Food, Water, Air Contamination Fueling Brain Disease

Alzheimer’s Disease, Autism Now 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 Diseaese 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.

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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.

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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.

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.

Alzheimer’s Disease Awareness Month

Answers To Alzheimer’s Begin With The Truth

President Ronald Reagan designated November as National Alzheimer’s Disease Awareness Month in 1983. At the time, fewer than 2 million Americans had Alzheimer’s; today, the number of people diagnosed (and still alive) with the disease has soared to nearly 5.4 million. The X factor is the millions who are going undiagnosed and misdiagnosed.

Mayors in cities around the nation are declaring November Alzheimer’s Disease Awareness and Caregivers Month.

Alzheimer’s disease is the sixth-leading cause, and the fastest-growing cause, of death in the United States (and the world), which has some of the highest rates of Alzheimer’s disease in the world. Finland, Sweden and Iceland also are at the top of the list. However, states such as Washington, North Dakota and South Dakota rival the rates found in Scandinavian countries.

Alzheimer's disease treatment

Unfortunately, Alzheimer’s disease is going undiagnosed and misdiagnosed at an escalating pace. Many people, for example, have had diagnoses withheld by their doctors. The epidemic is more widespread than anyone knows. Physicians have withheld millions of diagnoses from patients and their families. According to the Alzheimer’s Association, physicians in the U.S. only inform 45 percent of patients about their Alzheimer’s diagnosis. The same suppression is likely at work in most countries. Meanwhile, millions more go undiagnosed and misdiagnosed.

A groundbreaking study suggested that Alzheimer’s disease causes six times as many deaths as the official statistics would indicate. The Centers for Disease Control and Prevention estimated that, in 2010, Alzheimer’s 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. But, in reality, the study said Alzheimer’s 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.

Meanwhile, no one is talking about the fact that most forms of neurodegenerative disease, including Alzheimer’s disease, is transmissible. Spouses of those with Alzheimer’s disease, for example, are 600 percent more likely to contract the disease. Other caregivers also are in harm’s way. In fact, entire communities are at risk of exposure.

prion disease spectrum

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.

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.

On average, Alzheimer’s follows a 14-year course from onset of symptoms until death. For most patients, symptoms go undiagnosed and untreated for at least seven years. For most patients, symptoms go undiagnosed and untreated for at least seven years, during which time the lesions spread through the brain and cause irreparable damage, said Dennis Fortier, author of the Brain Today blog.

 

“With a good diet, physical exercise, social engagement, and certain drugs, many patients (especially those detected at an early stage) can meaningfully alter the course of Alzheimer’s and preserve their quality of life,” Fortier said. “No cure does not mean that there is no treatment.”

The health of the brain is affected by our overall health. Research shows that high cholesterol, high blood pressure, and obesity increase the risk for cognitive decline. A healthy brain requires strong blood flow and plenty of oxygen.

Meanwhile, we can’t forget that:

  • Women are contracting neurodegenerative disease at twice the rate of men;
  • Spouses of those with Alzheimer’s disease are 600% more likely to contract the disease, which is further evidence that it is a transmissible disease. Caregivers, family members and others are in harm’s way because of disease mismanagement and misinformation;
  • People in Finland, Iceland, Sweden and the United States have the highest prevalence of Alzheimer’s disease. Rates in North Dakota, South Dakota and Washington rival the highest rates in the world. Sewage mismanagement and the mismanagement of other forms of infectious waste are responsible for much of the epidemic in these regions and beyond;

We can’t ignore that the global Alzheimer’s disease epidemic and the autism epidemic both began to rise in the late 1970s. They proceeded to spike dramatically in the late 1980s and early 1990s. The spikes in autism and Alzheimer’s disease are almost identical in terms of timing and trajectory. The surge in chronic wasting disease among deer also follows the same trend. These devastating diseases are symptoms of a much bigger problem associated with toxic and infectious waste. Industry policies and practices changed dramatically, which triggered an explosion in brain disease.

According to a 2010 study by the Centers for Disease Control, Utah, North Carolina and New Jersey have the highest rates of autism. ASD strikes one in every 32 Utah boys, and one in every 85 girls. In New Jersey, one in every 28 boys has ASD. The numbers are likely still rising.

Thanks to modern sewage disposal and antiquated 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, valley fever, meningitis, hepatitis, and other threats to public health.

biosolids land application sewage sludge

Read more about the autism epidemic and its connection to infectious proteins and other neurotoxins that are spreading through biosolids and wastewater reclamation. Please contact us to share your insights, opinions and support for critical reforms.

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.

 

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/

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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.