.

Read The Full Story About Neurodegenerative Disease and Neurotoxins

PR firm and public health

Crossbow is an award-winning and record-setting communications firm that influences public opinion, public policy and business decisions around the world. We have generated millions of dollars in revenue, stockholder equity and media coverage for our clients. We’re helping stakeholders around the world tackle some of the most urgent issues of our time, including Alzheimer’s disease, Creutzfeldt-Jakob disease and autism.

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.

Alzheimer's disease public affairs firm

Crossbow is an award-winning and record-setting communications firm that influences public opinion, public policy and business decisions around the world. We have generated millions of dollars in revenue, stockholder equity and media coverage for our clients. We’re helping stakeholders around the world tackle some of the most urgent issues of our time, including Alzheimer’s disease, Creutzfeldt-Jakob disease and autism.

Food, Water, Air Contamination Fueling Brain Disease

Alzheimer’s Disease, Autism Are Industrial Diseases

The EPA is drawing more attention and criticism than usual lately, but its history of mismanagement is nothing new.

EPA failures regarding wastewater treatment, reuse and the land application of sewage sludge go back decades. For example, sewage sludge was deemed too toxic to dump in the ocean in 1972, so the EPA started pimping it as fertilizer for our food supply, gardens, parks and school grounds.

Sewage sludge certainly has some beneficial nutrients for plants, including phosphorous and nitrogen. Unfortunately, the so-called biosolids also include pathogens, prions, heavy metals, pharmaceutical residues, carcinogens and other harmful ingredients. After all, sewage comes from slaughter houses, nursing homes, hospitals, dental offices, veterinarians, street runoff, factories, and beyond. It also includes all of the things that millions of homes choose to dump.

land application sewage sludge

The EPA never conducted a legitimate risk assessment regarding the land application of sewage sludge. It never issued official policy. It issued something known to industry insiders as the sludge rule back in the 1990s. It’s the government equivalent of a wink-wink.

The EPA stood behind the sludge rule and allowed each state to develop random regulations and practices on sewage discharges. Places such as Milwaukee, Wisconsin started pimping its sewage sludge as fertilizer long ago. In Milwaukee, they branded the toxins Milorganite, which is registered for sale in all 50 states. Farmers are eating the stuff up. So do livestock, crops, gardeners and our wildlife. It’s running off into streams, rivers, lakes and oceans. Tornadoes carry it into the sky and into homes, offices and schools. The treated wastewater is discharged to Lake Michigan, where Chicago and other municipalities tap drinking water.

Since the EPA’s infamous sludge rule darkened our world, we now know about a deadly form of protein known as a prion. Prions are in the bodily fluids of victims, including blood, saliva, mucus, urine, feces, etc.—everything that’s destined for a wastewater treatment plant and a farmer’s field (or a soccer field).

Prions aren’t alive, so they can’t be killed. Wastewater treatment does little more than separate the stuff that floats from the stuff that doesn’t float. What’s left is pumped right back into your world. Including wastewater that’s being touted as drinking water (per the next section, look for the word “prion” in the risk assessments).

Prion disease and Alzheimer's disease

Dr. Stanley Prusiner earned the Nobel Prize in physiology in 1998 for his study of prions and prion disease. Unfortunately, government and industry are ignoring the ramifications of his science. As such, neurodegenerative disease is now the fastest-growing cause of death in the world. The autism epidemic is likely related to the same mismanagement of neurotoxins. Meanwhile, valley fever has evolved into an umbrella term for a variety of ailments spread through infectious waste in soil and air.

Prion disease is prion disease, but misguided public servants are blinding us with pseudo science. We know that prions migrate, mutate, multiply and kill with unparalleled efficiency. Yet, we are being told that various threats are unproven. We are being told that prions deplete themselves.

We are being told that there is no connection between the various forms of prion diseases among humans and other mammals, including Alzheimer’s disease, Parkinson’s disease, Creutzfeldt-Jakob disease, chronic wasting disease, and mad cow disease.

We are told that autism is caused by vaccines, not food and water contamination. We are being told that infectious waste is fertilizer. It’s time to read between the lines and think for ourselves, while we can still think at all.

The wastewater treatment plant in Milwaukee, for example, has been serving people with prion disease for decades. Wastewater treatment plants around the world are prion collectors, incubators and distributors. As more and more people get neurodegenerative disease, the deadlier the waste stream becomes. They have become weapons of mass destruction, yet no regulation exists. Highly toxic garbage in—fertilizer out.

land application sewage sludge and disease

Prions + Pathways = Victims

Humans Transmitting Prion Disease To Wildlife

Thanks to the indiscriminate dumping of sewage sludge laden with prions from sick people, the dairy state is a now a leader in chronic wasting disease among its wildlife. Since wildlife are serving as the proverbial bird in a coal mine, we know that livestock and humans also are being poisoned. The prion pathway goes both directions–people can contract it from infected animals and animals can contract it from human infectious waste (sewage). Few, if any mammals are immune. Few corners of the earth are safe.

The risk assessments for biosolids and wastewater reclamation were prepared before the world of science knew about deadly, unstoppable prions. Prions don’t deplete themselves over time. They don’t have a half-life. They migrate, mutate and multiply. Prions are being mismanaged in a criminal way on an industrial scale.

Although there are several pathways for deadly prion disease to infect a herd, the greatest prion pathway is being ignored. Sick deer, elk, moose and reindeer are just canaries in a proverbial coal mine. You and your family are caught in the crossfire of misinformation and mismanagement. Neurodegenerative disease is now the fastest-growing cause of death in the world.

Municipalities around the world were asked to stop dumping their sewage sludge in rivers and oceans and start dumping the toxic soup onto farms, forests, parks, school grounds, gardens and golf courses. Cities also are dumping the toxins in the deserts around the world, where it bakes and blows back in the faces of the cities that are trying to get rid of the sewage. The death dust from sewage sludge alone includes infectious waste, radioactive waste, heavy metals, carcinogens, pharmaceutical residues and other threats.

Alzheimers disease treatment

Humans Transmitting Brain Disease To Humans

Most forms of neurodegenerative disease are prion disease. The clinical term is transmissible spongiform encephalopathy (TSE). The operative word is “transmissible.” Victims are producing and discharging infectious waste. Prions from people are the most deadly and aggressive because people are at the top of the food chain. It’s a vicious cycle. People are giving it back and forth to each other, but in different mutations. People are transmitting prion disease to animals through sewage. Animals are transmitting it to people through milk and meat. Government and industry are fanning the flames.

Thanks to modern sewage disposal (biosolids) and antiquated (if not fraudulent) risk assessments, we’re witnessing a public health disaster that’s still unfolding in the form of autism, Alzheimer’s disease, west Nile virus, Zika virus, chronic wasting disease, mad cow disease, valley fever, meningitis, hepatitis, and other threats to public health.

The spike in autism and Alzheimer’s disease began shortly after we started dumping toxic sewage on open lands in urban and rural areas. The spike in chronic wasting disease and mad cow disease began about the same time. It’s time to divert all sewage sludge to lined landfills to protect human health, animal health and entire watersheds. Infectious waste isn’t fertilizer.

Alzheimer's disease prevention

Crossbow Communications specializes in issue management and public affairs. Alzheimer’s disease, Creutzfeldt-Jakob disease, chronic wasting disease and the prion disease epidemic is an area of special expertise. Please contact Gary Chandler to join our coalition for reform gary@crossbow1.com.

Brain Trauma Increases Risk For Parkinson’s Disease

Concussions Contribute To Neurodegenerative Disorders

By Nicholas Bakalar, New York Times

A traumatic brain injury, even a mild concussion, increases the risk for Parkinson’s disease, a new study reports.

Researchers identified all patients diagnosed with T.B.I. in a Veterans Health Administration database — 162,935 men and women — and matched them with the same number of people with similar health and behavioral characteristics but who had not had a brain injury. The study is in Neurology.

Of the T.B.I. cases, half were mild, involving a blow to the head with some subsequent symptoms but with little or no unconsciousness. The rest were moderate to severe, involving extended unconsciousness or long-term symptoms.

Muhammad Ali fighting Parkinson's

After controlling for age, race, income and many medical and psychiatric diseases, they found that compared with those who had had no T.B.I., those with a mild T.B.I. had a 56 percent increased risk for Parkinson’s disease; those with moderate to severe T.B.I. had an 83 percent increased risk.

“We don’t have brain autopsies, so we don’t know what the underlying biology is,” said the lead author, Dr. Raquel C. Gardner, an assistant professor of neurology at the University of California, San Francisco. “But in Parkinson’s you see abnormal protein accumulation, and there’s some evidence that T.B.I. is linked to deposits of these abnormal proteins. This study provides the most definitive evidence that there is this association.”

Read The Full Article About TBI and Neurological Disorders.

The new findings could be problematic for the increasingly-embattled NFL, which has spent years – and billions of dollars – trying to dismiss the idea that tackle football is not as dangerous to players as scientists claim.  The findings come amid a huge swell in research showing that attempts to curb the rate of concussions may not be enough: even subconcussive hits, or just one debilitating hit, could sew the seeds for crippling neurodegenerative diseases including CTE, Alzheimer’s and Parkinson’s.

Chronic Traumatic Encephalopathy

“Previous research has shown a strong link between moderate to severe traumatic brain injury and an increased risk of developing Parkinson’s disease but the research on mild traumatic brain injury has not been conclusive, said Senior study author Professor Kristine Yaffe, of the University of California, San Francisco. “Our research looked at a very large population of U.S. veterans who had experienced either mild, moderate or severe traumatic brain injury in an effort to find an answer to whether a mild traumatic brain injury can put someone at risk.”

Moderate to severe traumatic brain injury was defined as a loss of consciousness for more than 30 minutes, alteration of consciousness of more than 24 hours or amnesia for more than 24 hours.

Mild traumatic brain injury was defined as loss of consciousness for zero to 30 minutes, alteration of consciousness of a moment to 24 hours or amnesia for zero to 24 hours.

The researchers identified 325,870 veterans from three US Veterans Health Administration medical databases. Half of the study participants had been diagnosed with either a mild, moderate or severe traumatic brain injury and half had not.

The study participants, who ranged in age from 31 to 65, were followed for an average of 4.6 years. At the start of the study, none had Parkinson’s disease or dementia. All traumatic brain injuries were diagnosed by a physician.

A total of 1,462 of the participants were diagnosed with Parkinson’s disease at least one year and up to 12 years after the start of the study. The average time to diagnosis was 4.6 years.

A total of 949 of the participants with traumatic brain injury (0.58 percent) developed Parkinson’s disease, compared to 513 of the participants with no traumatic brain injury (0.31 percent).

A total of 360 out of 76,297 with mild traumatic brain injury (0.47 percent) developed the disease and 543 out of 72,592 with moderate to severe traumatic brain injury (0.75 percent) developed the disease.

After researchers adjusted for age, sex, race, education and other health conditions such as diabetes and high blood pressure, they found that:

  • Those with any kind of traumatic brain injury had a 71 percent increased risk of Parkinson’s disease;
  • Those with moderate to severe traumatic brain injury had an 83 percent increased risk, and those with mild traumatic brain injury had a 56 percent increased risk of Parkinson’s; and
  • Researchers found that those with any form of traumatic brain injury were diagnosed with Parkinson’s disease an average of two years earlier than those without traumatic brain injury.

“This study highlights the importance of concussion prevention, long-term follow-up of those with concussion, and the need for future studies to investigate if there are other risk factors for Parkinson’s disease that can be modified after someone has a concussion,” said study lead author Assistant Professor Raquel Gardner, also of the University of California, San Francisco. “While our study looked at veterans, we believe the results may have important implications for athletes and the general public as well.”

Alzheimer's disease prevention

Crossbow Communications specializes in issue management and public affairs. Alzheimer’s disease, Parkinson’s disease, Creutzfeldt-Jakob disease, chronic wasting disease and the prion disease epidemic is an area of special expertise. Please contact Gary Chandler to join our coalition for reform gary@crossbow1.com.

Caregivers At Risk In Battle Against Brain Disease

Spouses Of Those With Brain Disease More Likely To Contract Brain Disease

Millions of people are becoming caregivers for friends and family members with Alzheimer’s disease. It’s a silent epidemic that’s creating family crises around the world. In addition to the shock of the sudden dependency, at least some caregivers (family members and professionals) are being misinformed and exposed to deadly pathogens that can spread the disease.

“A good caregiver who understands the disease, its symptoms and progression is crucial to the overall well-being of people with Alzheimer’s disease,” said Dr. Fred Kobylarz, a dementia expert at the Robert Wood Johnson Medical School at Rutgers University. “Alzheimer’s has become pervasive in the United States and around the world. It affects people in all walks of life,” Kobylarz said. “It is a problem that needs action and attention.”

Memory problems are typically one of the first signs of cognitive impairment related to Alzheimer’s disease. Some people with memory problems have a condition called mild cognitive impairment (MCI). In MCI, people have more memory problems than normal for their age, but their symptoms do not interfere with their everyday lives. Movement difficulties and problems with the sense of smell have also been linked to MCI. Older people with MCI are at greater risk for developing Alzheimer’s disease, but not all do. Some may even go back to normal cognition.

The first symptoms of Alzheimer’s disease vary from person to person. For many, decline in non-memory aspects of cognition, such as speech, vision, and impaired reasoning or judgment, may signal the very early stages of Alzheimer’s disease.

Alzheimer's disease treatment

Researchers are studying biomarkers (brain images, cerebrospinal fluid, and blood) to see if they can detect early changes in the brains of people with MCI and in cognitively normal people who may be at greater risk for Alzheimer’s. Studies indicate that such early detection may be possible, but more research is needed before these techniques can be relied upon to diagnose Alzheimer’s disease in everyday medical practice.

For instance, people early on might show signs of memory loss that don’t affect their ability to function day to day. “Some memory loss can also be a sign of the normal aging process,” Kobylarz explained.

“Families should look for memory impairment and trouble managing aspects of their daily lives — like paying bills or taking their medication,” he said.

It’s also important to know your family history and share that with your doctors, Kobylarz said. Though older age is the biggest risk factor for Alzheimer’s, he explained, genetics and family history also play a role.

If you notice worrisome changes in an older family member, talk with a doctor, he said.

Scientists don’t yet fully understand what causes Alzheimer’s disease in most people. There is a genetic component to some cases of early-onset Alzheimer’s disease. Late-onset Alzheimer’s arises from a complex series of brain changes that occur over decades. The causes probably include a combination of genetic, environmental, and lifestyle factors. The importance of any one of these factors in increasing or decreasing the risk of developing Alzheimer’s may differ from person to person.

Alzheimers disease epidemic

To diagnose Alzheimer’s, doctors often:

  • Ask the person and a family member or friend questions about overall health, past medical problems, ability to carry out daily activities, and changes in behavior and personality;
  • Conduct tests of memory, problem solving, attention, counting, and language;
  • Carry out standard medical tests, such as blood and urine tests, to identify other possible causes of the problem; and
  • Perform brain scans, such as computed tomography (CT), magnetic resonance imaging (MRI), or positron emission tomography (PET), to rule out other possible causes for symptoms.

These tests may be repeated to give doctors information about how the person’s memory and other cognitive functions are changing over time. If the diagnosis is Alzheimer’s, beginning treatment early in the disease process may help preserve daily functioning for some time, even though the underlying disease process cannot be stopped or reversed. An early diagnosis also helps families plan for the future. They can take care of financial and legal matters, address potential safety issues, learn about living arrangements, and develop support networks.

In addition, an early diagnosis gives people greater opportunities to participate in clinical trials that are testing possible new treatments for Alzheimer’s disease or other research studies.

Alzheimer’s disease can be definitely diagnosed only after death, by linking clinical measures with an examination of brain tissue in an autopsy.

People with memory and thinking concerns should talk to their doctor to find out whether their symptoms are due to Alzheimer’s or another cause, such as stroke, tumor, Parkinson’s disease, sleep disturbances,side effects of medication, an infection, or a non-Alzheimer’s dementia. Some of these conditions may be treatable and possibly reversible.

Alzheimer’s cannot yet be cured, but medications and lifestyle changes can often help slow the progression of the disease, Kobylarz said. This requires the doctor, patient and family to work together to develop a plan to maintain cognitive function, he added.

Caring for a person with Alzheimer’s disease can have high physical, emotional, and financial costs. The demands of day-to-day care, changes in family roles, and decisions about placement in a care facility can be difficult. There are several evidence-based approaches and programs that can help, and researchers are continuing to look for new and better ways to support caregivers.

Becoming well-informed about the disease is one important long-term strategy. Programs that teach families about the various stages of Alzheimer’s and about ways to deal with difficult behaviors and other caregiving challenges can help.

Prion disease and Alzheimer's disease

Which Forms Of Neurodegenerative Disease Are Contagious

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.” Prions are a deadly and unstoppable form of protein that migrates, mutates, multiplies and kills with unparalleled efficiency. Prions cause fatal neurodegenerative diseases in humans and animals by converting the cellular prion protein PrPC into aggregation-prone PrPSc.

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 and we all are facing a public health disaster because of the negligence and reckless disregard for public health. Misinformed caregivers, family members, healthcare workers and others are caught in the crossfire of a deadly contagion known as a prion.

TSE is a spectrum disease also known as prion 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

Prion disease causes memory loss, impaired coordination, and abnormal movements. Abnormal proteins are now associated with autism. In fact, it appears that the biggest difference between the neurodegenerative disease spectrum and autism spectrum disorders is age. Both spectrums share common environmental causes and pathologies.

Caregivers Misinformed

It’s not known which patients with brain disease become infectious or when, but both CJD and Alzheimer’s patients are being mismanaged. Informed neurologists won’t touch patients with these symptoms because of the risk of transmission. They are making diagnoses from across the room.

“Creutzfeldt-Jakob disease behaves like Alzheimer’s disease on steroids,” said Dr. Jennifer Majersik, an associate professor of neurology at the University of Utah.

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. Misdiagnosis and misinformation regarding prion disease is a matter of life and death. The disease is now striking young people, including teenagers, with much greater frequency. It’s also killing clusters of people in the same communities with greater frequency. The mismanagement doesn’t end here.

Studies confirm that people and animals dying of prion disease contaminate the environment around them because infectious prions are in the urine, feces, blood, mucus and saliva of each victim. These infectious bodily fluids are contributing to the rapid spread of Alzheimer’s and other mutations of prion disease.

“There has been a resurgence of this sort of thinking, because 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 (prions).”

Alzheimer's disease research

Caregivers and other stakeholders are caught in the crossfire of misinformation and mismanagement. At the most basic level, this means that a sneeze, a drinking glass and eating utensils are permanent pathways of disease transmission. Anything that ever comes into contact with the bodily fluids of a victim is impossible to sterilize.

On a larger level, it means that entire communities and watersheds are at risk of permanent contamination from just a single victim, not to mention thousands of infectious victims. Alzheimer’s disease is an environmental nightmare–it’s a real-world version of Pandora’s box.

A study published in the journal Nature adds to the evidence about the transmissibility of Alzheimer’s disease between people. A second study by the same scientist in early 2016 adds to the claim. Meanwhile, there is absolutely no evidence to the contrary. Even wildlife are contracting brain disease from people because of the dumping of infectious waste on farms, ranches and forests.

Surgical instruments infected with prions, for example, are impossible to sterilize and hospitals throw them away. Prions are in the blood, saliva, urine, feces, mucus, and bodily tissue of its victims. Many factors are contributing to the epidemic. Prions are now the X factor. Industry and government are not accounting for prions or regulating them. They are ignoring the threat completely, which violates the Bioterrorism Preparedness and Response Act of 2002 in the United States. Other nations also are ignoring laws developed to protect food, air and water.

More Mismanagement Of Prion Disease

When the U.S. government enacted the Bioterrorism Preparedness and Response Act of 2002, it classified prions as select agents that pose an extreme risk to food, water and much more. Only two labs in the U.S. were allowed to handle them for research purposes. Unfortunately, the CDC quietly took prions off the list because the regulation criminalized entire industries and several reckless practices.

The U.S. Environmental Protection Agency (EPA) has confirmed that prions are in sewage and that there has been no way to detect them or stop them. As such, the EPA has never issued guidance on prion management within wastewater treatment plants.

land application sewage sludge

Unfortunately, the EPA’s risk assessment on sewage sludge and biosolids were prepared before the world of science knew about prions. The agency continues to cling to it’s antiquated sludge rule crafted back in the dark ages. It does, however, consider prions a “emerging contaminant of concern.” Meanwhile, its outdated risk assessments are promoting a public health disaster. The neurotoxins found in sewage, including heavy metals, also are contributing to the global spike in autism, which follows the same timing and trajectory as the spike in neurodegenerative diseases.

“Since it’s unlikely that the sewage treatment process can effectively deactivate prions, adopting measures to prevent the entry of prions into the sewer system is advisable,” said the Toronto Department of Health, November 2004.

Once unleashed on the environment, prions remain infectious. They migrate, mutate and multiply as they infect crops, water supplies, wildlife, livestock, sea mammals and humans. According to prion researcher Joel Pedersen at the University of Wisconsin, prions in soil become up to 680 times more infectious. From there, they migrate, mutate and multiply. It’s a real world version of Pandora’s Lunchbox.

“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.

Pedersen also found that sewage treatment does not inactivate prions. Therefore, prions are lethal, mutating, migrating and multiplying everywhere sewage is dumped.

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 pathogens, pharmaceutical residue and chemical pollutants found in sewage sludge are taken up by plants and vegetables.”

TSEs also include mad cow disease and chronic wasting disease in the deer family. Few, if any, mammals are immune. Thanks to the mismanagement of infectious waste, including sewage, the animal world is contracting prion disease from humans. They also are passing it among themselves via their own bodily fluids. Species barriers are a myth.

Unfortunately, prions linger in the environment, homes, hospitals, nursing homes, dental offices and beyond infinitely. Prions defy all attempts at sterilization and inactivation. If they can’t stop prions in the friendly and sterile confines of an operating room, they can’t stop them in the wastewater treatment plant.

biosolids land application

The risk assessments prepared by the U.S. EPA for wastewater treatment and sewage sludge are flawed and current practices of recycling this infectious waste is fueling a public health disaster. Many risks are not addressed, including prions and radioactive waste. They don’t mention prions or radiation because there is no answer. Most nations are making the same mistake. We’re dumping killer proteins on crops, parks, golf courses, gardens, ski areas, school grounds and beyond. Wind, rain and irrigation spread these contaminants and many more throughout our communities and watersheds.

Failure to account for known risks is negligent. Crops for humans and livestock grown in sewage sludge absorb prions and become infectious. We’re all vulnerable to neurotoxins and right now due to widespread denial and mismanagement. It’s time to stop the land application of sewage sludge (LASS) in all nations. Safer alternatives exist.

Alzheimer's disease public relations firm

Crossbow Communications specializes in issue management and public affairs. Alzheimer’s disease, Creutzfeldt-Jakob disease, chronic wasting disease and the prion disease epidemic is an area of special expertise. Please contact Gary Chandler to join our coalition for reform gary@crossbow1.com.

Tau Proteins Very Similar To Prions

Prion Science Still Unfolding

Neurodegenerative disease is the fastest-growing cause of death in the world. Prion disease is responsible for the vast majority of the surge in humans and other mammals.

Professor Goedert, a program leader at the MRC Laboratory of Molecular Biology in Cambridge, believes our best hope of fighting dementia requires predicting who will get neurodegenerative disease and preventing its onset.

His work has just earned him – along with three other neuroscientists – the Brain Prize for 2018 from the Lundbeck Foundation in Denmark. Worth one million euros, it is the most valuable award there is for brain research.

Goedert won the prize for groundbreaking work dating back to the 1980s that was initiated at the LMB by Aaron Klug and Martin Roth and initially involved Claude Wischik, Tony Crowther, Michal Novak, John Walker, Cesar Milstein, Ross Jakes and Maria Grazia Spillantini.

neuroscience and prions

Using human brain tissues, transgenic mice, cultured cells and purified proteins, Professor Goedert demonstrated – despite considerable initial skepticism – the importance of tau protein in Alzheimer’s disease.

“The brains of people who have died of Alzheimer’s disease have two abnormalities – so-called plaques and tangles. These are protein aggregates,” he explains.

Ultimately, these abnormalities kill nerve cells and brain tissue. Plaques are caused by the clumping together of beta-amyloid protein pieces outside nerve cells, which block cell-to-cell signalling. Tangles, meanwhile, are inside the nerve cells and occur when tau protein assembles into clusters of filaments and becomes insoluble. These are the focus of Goedert’s work.

“We all have tau proteins in the brain. Its function is probably to stabilise microtubules inside cells,” he says.

Microtubules are a cellular transport system, like rails, that help material to move in our bodies.

“But it is not a loss of function disease,” Goedert stressed. “It’s a gain of toxic function. The tau protein is one of many proteins that can stabilise these microtubules.

“It looks like if a portion of it turns into these abnormal structures, it’s not sufficient to disrupt this process. The formation of these inclusions is what causes the disease of the cell.”

A pathological pathway leads from the soluble to insoluble filamentous tau.

“Somewhere along it lies the cause of the disease, in the sense of why the nerve cells degenerate and die, which leads to the symptoms of the disease,” explains Goedert.

“Everybody would agree that something on this pathway causes neurodegeneration. Some would argue that there are aggregate species – not the final filaments, but smaller – that have a very active toxic effect.

“I would think it’s equally likely that if you have loads of these filaments inside cells, over a long period of time they are like space-occupying lesions inside a cell body and particularly inside very fine processes.

“They would disrupt all sorts of things inside the cells, including the transport of materials to the periphery, and then at the end the cell dies.

“In the past 10 years, we’ve also found tau proteins exhibit prion-like properties – they can fold in ways that can be transmitted to soluble tau molecules.”

Prions are the misfolded protein equivalent of viral infections and enable a neurodegenerative disease to spread. In the case of Alzheimer’s disease, it means the tau protein aggregates gradually take over.

Prion disease and Alzheimer's disease

“These aggregates form in a small region of the brain and over a long period of time spread to the brain as a whole, and then symptoms appear. Initially, when you have small numbers of these aggregates, there are no symptoms,” adds Goedert.

Much of the group’s work now is focused on the mechanisms behind the spread. Prions migrate, mutate and multiply. There is no species barrier. As such, other mammals are now contracting brain disease from human sewage.

“If we understand more, we might be in a position to prevent the spread from happening and develop compounds that can prevent the symptoms. In addition, you need to be able to predict who is going to get the disease.

“These very early aggregates that form, before the spread occurs, are probably present in people’s brains for decades before the symptoms appear. If you could detect those and predict at an individual level for example that if a person lives another 20 years they are going to get the disease, then you would be in a position to treat that person and prevent the symptoms,” says Professor Goedert, who is an honorary professor of experimental molecular neurology at the University of Cambridge.

“You could give the compounds to everyone over the age of 50. But every treatment has some sort of side effect. Then you would have to treat people who are perfectly healthy.”

No compounds yet exist to deal with the aggregation of tau proteins. And those that have been trialled to tackle amyloid plaques have so far failed.

“One possibility is that the compounds were perfectly good but were given too late,” suggests Prof Goedert. “I think identifying people at risk of developing the disease at a point when they have no symptoms but have some of these pathologies in the brain is really crucial. These are the biomarkers. But until recently it was not possible to detect these things inside living people.”

Studies of the brains of thousands of people have shown that the vast majority have small numbers of these aggregates. Those who had Alzheimer’s disease had many more of them.

“When you see small numbers of aggregates in the brain, you extrapolate that had the person lived for another 20-30 years, they would have got the disease,” says Goedert.

“More recently, it’s become possible to identify aggregates in the brains of living people using PET (positron emission tomography) scanning. You inject mildly radioactive compounds that bind specifically to the aggregates – they don’t see the protein where it’s not aggregated. Then using imaging techniques, you can detect the aggregates.”

PET scans can now be used to detect both beta-amyloid plaques and aggregated tau protein, although the test is not yet sophisticated enough.

“It’s still very early but I think this is going to revolutionise everything,” says Prof Goedert. “In principle you could take a person and image them every year and see whether the pathology progresses. The problem is resolution. Are you going to detect very small numbers of these things? Over time that will improve – but at the moment it’s not there.

“In the long run, it could be like breast cancer screening for women or colonoscopies for men and women. You would take people at the age of 50 and have a PET scan every five or 10 years.”

Current therapies – cholinesterase inhibitors and glutamate receptor antagonists – treat some of the symptoms of Alzheimer’s disease, but do not tackle the underlying biological causes.

These symptoms often begin with memory lapses and gradually progress through to problems with communication, reasoning and orientation. In the latter stages, patients may have difficulties eating or walking, and become increasingly frail and needing help with all aspects of daily life.

prion disease spectrum

“There are so many people working on it now, one can be reasonably optimistic in terms of the timeframe. It’s reasonably clear now what one has to do,” says Prof Goedert.

Understanding the mechanisms of the disease is key – and the work of Professor Goedert and those he shared the prize with is likely to play a critical role in future treatments. Most recently, he has been examining the structure of the tau filaments.

“This lab is very famous for its cryo-electron microscopy technique, which Richard Henderson got a Nobel Prize for last year, and we are collaborating with the group of Sjors Scheres to look at high resolution structures of these tau filaments for Alzheimer’s disease. It tells you how similar or different they are, which I think has a bearing on the prion-like properties of these aggregates,” he said.

Different tau filaments feature in the distinct neurodegenerative diseases such as Pick’s disease and progressive supranuclear palsy, where they form in the absence of beta-amyloid deposits outside brain cells.

Goedert’s recent work in mouse models and in cell cultures suggests filamentous tau clusters propagate through self-seeding (replication, infection and mutation).

“Experimentally, they do. But proving the mechanism takes place in the human brain is difficult. We must interfere with the process and block to prove the theory,” he said. “In the long run, prevention is the thing to do.”

Goedert shares the 2018 Brain Prize with Bart De Strooper (London and Leuven), Christian Haass (Munich) and John Hardy (London) for their groundbreaking research on the genetic and molecular basis of Alzheimer’s disease.

Although he knows them all, Professor Goedert has not collaborated with the others because they all work primarily on beta amyloid plaques.

Unfortunately, prions migrate, mutate and multiply. There is no species barrier. As such, other mammals are now contracting brain disease from human sewage that’s being dumped into our food and water supplies. Sick wildlife and sick livestock are just the tip of the iceberg. Infectious waste isn’t fertilizer for farms, ranches, golf courses, school grounds, parks, gardens or elsewhere. Spreading infectious waste is now spreading brain disease at the speed of light. Preventing brain disease begins with the truth. http://crossbowcommunications.com/wildlife-contracting-brain-disease-from-biosolids/

Alzheimer's disease prevention

Crossbow Communications specializes in issue management and public affairs. Alzheimer’s disease, Creutzfeldt-Jakob disease, chronic wasting disease and the prion disease epidemic is an area of special expertise. Please contact Gary Chandler to join our coalition for reform gary@crossbow1.com

Neil Diamond Retires Due To Parkinson’s Disease

Neurodegenerative Disease Gaining Momentum

After nearly 50 years on the pop charts, Neil Diamond announced his retirement to tackle Parkinson’s disease.

Concert dates in Australia and New Zealand that were set for March and April as part of Mr. Diamond’s 50th anniversary tour have been canceled. With 38 songs in the Top 10 on the Billboard Adult Contemporary charts, he is one of the world’s best-selling artists of all time.

“It is with great reluctance and disappointment that I announce my retirement from concert touring,” Mr. Diamond said in a statement on his website. “I have been so honored to bring my shows to the public for the past 50 years.”

Parkinson's disease Neil Diamond

Mr. Diamond, who turns 77 this week, will continue writing and recording music, but would no longer play to live audiences. As part of the anniversary tour, he had already performed concerts across the United States and Europe, including dates in New York; Nashville; London; and Hamburg, Germany, when he made the announcement.

Mr. Diamond was inducted into the Rock and Roll Hall of Fame in 2011. He will receive a Lifetime Achievement Award at this year’s Grammys.

Mr. Diamond was on his 50th anniversary tour when he announced his retirement from live performances. As part of that tour, he performed at the Royal Farms Arena in Baltimore in June 2017, where he sang probably his best-known and most-beloved hit, “Sweet Caroline.” In the statement announcing his retirement, he cited a line from the song: “This ride has been ‘so good, so good, so good’ thanks to you.”

Neurodegenerative disease is now the fastest-growing cause of the death in the world. It’s vastly undiagnosed and misdiagnosed.

Alzheimer’s disease alone is taking the lives of 50-100 million people now. Despite millions of deaths, experts suggest that the prevalence of the disease will quadruple by 2050, if not sooner. Unfortunately, there is a growing stack of evidence that Alzheimer’s disease and Parkinson’s disease are forms of prion disease–a transmissible disease–which means that millions of caregivers, friends and family members are at risk.

Prion disease and Alzheimer's disease

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.” Prions are a deadly and unstoppable form of protein that migrates, mutates, multiplies and kills with unparalleled efficiency. Prions cause fatal neurodegenerative diseases in humans and animals by converting the cellular prion protein PrPC into aggregation-prone PrPSc.

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 and we all are facing a public health disaster because of the negligence and reckless disregard for public health. Misinformed caregivers, family members, healthcare workers and others are caught in the crossfire of a deadly contagion known as a prion.

TSE is a spectrum disease also known as prion 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.

Parkinson’s disease is the second most common diagnosis in the prion spectrum. It’s estimated that between 7-10 million people around the world have Parkinson’s disease today.

The US National Institute for Neurological Disorders and Stroke (NINDS) estimated in a 2006 report that about 50,000 new cases of Parkinson’s disease are diagnosed in the US each year, and the total number of cases in the US is at least 500,000. The true prevalence (total number of cases) of Parkinson’s disease is difficult to assess, because the disease is typically not diagnosed until the disease process is already far advanced. Therefore the actual number of Americans with the disease is almost certainly higher than the diagnostic numbers would suggest.

The prion epidemic is worse in some regions of the world than others. Finland and Iceland are at the top of the list. The United States is third, where deaths from Alzheimer’s disease increased 71 percent from 2000 to 2013. Over the same time, deaths from heart disease decreased 14 percent.

Researchers have more questions than answers, but we know that neurotoxins, head trauma and genetics can all trigger neurodegenerative disease. Unfortunately, that’s where our knowledge gets fuzzy. Most diagnoses are a process of elimination. After eliminating all other possibilities, the medical guesswork begins:

  • If the patient has a memory disorder, it’s Alzheimer’s disease.
  • If they have a movement disorder, it’s Parkinson’s disease.
  • If the patient shows both symptoms, flip a coin.
  • If they ever had a concussion, it’s possibly CTE.
  • If the person is incapacitated, it’s Creutzfeldt-Jakob disease (CJD).

Prion disease causes memory loss, impaired coordination, and abnormal movements. Abnormal proteins are now associated with autism. In fact, it appears that the biggest difference between the neurodegenerative disease spectrum and autism spectrum disorders is age. Both spectrums share common environmental causes and pathologies.

Alzheimer's disease public relations firm

Crossbow Communications specializes in issue management and public affairs. Neurodegenerative disease is among our special areas of practice. Please contact Gary Chandler to join our coalition for reform gary@crossbow1.com.

Burden Of Care For Alzheimer’s Disease Rising Fast

Neurodegenerative Disease The Fastest-Growing Cause Of Death

Someone in the world develops dementia every three seconds. There were an estimated 46.8 million people worldwide living with dementia diagnoses in 2015 and this number is believed to be close to 50 million people in 2017. This number will almost double every 20 years, reaching 75 million in 2030 and 131.5 million in 2050. The X factor is the number of people who have dementia, but have not been diagnosed. It’s estimated that the real number is drastically higher.

Much of the increase will be in developing countries. Already 58 percent of people with dementia live in low and middle income countries, but by 2050 this will rise to 68 percent.

The total estimated worldwide cost of dementia is US$818 billion in 2015, which represents 1.09 percent of global GDP. By 2018, the global cost of dementia will rise above a US$1 trillion.

This figure includes costs attributed to informal care (unpaid care provided by family and others), direct costs of social care (provided by community care professionals, and in residential home settings) and the direct costs of medical care (the costs of treating dementia and other conditions in primary and secondary care).

In the U.S. alone, it’s estimated that Alzheimer’s disease is already costing citizens $277 billion annually, including $186 billion in Medicare and Medicaid payments. 

Between 2000 and 2015, deaths from Alzheimer’s disease as recorded on death certificates increased 123 percent, while deaths from the number one cause of death (heart disease) decreased 11 percent. Unfortunately, Alzheimer’s disease isn’t always diagnosed and it isn’t accurately reported as the cause of death in the majority of cases. Eighty-three percent of the help provided to older adults in the United States comes from family members, friends or other unpaid caregivers. Nearly half of all caregivers who provide help to older adults do so for someone with Alzheimer’s disease or another dementia.

Alzheimers disease epidemic

Direct medical care costs account for roughly 20 percent of global dementia costs, while direct social sector costs and informal care costs each account for roughly 40 percent. The relative contribution of informal care is greatest in the African regions and lowest in North America, Western Europe and some South American regions, while the reverse is true for social sector costs.

This means that if global dementia care were a country, it would be the 18th largest economy in the world. The annual costs exceed the market values of companies such as Apple (US $742 billion) and Google (US $368 billion).

Research shows that most people currently living with dementia have not received a formal diagnosis. In high income countries, only 20-50 percent of dementia cases are recognised and documented in primary care. This ‘treatment gap’ is certainly much greater in low and middle income countries, with one study in India suggesting 90 percent remain undiagnosed. If these statistics are extrapolated to other countries worldwide, it suggests that approximately three quarters of people with dementia have not received a diagnosis, and therefore do not have access to treatment, care and organized support that getting a formal diagnosis can provide.

Earlier diagnosis and early intervention are important mechanisms by which the treatment gap can be closed. Among all people alive today, if those who will get Alzheimer’s disease were diagnosed when they had mild cognitive impairment (MCI) — before dementia — it would save trillions of dollars in health and long-term care costs.

Alzheimer's disease prevention

Crossbow Communications specializes in issue management and public affairs. Alzheimer’s disease, Creutzfeldt-Jakob disease, chronic wasting disease and the prion disease epidemic is an area of special expertise. Please contact Gary Chandler to join our coalition for reform gary@crossbow1.com.

Prions Detected In Human Skin

Raises Concerns About Prion Pathways

Researchers have found abnormal prion protein in the skin of 23 people who died from Creutzfeldt-Jakob Disease (CJD). Meanwhile exposing mice to skin tissue taken from the CJD patients caused them to develop prion disease.

The study has raised questions about the possibility of prion diseases being transmitted during medical procedures that involve the skin, as well as the possibility of using skin samples to detect the diseases.

Creutzfeldt-Jakob disease (CJD)—the human equivalent of mad cow disease—is caused by rogue, misfolded protein aggregates termed prions, which are infectious and cause fatal damages in the patient’s brain. CJD patients develop signature microscopic sponge-like holes in their brains. The initial signs of CJD include memory loss, behavior changes, movement disorder, and vision problems, which usually rapidly progress to death. According to the National Institutes of Health (NIH), 90 percent of CJD patients die within one year of onset, and hundreds of Americans are diagnosed annually. There is no available treatment or cure.

prion disease spectrum

There are numerous types of prion diseases in humans, and CJD is the most common. About 90 percent of CJD cases have a sporadic origin. Prion infectivity is highly concentrated in CJD patient brain tissue. Inter-personal CJD transmission has occurred after patients were exposed to surgical tools previously contaminated by CJD brain tissues.

In a Science Translational Medicine study published today, Case Western Reserve University School of Medicine researchers found that CJD patients also harbor infectious prions in their skin, albeit at lower levels. In the study, the researchers collected skin samples from 38 patients with assistance from the National Prion Disease Pathology Surveillance Center at Case Western Reserve School of Medicine and measured their prion levels. Using a highly sensitive in vitro assay developed and conducted by Byron Caughey’s group at the NIH, they detected prion protein aggregates in the skin samples from all of CJD patients. Prion levels were 1,000-100,000 times lower in the skin than in the brain, and only detectable by this extremely sensitive assay. The researchers further demonstrated that such skin prions are infectious, since they are capable of causing disease in humanized mouse models.

“It is well known that CJD is transmissible via surgical or medical procedures involving prion-infected brain tissue. Our finding of infectious prions in skin is important since it not only raises concerns about the potential for disease transmission via common surgeries not involving the brain, but also suggests that skin biopsies and autopsies may enhance pre-mortem and post-mortem CJD diagnosis,” said Wenquan Zou, Associate Professor of Pathology and Neurology and Associate Director of the National Prion Disease Pathology Surveillance Center at Case Western Reserve School of Medicine. Zou led the study involving a consortium of research groups and researchers across Case Western Reserve School of Medicine, University Hospitals Cleveland Medical Center, the NIH, and the People’s Republic of China.

Prions and Alzheimer's disease

“The level of prion infectivity detected in CJD skin was surprisingly significant, but still much lower than that in CJD brains,” cautioned Qingzhong Kong, Associate Professor of Pathology and Neurology at Case Western Reserve School of Medicine. “Prion transmission risk from surgical instruments contaminated by skin prions should be much lower than that of instruments contaminated by brain tissue.” In the study, the Kong group assisted by the Zou group demonstrated that CJD patient skin is infectious using humanized transgenic mouse models.

Current diagnostic tools for CJD rely on brain tissue samples collected at either biopsy or autopsy, or cerebral spinal fluid obtained by spinal taps. The new study may lay the foundation for less invasive techniques. “Using the skin instead of brain tissue for post-mortem diagnosis could be particularly helpful in cultures that discourage brain autopsy, such as China and India. These countries have the largest populations with the greatest number of patients, but brain autopsy is often not performed,” said Zou.

“Further investigation is necessary to determine whether extra precautions should be taken during non-neurosurgeries of CJD patients, especially when surgical instruments will be reused,” said Zou. Case Western Reserve School of Medicine researchers plan to further evaluate the potential risk of skin prion transmission through non-neurosurgeries, primarily using mouse models.

The study was conducted by scientists from the National Institute of Allergy and Infectious Diseases (NIAID) and various other collaborating groups.

Generally, people associate prion diseases with the brain, although it has been shown that clusters of the abnormal prion protein, which cause sponge-like holes in the brain, can accumulate in other organs including the liver, spleen, lungs and kidney. It is known that Sporadic CJD, which is the most common human prion disease, can be transmitted via invasive medical procedures involving the central nervous system and cornea, but transmission via the skin has not generally been considered a concern.

The authors want to study the risk of surgical instruments becoming contaminated and the risk associated with procedures that involve CJD patients. They also suggest the possibility of using the skin-based diagnostic test for prion diseases in humans and animals.

Alzheimer's disease public relations firm

Crossbow Communications specializes in issue management and public affairs. Alzheimer’s disease, Creutzfeldt-Jakob disease, chronic wasting disease and the prion disease epidemic is an area of special expertise. Please contact Gary Chandler to join our coalition for reform gary@crossbow1.com.