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

Simple Steps To Protect Your Brain

Nutrition, Exercise The Best Defense Against Alzheimer’s Disease

As we age, cognitive decline is common, there is much that we can do to boost our brainpower, while promoting overall health.

Neuroplasticity means the brain can grow, rewire, adapt and strengthen when properly stimulated. Recent studies suggest physical and mental exercise, a healthy diet and other common lifestyle changes can improve brain function, delay dementia symptoms and even lower the risk for Alzheimer’s disease.

“Even though we cannot predict exactly who will get Alzheimer’s disease and when, we do know that people who practice Alzheimer’s prevention strategies improve their quality of life and reap immediate benefits in memory and health,” says Dr. Gary Small, director of UCLA’s Longevity Center and co-author of The Alzheimer’s Prevention Program: Keep Your Brain Healthy for the Rest of Your Life.

Alzheimer's disease treatment

Here are some smart ways to boost your brain, while building total body health:

Lose Weight and Lower Your Blood Pressure

Carrying around a lot of belly fat is often a sign of increased cell inflammation throughout the body, including the brain. In one study, men who had the most abdominal fat in their 40s were the most likely to develop dementia later on. Just another reason to improve your diet and lace up your walking shoes.

A sharp, healthy brain needs a good supply of oxygen and glucose to operate. Better blood flow gets it there. Increased blood flow helps brain cells communicate better, says Small, who believes that as little as 15 to 20 minutes of cardiovascular exercise a day can lower Alzheimer’s risk.

Have it checked every year. If it’s high — that is, above 120/80 mmHg — work with your doctor to get it down. High systolic blood pressure limits blood and nutrients to the brain, making it more likely that you will lose gray matter in critical areas as you age.

Consume Salmon

Studies have shown that eating foods like salmon, tuna and other oily fish — along with flaxseed and walnuts — that are rich in omega-3 fatty acids is a good bet for all-around brain and heart health. Omega-3 fatty acids contain DHA and EPA, which are highly concentrated in the brain and crucial for optimal brain function, according to the Academy of Nutrition and Dietetics.

prevent Alzheimer's disease

These fatty acids are important to consume, because our neurons use them to build brain cell walls and maintain good brain health. In studies, people with low blood levels of omega-3s had lower brain volume than people with higher levels, suggesting their brains were aging more rapidly. One study at Tufts University found that people who ate oily fish three times a week reduced their risk of Alzheimer’s disease by nearly 40 percent.

Eat Leafy Green Vegetables

The ideal side dish to your salmon entrée is a leafy green vegetable like spinach, kale, Swiss chard or collards. All have been linked to slowing cognitive decline, thanks to their high concentration of vitamin K. According to a new study from Rush University Medical Center, people who ate one to two servings of leafy greens each day had the cognitive ability of a person 11 years younger than those who consumed none.

Eat Blueberries

And eat a bucketful. Inside each berry is a special antioxidant called anthocyanin, which can cross the blood-brain barrier and protect brain cells from oxidation damage. A Harvard Nurses’ Health Study of 16,000 women older than 70 found that women who consumed two or more half-cup servings of blueberries or strawberries per week remained mentally sharper than those who didn’t eat berries.

treat Alzheimer's disease

Brain Stimulation

Word-recall tasks and other brain challenges like Sudoku and crossword puzzles might decrease your risk of dementia, according to a recent study at the University of California, Berkeley. The scientists believe brain challenges prevent the buildup of beta-amyloid in the brain, the protein that accumulates in the brain of Alzheimer patients.

Olive Oil

A study from Spain showed that men who ate about four tablespoons of extra-virgin olive oil a day showed better language comprehension, attention and abstract thinking than those on a low-fat diet. Its antioxidants may reduce brain inflammation.

Social Interaction

In an eight-year study reported in The Lancet Neurology, researchers gave cognitive-performance tests to 89 elderly people and then compared the results of testing with autopsy findings some years later. They found that the larger a person’s social network, the smaller an effect the neurological tangles and plaques associated with Alzheimer’s disease had on cognitive ability. Researchers say the protective effects of having many friends were more evident for the parts of the brain where we store general knowledge, language and factual information.

Alzheimer’s Disease News via https://scoutingmagazine.org/2017/10/nine-easy-ways-protect-brain/

Alzheimer's disease public relations firm

Crossbow Communications specializes in issue management and public affairs. Its expertise includes health and environmental issues, including Alzheimer’s disease. Please contact Gary Chandler at gary@crossbow1.com to join our network.

Patients With Neurodegenerative Disease Produce Infectious Waste

Caregivers Caught In The Crossfire Of Misinformation, Mismanagement

Neurodegenerative disease is the fastest-growing cause of death in the world. Alzheimer’s disease alone is taking the lives of 50-100 million people now. Despite millions of Alzheimer’s-related fatalities annually, experts suggest that the prevalence of the disease among the living will quadruple by 2050, if not sooner. Some advocates are warning that the surging epidemic could bankrupt entire nations.

Unfortunately, there is a growing stack of evidence that Alzheimer’s disease is a transmissible disease, which means that millions of caregivers, friends and family members are at risk.

The epidemic is more widespread than anyone knows. A groundbreaking study suggested that Alzheimer’s disease causes six times as many deaths than official statistics indicate. The Centers for Disease Control and Prevention estimated that, in 2010, Alzheimer’s disease caused almost 84,000 deaths in the United States, a number derived from death certificates in which Alzheimer’s disease was listed as the main cause. In reality, the study said Alzheimer’s disease was the underlying cause in more than 500,000 deaths in 2010 that were often attributed to conditions, such as pneumonia, caused by complications of Alzheimer’s. Those numbers make Alzheimer’s disease the third-leading cause of death in the United States, behind heart disease and cancer. The study was led by researchers at the Rush University Medical Center in Chicago and published in 2013 in the medical journal Neurology.

Prions 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.

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

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).”

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.

Alzheimer's disease diagnosis

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 contrary. Even wildlife are contracting brain disease from people because of the dumping of infectious waste on farms, ranches and forests.

Caregivers are being misinformed about the risks associated with exposure to people with Alzheimer’s disease and Creutzfeldt-Jakob disease. 

Surgical instruments infected with prions, for example, are impossible to sterilize. 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.

Wastewater treatment plants are collecting points for prions from infected humans. The sewage treatment process can’t stop prions from migrating, mutating and multiplying before being discharged into the environment where they can kill again. Wastewater treatment plants are spreading infectious waste far and wide because they are incapable of stopping prions. As such, all by-products and discharges from wastewater treatment plants are infectious waste, which are contributing to the global epidemic of neurodegenerative disease among humans, wildlife and livestock.

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. 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.

wastewater treatment plant

“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.

biosolids land application sewage sludge

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

Unfortunately, prions linger in the environment, homes, hospitals, nursing homes, dental offices and beyond infinitely. Prions defy all attempts at sterilization and inactivation. Answers begin with the truth.

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.

Preventing Dementia A Major Challenge

New Report Offers Little Hope In Battle Against Neurodegenerative Disease

By Sharon Begley, STAT

Alzheimer’s disease drug treatments have met failure after failure. Many people have decided that prevention is the only hope. Unfortunately, a U.S. panel of experts claims that prevention might be just as elusive as a cure.

From physical activity to avoiding high blood pressure to brain training, a 17-member committee assembled by the National Academies of Sciences concluded, no interventions are “supported by high-strength evidence.” Instead, some high-quality studies found that one or another intervention worked, but other equally rigorous studies found they didn’t.

Alzheimer's disease diagnosisThe three prevention strategies that the report focused on were cognitive training, blood pressure control, and physical activity. (Unfortunately, it didn’t track dietary factors.)

  1. Cognitive training: The evidence for programs aimed at boosting reasoning, problem-solving, memory, and speed of processing does include randomized trials that reported benefits from brain training, but the report calls that evidence “low to moderate strength.” One problem: There seemed to be benefits for two years, but not after five or 10. Results in other randomized studies were even more equivocal. There are also data from studies that are less rigorous, leading the committee to conclude that brain training (computer-based or not) can delay or slow age-related cognitive decline — but not Alzheimer’s.
  2. Blood pressure: Evidence that this helps is weaker still. It’s mostly not based on randomized controlled trials, but the committee decided there is “sufficient” evidence from other kinds of studies as well as from understanding how the brain works to conclude that managing hypertension (especially from ages 35 to 65) can prevent, delay, or slow Alzheimer’s disease, and therefore to include it in public health messages. But there’s no good evidence on how best to reduce high blood pressure; of all the kinds of drugs that do so, however, angiotensin receptor blockers seem to be the best for cognition, for unknown reasons.
  3. Physical activity: Evidence for this is on a par with that for blood pressure: “evidence is insufficient to conclude whether increasing physical activity” prevents or slows Alzheimer’s disease. Randomized controlled trials only sometimes showed benefit, though there is some evidence from other kinds of studies shows that exercise delays or slows age-related cognitive decline (but not Alzheimer’s disease).

“Even though clinical trials have not conclusively supported the three interventions,” Alan Leshner, chair of the committee and CEO emeritus of the American Association for the Advancement of Science, said in a statement, “the evidence is strong enough to suggest the public should at least have access to these results to help inform their decisions.”

The disappointing conclusion comes in the wake of a review published last month of the 105 experimental anti-Alzheimer’s compounds in development. It concluded that their immediate prospects are so poor that the U.S. is unlikely to meet its goal of having a “meaningful” therapy for Alzheimer’s by 2025. That makes the need for prevention strategies greater than ever.

Some experts outside the committee said it had set too high a bar. Henry Mahncke, CEO of brain-training company Posit Science, criticized the committee for lumping together all kinds of cognitive training. That diluted the results showing that the kind that taps into neuroplasticity, the brain’s ability to change its structure and function, “consistently works,” while other forms have “poor to mixed results.”

prevent Alzheimer's disease

The Alzheimer’s Association said it is sticking with its “10 Ways to Love Your Brain” and reduce the risk of dementia. The 10 include physical activity, lifelong learning, heart health, and sound sleep.

“No one is promising this is going to prevent Alzheimer’s,” said spokesman Niles Frantz, “but we think there is enough evidence to say it can reduce your risk.” Unlike the committee, he said, “we believe it is worth talking publicly about these things.”

The neurobiology of dementia suggests that “a multifaceted approach [to prevention] may be most effective,” the report notes. But it is fiendishly complicated to do randomized controlled trials on more than one intervention at a time.

However, STAT has learned, a large-scale, U.S.-based lifestyle intervention study to prevent cognitive decline and dementia will be introduced at the Alzheimer’s Association International Conference in London in July. It is expected to be modeled on a Finnish study that found that a kitchen sink approach — healthy eating, brain training, exercise, and managing diabetes and cardiovascular risk — slows cognitive decline.

Neurodegenerative Disease News via STAT https://www.statnews.com/2017/06/22/preventing-dementia-strategies/

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.

Alzheimer’s Disease Influenced By Acidity

pH Level Might Deter, Slow Progression Of Alzheimer’s Disease

Prion diseases are scary, incurable and fatal. They first gained notoriety when cows became infected by prion proteins and, in turn, infected people. Fervor surrounding mad cow disease resulted in the U.S. banning imports of beef from the European Union for 15 years.

New research led by Michigan State University and published in the current issue of the Proceedings of the National Academy of Sciences, offers hope by showing how we might prevent prions from aggregating or growing into deadly diseases.

Lisa Lapidus, MSU professor of physics and astronomy, has pioneered a laser technique to advance her medical discoveries. The two-laser approach measures the speed at which proteins rearrange before beginning to clump, or aggregate — the critical beginning of many neurodegenerative diseases.

Alzheimer's disease diagnosis

“While prion’s transmission method is quite unusual, the process of protein clumping is quite common in a number of diseases, such as Alzheimer’s and Parkinson’s disease,” said Lapidus, who published the paper with Kinshuk Raj Srivastava, former postdoctoral fellow at MSU. “We’ve discovered that there is a ‘dangerous middle range,’ a speed that individual proteins rearrange in which clumping happens fastest. We were also able to find a way to bump the proteins out of the danger zone and reduce the chances of clumping from happening.”

Bumping proteins out of the danger zone could help advance research on prion diseases, such as fatal familial insomnia and kuru in humans, mad cow disease, and chronic wasting disease in deer.

What these prion diseases have in common, the team discovered, is the key speed changer of pH. Using the protein from a hamster, a mammal with a history of suffering from prion diseases, the team found that prion-related protein chains reconfigure slowly at neutral pH, thus avoiding the sticky middle speeds.

However, at low pH, the scientists found the protein rearranged in the dangerous middle range, confirming that prions thrived and grew when pH levels were low. To further prove this middle regime is really dangerous, they compared the speed of hamster at low pH to rabbit, an animal that doesn’t get prion disease. Rabbit prion was much faster than hamster.

“If rearrangement is fast, when two chains come into contact, they can rearrange rapidly enough to avoid making interactions that lead to clumping,” Lapidus said. “When moving slow, neither chains will have sticky patches exposed. But when the rearrangements are happening at the same speed as the random collisions between two proteins, then clumping can occur more quickly.”

Taking the research one step further, Lapidus and her team decided to see if any drugs could move hamster prions out of this danger zone. Lapidus proved that astemizole is effective in speeding up protein self-interactions even further and preventing prion clumping.

Astemizole was once used to treat allergies, but it was pulled from the market due to rare but sometimes fatal side effects. The antihistamine, however, also has shown promise in some Alzheimer’s research.

This research didn’t directly examine disease transmission, but future research could tackle this and help understand how proteins rearranging in the danger zone can be recruited by an existing clump of protein.

Alzheimer’s Disease Prevention and Treatment Update via https://www.eurekalert.org/pub_releases/2017-03/msu-apb032017.php

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

Together We Can Prevent Alzheimer’s Disease.

Is Alzheimer’s Disease Contagious

Science, Evidence Proving Transmissibility

If you think that you and your family are immune to the surging epidemic of neurodegenerative disease, think again. Neurodegenerative disease, including Alzheimer’s disease, is the fastest-growing cause of death in the world. It’s getting worse every day thanks to mismanagement and misinformation.

Infectious proteins known as prions are involved with most forms of neurodegenerative disease. Prion disease is known in neurology as transmissible spongiform encephalopathy (TSE). The operative word is “transmissible.” The global epidemic has more to do with the prion contagion than age.

Dr. Stanley Prusiner, an American neuroscientist from the University of California at San Francisco, earned a Nobel Prize in 1997 for discovering and characterizing deadly prions and prion disease. Prusiner claims that all TSEs, including Alzheimer’s disease, are caused by prions.

Prions and Alzheimer's disease

President Obama awarded Prusiner the National Medal of Science in 2010 to recognize the importance of his research. According to Prusiner, TSEs are a spectrum disease. Creutzfeldt-Jakob disease, which is extremely aggressive and extremely transmissible, is at the extreme end of the spectrum. Unfortunately, Prusiner’s science is being ignored and we are facing a public health disaster because of the negligence.

Neurologists are just guessing when they make a diagnosis on the prion spectrum. If the patient exhibits memory problems, they are labeled with Alzheimer’s disease. If they have a movement disorder, they are diagnosed with Parkinson’s disease. If the person exhibits extreme symptoms of both, they are diagnosed with Creutzfeldt-Jakob disease (CJD). It’s far from a science. Neurologists don’t know where along the spectrum the disease becomes transmissible. The entire spectrum could represent a transmissible disease. Unfortunately, neurologists are not warning these patients and their caregivers about the risks of exposure. Even those with Creutzfeldt-Jakob disease are not quarantined. They are sent home, where they can infect friends, family, caregivers, clinics, dental offices, restaurants and entire communities.

“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 renews concern about the transmissibility of Alzheimer’s disease between people. A second study released in early 2016 by the same scientist adds to the stack of evidence.

According to neuroscientist Laura Manuelidis, at least 25 percent of Alzheimer’s diagnoses are wrong. These misdiagnoses are actually CJD, which is further up the prion spectrum. CJD, without dispute, is extremely infectious to caregivers and loved ones.

Alzheimer's disease and caregivers

Studies confirm that people and animals dying of prion disease contaminate the environment around them with prions because prions are in the skin, urine, feces, blood, mucus and saliva of each victim. Each victim becomes an incubator and a distributor of the Pandora-like pathogen. Victims are contagious long before they exhibit clinical symptoms.

At the personal level, this is very bad news for caregivers, especially spouses, who are 600 percent more likely to contract neurodegenerative disease from patients (Duke University and Utah State University). A cough, sneeze, utensils and drinking glasses all become lethal pathways. Once an item is contaminated, it’s impossible to sterilize. The human prion is resistant to both heat and chemicals. It’s reported that prions released from people are up to a hundred thousand times more difficult to deactivate than prions from most animals. Prions are not alive, so they can’t be killed.

Wastewater treatment plants are collecting points for prions from infected humans. The sewage treatment process can’t stop prions from migrating, mutating and multiplying before being discharged into the environment where they can kill again. The bad news is that the prions are being released back into the environment and dumped openly on land. The wastewater is being reclaimed and used for irrigating crops, parks, golf courses. It’s even being recycled as drinking water.

wastewater treatment plant

Claudio Soto, PhD, professor of neurology at the University of Texas Medical School in Houston, and his colleagues confirmed the presence of prions in urine. Soto also confirmed that plants uptake prions and are infectious and deadly to those who consume the infected plants. Therefore, humans, wildlife and livestock are vulnerable to prion disease via plants grown on land treated with sewage sludge and reclaimed sewage water.

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.

joel pedersen prion research

“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 taken up by plants and vegetables.”

Thanks to more and more people dying from TSEs, wastewater treatment systems are more contaminated with prions than ever. Wastewater treatment plants are now prion incubators and distributors. The prion problem is getting worse every day.

biosolids land application sewage sludge

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. 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 its antiquated sludge rule crafted back in the dark ages. It does, however, consider prions a “contaminant of emerging concern.” Meanwhile, its outdated risk assessments are promoting a public health disaster.

“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.

Exposing crops and livestock to prions is a very bad idea. Plants absorb prions from the soil along with water and nutrient uptake, which makes the prions even more bioavailable and infectious to humans, wildlife and livestock.

chronic wasting disease

Unfortunately, the damage is real. Deer, elk, moose and reindeer are contracting an unstoppable prion disease now. In deer, the government calls prion disease chronic wasting disease. In cattle, prion disease is called bovine spongiform encephalopathy (they might as well call it what it is—transmissible spongiform encephalopathy). Mad cow disease is the term that most of us know. The government pretends that there is a specific prion responsible for each of these diseases. The fact is that there are thousands of mutations of prions spreading in the environment and food chain now. Some kill quickly, while some are less lethal. The only thing that we need to know is that a deadly prion is a deadly prion. There is no species barrier.

mad cow disease

If prion disease is killing these animals, livestock are not immune. Beef and dairy cattle are consuming these infected crops and the infected water supplies, too. Since humans are at the top of the food chain, and since we are often downstream from these infected farms, ranches and forests, our food and water supplies are being compromised. Wind and tornadoes transport the infectious waste even further.

So, is Alzheimer’s disease transmissible? There is absolutely no evidence to the contrary. The truth is your best defense against neurodegenerative disease. It’s time to demand reforms on many levels to safeguard caregivers, family members and our food and water supplies. Despite all of the warning signs, government and industry are insisting that we waste more time, money and lives studying these issues to death. The infection is real. The body count is real. The denial is disturbing.

Alzheimer’s Disease Research via http://crossbowcommunications.com/is-alzheimers-disease-contagious/

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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.

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 http://crossbowcommunications.com/wastewater-reclamation-reuse-based-on-outdated-risk-assessments/

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Crossbow Communications specializes in issue management and public affairs. Please join our coalition to help reform practices that are contributing to the Alzheimer’s disease epidemic.

Asians At Higher Risk For Dementia

DNA Analysis Reveals Key Genetic Mutations, Therapies

By Joana Fernandes, PhD

Researchers reviewed the novel mutations found in genes associated with early-onset Alzheimer’s disease in Asian countries, arguing that identifying disease-associated mutations greatly contributes to the knowledge of the cause and effect of the disease. This information is also essential to develop preventive and therapeutic strategies.

Alzheimer's disease research

The study, “Mutations, Associated With Early-Onset Alzheimer’s Disease, Discovered In Asian Countries,” was published in the journal of Clinical Interventions in Aging. 

Alzheimer’s disease can be classified into the early-onset and late-onset types. The early-onset form is more rare and hereditary, developing before the age of 65. Essentially, three genes are known to be involved in this form of the disease: APPPSEN1, and PSEN2.

APP encodes the amyloid precursor protein which, when cleaved, will become the beta-amyloid protein, whose toxic accumulation is the hallmark of Alzheimer’s. The other two genes, PSEN1 and PSEN2, encode proteins that cleave the amyloid precursor protein, contributing to the formation of the beta-amyloid protein. Mutations in these three genes may promote beta-amyloid production and accumulation.

Here, researchers reviewed all of the known mutations in these three genes that were discovered in Asian countries, such as Japan, Korea, and China. According to the authors, 30 novel Asian mutations were found in APP, PSEN1, and PSEN2 comparing Caucasian and Asian patients. The unfolding epidemic could be more severe in these regions of the world.

Alzheimer's disease epidemic

Most mutations associated with early-onset Alzheimer’s disease have been detected in PSEN1, and novel PSEN1 mutations were recently identified in patients from various parts of the world, including Asia. Other studies discovered what were probably pathogenic PSEN2 mutations in Korea and China.

“Several mutations were discovered in APP, PSEN1, and PSEN2 that could contribute to disease progression,” the authors wrote. “Most of these mutations are associated with familial [early-onset Alzheimer’s]. However, several [new] cases of [Alzheimer’s] were reported in patients without any family history of dementia.”

“The majority of pathogenic mutations were found in PSEN1 gene,” they added. “Several PSEN1 mutations could be associated with early-onset [Alzheimer’s], which occurs at the age of 40 years, and with rapid and aggressive dementia progression. Mutations in APP and PSEN2 are quite rare but are possible causative factors [for early-onset disease]. Pathogenic mutations could result in disease onset at the age of 40-65 years.”

Although there is no known cure for Alzheimer’s disease, potential therapeutic approaches might be successful in early stages of the disease. The problem is that diagnosing the disease before clinical symptoms occur is complicated.

The identification of proteins and genes that can act as biomarkers for disease onset is essential to improve diagnosis, especially given that several genes have already been described as causative or risk factor genes for dementia.

For this reason, knowing which mutations are associated with Alzheimer’s disease may become a powerful strategy to predict the development of this disease before the appearance of symptoms, and allow the start of prevention therapies in patients.

Alzheimer’s Disease News Source: https://alzheimersnewstoday.com/2016/10/19/novel-mutations-linked-early-onset-alzheimers-found-asian-countries

Pomegranate Seeds Treat Neurodegenerative Disease

Alzheimer’s Disease Treated With Antioxidant

Granalix BioTechnologies has developed a new treatment for those with Alzheimer’s disease. The company announced the availability of GranaGard™ a food supplement based on pomegranate oil that helps prevent neurodegeneration.

Alzheimer's disease prevention tips

GranaGard, is a submicron Pomegranate Seed Oil (PSO) emulsion, and is an innovative formulation of one of the strongest natural antioxidants, Punicic acid (an Omega 5 lipid), which constitutes 80 percent of PSO. The novel patented formulation was shown to delay disease onset and prevent neuronal death in a model of genetic prion disease (a form of Mad Cow Disease)[i] and to reduce disease burden in a mouse model of Multiple Sclerosis[ii], while showing no toxicity after long term administration. In both diseases, GranaGard administration results in reduction of brain lipid oxidation, which is caused by increased levels of reactive oxygen species (ROS).

Prof. Ruth Gabizon, Founder and acting CEO of Granalix BioTechnologies, explained, “Reactive Oxygen species (ROS) are chemically active molecules that can lead to significant damage to cells, and in particular in the central nervous system. It is therefore widely accepted that this chemical agent contributes to chronic inflammation and neurodegenerative diseases. And while antioxidants that can counteract ROS are ubiquitously present in a healthy human diet, their activity is limited by chemical degradation, poor bioavailability, reduced distribution to the CNS, and sub-pharmacological doses.

Alzheimer's disease treatment

To overcome these limitations, we generated GranaGard, a novel neuroprotective formulation with high bioavailability. In addition to its protective role in subjects at risk of neurodegenerative conditions, GranaGard is expected to be effective for general neurological well-being for the larger public. We are also currently testing GranaGard for its effect in various non-neurological diseases and as a protective agent during intense exercise.”

PSO submicron droplets have several advantages. First, the nano formulation may avoid the first passage of the oil through the liver, thereby enhancing the availability of the droplets to other organs such as the CNS. GranaGard is then able to enter the brain and protect membrane lipids from ROS attacks that occur as a result of both every-day efforts and pathological events. In vivo, Punicic Acid is metabolized into Conjugated Linoleic Acid (CLA), a compound known for its neuroprotective and other beneficial effects. When mice are given the GranaGard formulation, CLA was found to accumulate in the brain and can directly exert its neuroprotective effect.

Neurodegenerative diseases, such as Alzheimer’s disease, Creutzfeldt-Jakob disease, Parkinson’s or Amyotrophic Lateral Sclerosis (ALS) are late onset brain disorders that together affect millions of people around the globe. Alzheimer’s disease is already the 5th leading cause of death for people aged 65 or older in the US. It’s also the fastest-growing cause of death globally. Currently, there are no preventive or curative treatments for these conditions.

“GranaGard can currently be purchased at the Company’s website. We are seeking additional partners for worldwide distribution,” added Prof. Gabizon. GranaGard™ is produced by Supherb and can be purchased at the Company’s website at https://granalix.com/

Granalix BioTechnologies focuses on developing science-based novel formulations of natural antioxidants that can be used for the prevention and treatment of neurodegenerative conditions. The Company was established in 2014 by Prof. Ruth Gabizon from the Department of Neurology at Hadassah Medical Center, Jerusalem, Israel and Prof. Shlomo Magdassi at the Casali Center for Applied Chemistry, the Institute of Chemistry and the Center for Nanoscience and Nanotechnology at the Hebrew University of Jerusalem.

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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.

Wildlife Contracting Brain Disease From Humans

Chronic Wasting Disease Further Proof Of Infectious Disease

Alzheimer’s disease, Parkinson’s disease and other forms of neurodegenerative disease are collectively becoming the leading cause of death around the world. Brain disease also continues to expand in wildlife. Is there a connection?

biosolids land application contaminates food water

Keep reading to find out why:

  • Alzheimer’s disease is part of a spectrum disease known as prion disease, which also includes Creutzfeldt-Jakob disease. The spectrum also is known as transmissible spongiform encephalopathy (TSE);
  • Alzheimer’s disease is an infectious prion disease, which is often misdiagnosed and undiagnosed. Millions of diagnoses are being suppressed by physicians;
  • The bodily fluids of those with prion disease are infectious;
  • Wastewater treatment plants are contaminating our food and water supplies by spreading deadly prions via sewage sludge, biosolids and reclaimed wastewater. The risk assessments involving these facilities and their by-products were prepared before prions were discovered and characterized;
  • Wildlife, sea mammals, livestock and people are contracting prion disease from mismanaged sewage; 
  • Caregivers are in harm’s way because of disease mismanagement; 
  • It’s time to reclassify sewage sludge, biosolids and reclaimed wastewater as infectious waste; and 
  • It’s time to defend our food, water and air from infectious waste by enforcing the Bioterrorism Preparedness and Response Act Of 2002 and similar laws around the world.

The Brain Disease Epidemic

Alzheimer’s disease alone is killing 50-100 million people now. Millions more will contract the disease this year, while just as many will go undiagnosed and misdiagnosed.

Thanks to misinformation and the mismanagement of infectious waste and bodily fluids, people of all ages are now exposed to an expanding spectrum of brain disease. So are other mammals.

Prions and Alzheimer's disease

The most common forms of neurodegenerative disease include Alzheimer’s disease, Parkinson’s disease, ALS and Creutzfeldt-Jakob disease–the most aggressive and infectious of them all. According to Nobel Prize Laureate Stanley Prusiner, these brain diseases are part of the same disease spectrum—prion disease. It’s also known as transmissible spongiform encephalopathy (TSE). The operative word is transmissible.

Pandora’s Lunchbox

Many factors are contributing to the epidemic. Unfortunately, it appears that Alzheimer’s and Parkinson’s are just as infectious as Creutzfeldt-Jakob disease (CJD). The bodily fluids of people with prion disease are infectious. Prions are the X factor in the global epidemic.

infectious waste and food contamination

Prion disease is a spectrum disease that varies in severity. It also varies depending on which region of the brain is impacted first. It affects most, if not all, mammals. Prion disease causes memory loss, impaired coordination, and abnormal movements. Prions are an infectious form of glycoprotein that can propagate throughout the body. TSE surveillance is important for public health and food safety because TSEs have the potential of crossing from animals to humans, as seen with the spread of mad cow disease. TSEs also have the potential of being transmitted from humans to animals. The most common example is chronic wasting disease (CWD) among deer species. Sick wildlife are a canary in the proverbial coal mine. CWD is part of a larger epidemic of neurological disease that is killing people, wildlife and livestock around the world. The warning signals are being ignored.

land application sewage sludge and chronic wasting disease

CWD was first detected in deer in North America. Then it was detected in a variety of other animals, including an elephant at the Oakland zoo. It’s been found in a variety of animals across the United States and Canada. All hypotheses seem to center around contaminated feed and deer farmers. Then the deer spread the disease via nose-to-nose contact. Those theories were just rocked by the discovery of CWD in Norway in moose and reindeer. The disease didn’t jump the Atlantic from the Americas. However, Norway dumps tons of infectious waste on land every year–infectious waste from people with prion disease.

It’s not known which patients with brain disease become infectious or when. The medical community prefers to ignore the topic. The legal industry is about to have a bonanza because negligence is the rule and not the exception regarding Alzheimer’s disease and the mismanagement of infectious waste. Savvy neurologists won’t touch patients with these symptoms because of the risks. Unfortunately, caregivers aren’t warned accordingly.

Prions are unstoppable. The pathogen spreads through the bodily fluids and cell tissue of its victims. The blood, saliva, mucus, milk, urine and feces of victims are infectious. Wastewater treatment doesn’t touch prions. In fact, these facilities are now helping incubate and distribute prions via solids and wastewater released. Once unleashed on the environment, prions remain infectious. They migrate, mutate and multiply as they infect crops, water supplies and more.

chronic wasting 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. Unfortunately, the CDC quietly took prions off the list because the regulation criminalized entire industries and several reckless practices.

Unfortunately, prions linger in the environment, homes, hospitals, nursing homes, dental offices and beyond infinitely. Prions defy all attempts at sterilization and inactivation.

Prions shed from humans are the most deadly. They demand more respect than radiation. They’re being ignored by regulators and industry alike. As such, food and water sources are being contaminated with the deadliest forms of prions. Municipal water systems can’t stop them from reaching water taps in millions of homes. Filtration doesn’t phase them.

Alzheimer's disease research

Scientists have shown that infected tissues can transmit prion disease between animals. There is no species barrier. A new study published in the journal Nature renews concern about the transmissibility of Alzheimer’s disease between people. A second study by the same scientist in early 2016 adds to the stack of evidence. There is no evidence that Alzheimer’s disease is not infectious.

Although there are many causes and pathways contributing to prion disease, many pathways are being mismanaged around the globe. Not only are homes and hospitals exposed to the prion pathogen, so are entire sewage treatment systems. Wastewater treatment plants are prion incubators. Sewage sludge and wastewater pumped out spread the disease.

biosolids land application

The risk assessments prepared by the U.S. EPA for wastewater treatment and sewage sludge are flawed. 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. Failure to account for known risks is negligent. Crops for humans and livestock grown grown in sewage sludge absorb prions and become infectious. We’re all vulnerable to Alzheimer’s and other forms of prion disease right now due to widespread denial and mismanagement.

Sewage treatment plants can’t detect or stop prions. Just ask the U.S. EPA. If sick deer are serving as a canary in a coal mine, what is this infectious waste doing to livestock and humans?

mad cow disease

It’s time to stop the land application of sewage sludge (LASS) in all nations. Safer alternatives exist. Please join our coalition for reform.