Prion Test Improves Diagnosis For Neurodegenerative Disease

Prion Disease A Spectrum Disease

By the time Kay Schwister got her diagnosis last summer, she couldn’t talk anymore. But she could still scowl, and scowl she did.

After weeks of decline and no clue what was causing it, doctors had told Schwister — a 53-year-old vocational rehab counselor and mother of two from Chicago — that she had an incurable disease called Creutzfeldt-Jakob disease, or CJD.

The disease was shrinking Kay’s brain, and riddling it with holes. She would likely live only a few more weeks, the doctors said.

It was a diagnosis that no one could ever want. But the fact that Schwister was able to get a firm diagnosis while still alive is a relatively new development that represents a step forward in understanding a group of devastating neurological disorders. And, some biochemists say, it could lead to better ways of diagnosing brain diseases that are much more common, including Parkinson’s disease and Alzheimer’s disease.

For Kay Schwister, it all started in the spring of 2016, when she started getting headaches and feeling dizzy all the time. Aging, she told herself, just didn’t feel very good. Over the next few weeks, she got steadily worse.

Kay Schwister and CJD

“She got to the point where she was so nauseous and so dizzy that she stopped driving and working,” says her husband, Tim Schwister.

By the time Kay entered the emergency room last June, her speech had changed. She was enunciating things in a strange way, and finishing each sentence on a really high note.

Doctors drew blood and spinal fluid and tested it for things like multiple sclerosis and mercury poisoning. Those tests came back negative.

Soon, Kay couldn’t talk or walk.

“Not knowing what we were dealing with was probably one of the hardest things to ever go through in life,” says Tim. “We really wanted to know what we were up against, and if there was anything that we could do.”

Ultimately, Kay’s doctors ordered a newly developed test for Creutzfeldt-Jakob disease — a very rare condition that’s thought to kill about 1 in a million people worldwide every year, including about 300 deaths annually in the U.S.

prion disease spectrum

That test came back positive. About a month after Kay entered the hospital, the Schwisters had their answer. It was ugly, but still an answer.

Normal proteins in Kay’s brain had started misfolding, bending themselves into an unnatural shape and coaxing other proteins to do the same, like some kind of malicious origami. These misshapen proteins, known as prions, formed clumps in the brain, causing neurons to die.

“It’s almost as if it starts to turn certain portions of your brain off,” says Tim.

The vast majority of CJD cases worldwide are like Kay’s, popping up for no apparent reason. Other cases seem to be inherited. A very small number of patients have contracted the illness through close contact with material from an infected person’s brain or nervous system — during certain transplant procedures or via contaminated surgical equipment, for example. And another form, variant CJD, is the human version of mad cow disease, and has been linked to eating infected beef.

Prions and Alzheimer's disease

There is no cure or treatment for CJD. All Tim could do for his life partner of 35 years was to try to make her as comfortable as possible. Still, having a diagnosis spurred the many people who loved Kay into action, Tim says. Family and friends flew in from all over the country to visit. She was rarely alone.

“Every day, it was nonstop,” Tim says. “People that were there to visit with her, just to try to keep her spirits up.”

She never went home. Kay Schwister died within seven weeks of entering the hospital.

Until recently, families like the Schwisters wouldn’t have known what their loved one was suffering from until it was all over, when an autopsy might have shown that the brain was smaller than expected. Under a microscope and using a special stain, a pathologist would have seen holes in the brain, along with tangles and clumps of misfolded proteins (prions).

But diagnosis after death is too late — not just for the patient and families, but also for researchers trying to study potential therapies to slow down or stop the progression of the disease. These same diagnostic frustrations apply to some of the most common forms of dementia, including Parkinson’s and Alzheimer’s disease, which are also associated with protein misfolding.

“The trouble with many of these diseases, some of which are incredibly prevalent, is that it can take months or years to diagnose,” says Byron Caughey, a biochemist at Rocky Mountain Laboratories in Hamilton, Mont., a part of the National Institute of Allergy and Infectious Disease.

A previous spinal fluid assay for CJD could identify brain cell injury, but not the cause of that injury. That’s why Caughey recently teamed up with scientists in Italy, Japan and the U.K. to develop a different test. It’s called RT-QuIC, which stands for “real-time quaking-induced conversion.”

The test, developed a few years ago and still available via only a few laboratories, harnesses the bad protein’s ability to induce normal, neighboring proteins to take on its twisted form. The test takes about 90 hours and involves getting a sample of spinal fluid, shaking it up with normal proteins and waiting to see if the normal proteins misfold.

Alzheimer's disease diagnosis

Caughey and some Italian scientists have even figured out how to avoid the spinal tap; they can make the test work with a sample of cells taken from deep inside a patient’s nostril, from a spot that is separated from the brain by just a bony partition.

“So, we now have the ability to collect a little bit of spinal fluid or nasal brushing from patients while they’re still alive, and with quite a high degree of certainty, tell whether or not they have a prion disease,” says Caughey. In several studies now, he says, the RT-QuIC test has sensitively and specifically identified CJD prions in symptomatic patients; the test has since been distributed to CJD surveillance centers in multiple countries.

“Technologically, it’s a major new paradigm for testing protein misfolding,” says Dr. Jiri Safar, director of the National Prion Disease Pathology Surveillance Center at Case Western Reserve University in Cleveland and one of Caughey’s collaborators. Since the center started using the assay in April 2015, it has tested more than 5,000 samples from patients referred by doctors scattered around the U.S., Canada and Mexico. And within that group, Safar says, about 500 people tested positive for CJD. The assay costs about $50 to run.

“It’s a major game changer,” says Safar, who hopes wider use of the test in suspected cases will help to completely eliminate the possibility of transmitting CJD through infected blood, bodily fluids or organs.

Caughey, Safar and colleagues reported in late November in the journal Annals of Neurology that a second-generation version of their test was just as effective in diagnosing the disease as an autopsy or biopsy of a living brain (which is another diagnostic option, but a risky, invasive one).

Alison Green, a biochemist at the University of Edinburgh in the U.K., is now working on a modified version of the test that has been shown capable of detecting Parkinson’s disease and Lewy body dementia.

“It’s very important, because there is no other diagnostic test for Parkinson’s disease,” Green says. “It’s purely a clinical diagnosis at present.”

Parkinson’s is a chronic and progressive movement disorder that eventually includes symptoms of dementia in an estimated 50 to 80 percent of cases. Diagnosing it sometimes requires years of observation, at which point a patient has already lost a lot of neurons.

In a small study published last summer, Green used a version of RT-QuIC that looks for alpha-synuclein (a protein that’s associated with Parkinson’s) on 20 people who had a Parkinson’s diagnosis, and 15 people in a control group.

“And you can get a nice, clear-cut positive result after 120 hours,” she says. Nineteen out of 20 patients with Parkinson’s were correctly identified, and there were no false positives. Green is now replicating the study with 110 subjects.

If the test proves to be as reliable as it was in her first study, Green says, it could become an important diagnostic tool for doctors to rapidly identify a patient’s ailment and start therapies as soon as possible, when they might still make a difference.

“A lot of these drugs or therapies are being introduced way too late because patients aren’t diagnosed early enough,” Green explains. “And they may be effective treatments if you give them earlier.”

She’s also applied for funding to develop a test that would look for abnormal beta-amyloid peptides, possible indicators of Alzheimer’s disease.

The ultimate goal, says Green, is to have a whole bank of RT-QuIC assays so that patients with any kind of undiagnosed dementia can get answers.

Knowing the prognosis earlier, she says, could give some patients and families more choices.

“If you have early onset dementia, do you really want to spend the last few years of your life working, or do you want to take early retirement?” says Green.

And even for diseases that have no option of being slowed or reversed, she says, a firm and accurate diagnosis can still offer something essential to families — a spur to move beyond tests and treatments.

“We really, truly wanted to know if there was something that we could do for her,” says Tim Schwister of his wife, Kay. The diagnosis let him and his sons know that chasing further treatment at that point wouldn’t help, and that the best they could do was to turn their attention to making Kay comfortable, and spending time with her.

The diagnosis also helped the Schwisters connect with other families who’d gone through the same experience.

In a time of such great loss, Tim says, “it’s nice to know that you’re not alone.”

Prion Disease Diagnosis via http://www.npr.org/sections/health-shots/2017/02/06/508241181/prion-test-for-rare-fatal-brain-disease-helps-families-cope

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.

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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.

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Is Alzheimer’s Disease Contagious

Science, Evidence Proving That Alzheimer’s A Transmissible Disease

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, includingAlzheimer’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 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/

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.

Posted in Alzheimer's Disease Caregivers, Alzheimer's Disease Causes, Alzheimer's Disease Prevention, Chronic Wasting Disease, Creutzfeldt-Jakob Disease, Disease Transmission, Infectious Disease, Prion Disease, Sewage Sludge | Tagged , , , , , , | Leave a comment

Neurodegenerative Disease A Global Epidemic

Neurodegenerative Disease The Fastest Growing Cause Of Death

Death rates from heart disease and cancer are dropping globally due to advances in nutrition, medicine and disease management. Meanwhile, neurodegenerative disease is exploding because it’s highly contagious in most cases.

In the U.S., deaths from Alzheimer’s disease increased 71 percent from 2000 to 2013, while those attributed to heart disease decreased 14 percent. Similar trends are emerging around the world. Unfortunately, the global spike in autism shares the same timing and trajectory as the surge in neurodegenerative disease. It’s not just a coincidence. The correlation is real thanks to reckless policies and practices. It appears that the biggest difference between autism and classic forms of neurodegenerative disease is age of onset.

The actual epidemic is larger than anyone knows. Physicians are withholding 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 disease diagnosis. The same suppression is likely at work in most countries. Meanwhile, millions more go undiagnosed and misdiagnosed. Women face an elevated risk of Alzheimer’s disease.

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.

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 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. It’s not known which patients with brain disease become infectious or when, but both CJD and Alzheimer’s patients are being mismanaged. The most savvy neurologists won’t touch patients with these symptoms because of the risk of infection. They are making diagnoses from across the room. Unfortunately, caregivers aren’t warned accordingly.

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

According to neuroscientist 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. 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 mismanagement doesn’t end here.

Prions are now the X factor and they are not being accounted for by industry or government. Prions are an infectious form of glycoprotein that can spread throughout the body.

Alzheimer's disease diagnosis

“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 recent study published in the journal Nature also 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 to other mammals.

Many factors are contributing to the epidemic. Unfortunately, it appears that Alzheimer’s disease and Parkinson’s disease are just as infectious as Creutzfeldt-Jakob disease. Studies confirm that people and animals dying of prion disease contaminate the environment around them with prions because prions are in the urine, feces, blood, mucus and saliva of each victim.

Alzheimer's disease infectious disease

Not only are homes, hospitals and nursing homes exposed to the deadly prion pathogen from those with prion disease, so are entire sewage treatment systems and their by-products. Wastewater treatment plants are prion incubators and distributors. The sewage sludge and wastewater released are spreading disease far and wide. 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.

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.”

Each victim becomes an incubator and a distributor of the Pandora-like pathogen. 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.

biosolids land application sewage sludge

Sewage from hospitals, nursing homes, slaughterhouses, morgues, mortuaries, veterinarians and other high-risk places enters the same sewage system. Thanks to more and more people dying from TSEs, sewage systems are more contaminated with prions than ever. Wastewater treatment systems are now prion incubators and distributors.

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.

“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.

Researchers have more questions than answers about brain disease, but we know that neurotoxins, head trauma and genetics can all trigger neurodegenerative disease. Unfortunately, that’s where our knowledge gets fuzzy.

Alzheimer's disease and caregivers

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. 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 among deer species. Deer, elk, moose, reindeer and many other animals are being exposed to infectious waste in sewage.

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. 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.

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. Homes, nursing homes, hospitals, clinics and restaurants are other examples of public places that are being contaminated by prions from victims of prion disease.

biosolids land application contaminates food water

The deadly prion spectrum also includes mad cow disease and chronic wasting disease among deer. Scientists have shown that infected tissues can transmit prion disease between animals. There is no species barrier.

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.

wastewater treatment plant

Sewage treatment plants can’t detect or stop deadly prions. Just ask the U.S. EPA. Dumping sewage sludge (biosolids) from billions of people on land and at sea spreads prions far and wide. It also spreads heavy metals, radioactive waste, carcinogens, pharmaceuticals and more. It’s time for the truth. It’s time for reforms that can safeguard us from this public health disaster.

Read more about the correlation between Alzheimer’s disease, autism and sewage mismanagement. http://alzheimerdisease.tv/autism/

autism population

Background On Sewage Sludge

In 1972, world leaders admitted that dumping highly toxic sewage sludge into the oceans killed entire underwater ecosystems and threatened public health. Some nations stopped the dumping immediately and started dumping it on land or burning it in incinerators. The most responsible cities started putting sewage sludge in landfills. Meanwhile, the United States allowed cities to keep dumping sewage sludge at sea for another 20 years. It finally passed the Ocean Dumping Ban Act of 1988, when beaches along the east coast were forced to close because of high levels of pathogens from sewage that washed up on shore.

land application sewage sludge and disease

The law prohibited all dumping of industrial waste and municipal sewage sludge into our oceans after December 31, 1991. It did nothing however, to keep cities such as Boston and Los Angeles from dumping millions of gallons of raw sewage directly into the oceans every day, but with the help of the U.S. EPA, the Act did redirect millions of tons of deadly toxins and pathogens from our oceans to farms, ranches, national forests, city parks, golf courses, playgrounds, fair grounds, race tracks, sport fields and beyond. From there, the pathogens began contaminating food, water and air as they were soaked up by crops, swept away by rainwater and picked up by windstorms, tornadoes and hurricanes and dumped on innocent citizens where they live, work and play. The runoff still contaminates our oceans after it filters through our creeks, lakes and rivers.

After the 1991 ban on ocean dumping, the EPA instituted a policy of sewage sludge reuse on agricultural land. It hired a PR firm to spin a new brand for the death dirt. They crafted the clever name “biosolids” to help disguise the hazards. The EPA promoted biosolids recycling throughout the 1990s. Unfortunately, the risk assessments were severely biased and flawed. The proof is in the pudding.

This new form of sewage dispersal has sparked a public health disaster that’s still unfolding in the form of autism, Alzheimer’s disease, west Nile virus, Zika virus, chronic wasting disease, meningitis, hepatitis, and other threats to public health. The risk assessments for these practices failed to account for heavy metals, pharmaceutical residue, radionuclides, carcinogens and a deadly form of protein known as a prion (which was unknown to the world of science at the time). The practice sparked a public health disaster in exchange for healthier oceans and a very profitable new industry. The EPA even took its show on the road and convinced other nations to use its faulty risk assessments to justify multi-million dollar contracts for these new corporations. Countries such as Canada took the bait hook, line and sinker and never conducted its own risk assessments.

chronic wasting disease

Chronic wasting disease is now rampant in Canada and it recently jumped the Atlantic to Norway’s reindeer herd. It’s spreading across the U.S. like wildfire as we spread more pathogens and lies. Land application sites often involve locations where poverty is high and economic prosperity is low, which means resistance is low. Sludge tends to be dumped where minorities live, leading to allegations of environmental racism. Unfortunately, contaminated food and water make it back to the cities where the infectious waste originated.

Treated sewage sludge has been used in the UK, Europe and China agriculturally for more than 80 years, though there is increasing pressure in some countries to stop the practice of land application due to farm land contamination and public outrage. In the 1990s there was pressure in some European countries to ban the use of sewage sludge as a fertilizer. Switzerland, Sweden, Austria, and others introduced a ban to safeguard public health. Others should follow their example.

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Crossbow Communications specializes in issue management and public affairs. Call 602-999-7204 or write to Gary Chandler to join our campaign and coalition for truth and reform. gary@crossbow1.com. Together, we can prevent Alzheimer’s disease and autism.

Posted in Alzheimer's Disease Caregivers, Alzheimer's Disease Causes, Alzheimer's Disease Epidemic, Alzheimer's Disease Prevention, Autism, Contagion, Disease Transmission, Infectious Disease, Prion Disease | Tagged , , , , , , | 2 Comments

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 and many other species of mammals. It’s the environmental equivalent of Pandora’s Box.

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.

Posted in Alzheimer's Disease, Alzheimer's Disease Causes, Alzheimer's Disease Prevention, Autism, Contagion, Disease Transmission, Infectious Disease, Water Contamination | Tagged , , , , | 1 Comment

Key Proteins Found In Early Phases Of Alzheimer’s Disease

Tau, Amyloid Detection Could Improve Diagnostic Capabilities

Researchers from Aberdeen have identified changes in the brains of those suffering early signs of Alzheimer’s disease.

A University of Aberdeen study confirmed for the first time that two proteins, assumed to contribute to the disease process, are both present at very early stages of Alzheimer’s disease. Both are present in an area of the brain that is involved in memory formation and information processing–the hippocampus.

Alzheimer's disease and caregivers

The Alzheimer’s Research UK funded the research, which will have implications for the development of new drugs, but may also provide important information for diagnosis of the disease. 

The team, led by Dr Koss and Professor Bettina Platt, used human brain samples provided by the Brains for Dementia Research platform to investigate changes in the brain at different stages of the disease. The researchers developed novel ways to study two proteins (tau and amyloid), both associated with Alzheimer’s disease, and determined how each one contributed to the onset, progression and symptoms of the disease.

“The entire research community is in agreement that it’s important to diagnose Alzheimer’s disease early,” said Dr. Koss. “Our findings will go some way to help achieve this. These early-stage changes in the brains of people with Alzheimer’s disease highlight key biochemical processes that may not only enable improved diagnostic procedures but may also inform drug development.”

Early diagnosis also can help protect caregivers and others from the transmission of Alzheimer’s disease. It’s likely spreading through the bodily fluids of victims. Items exposed, including drinking glasses, utensils are impossible to sterilize.

“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 and Alzheimer's disease

Alzheimer’s Disease Research Report via https://www.eveningexpress.co.uk/fp/news/local/study-identifies-disease-changes/

Posted in Alzheimer's Disease, Alzheimer's Disease Causes, Alzheimer's Disease Diagnosis, Alzheimer's Disease Research, Diagnosis, Early Onset Alzheimer's Disease | Tagged , | Leave a comment

Microcephaly One Of Many Symptoms Caused By Zika Virus

Zika Virus A Byproduct Of Infectious Waste

Published In MedScape

Zika infection can have devastating effects on the central nervous system of people of all ages. The infection can cause a wide range of brain abnormalities, including paralysis and death in adults, according to two new studies from Brazil.

Infection with mosquito-borne Zika virus is a cause of the neurological disorder Guillain-Barre Syndrome (GBS), in addition to microcephaly and other congenital brain abnormalities, according to a systematic review published in PLOS Medicine by Nicola Low of the University of Bern, Switzerland, and colleagues in the World Health Organization (WHO) Zika Causality Working Group.

“All radiologists must know about these typical symptoms because sometimes you don’t see the symptoms of Zika virus in the pregnant mother,” said Bianca Guedes Ribeiro, MD, from the Clínica de Diagnóstico por Imagem in Rio de Janeiro.

“If the microcephaly and calcifications don’t show until the third trimester, it’s late,” she said.

microcephaly and Zika virus

Microcephaly is a nonspecific term used to describe a small head circumference, and can be caused by maternal exposure to HIV, alcohol, radiation, or TORCH pathogens (Toxoplasma gondii, other, rubella virus, cytomegalovirus, and herpes simplex virus).

Most of these pathogens and toxins are found in the modern sewage stream, which is being dumped on crops, parks, golf courses and beyond. It is therefore important that radiologists know what to look for when it comes to “Zika.”

Dr. Guedes Ribeiro presented results from one of the studies here at the Radiological Society of North America 2016 Annual Meeting. She and her colleagues looked at pre- and postnatal images of the central nervous system in pregnant women exposed to the Zika virus. In their perinatal MRI and CT scans, they saw brain abnormalities presenting as multiple calcifications, both cortically and subcortically, and microcephaly. They diagnosed pachygyria, corpus callosum dysgenesis, and small anterior fontanel with premature closure of cranial sutures in their cohort.

microcephaly and Zika virus

During her presentation, Dr Guedes Ribeiro described one case in which a 27-year-old pregnant woman presented with fever, a telltale sign of Zika, and a rash at 12 weeks of gestation. In that case, the fetus did not show microcephaly or calcifications until 32 weeks. “In a case like this, the mother might only know she got the infection at the final ultrasound scanning,” Dr Guedes Ribeiro explained.

Now that Zika is showing up in many other countries around the world, radiologists in the United States should consider the Zika virus when they see these typical central nervous system findings, as they do now in Brazil, even when a pregnant woman has no clinical history of Zika, said Dr Guedes Ribeiro. “When you see these findings, think about Zika,” she advised.

“It’s important to look deep inside the brain because you will get the detailed information about brain malformations that you can’t get with clinical observations,” said Fernanda Tovar-Moll, MD, PhD, from the D’Or Institute for Research and Education in Rio de Janeiro.

Dr Tovar-Moll was involved in a recent study that showed that a number of brain abnormalities, beyond microcephaly, can affect fetuses exposed to intrauterine Zika virus infection. Radiologists need to be aware of these abnormalities so they can guide diagnoses and appropriate counseling for patients and their caregivers, the researchers explain.

All the babies she and her colleagues examined showed calcifications in the brain, “particularly between the grey and white matter junction,” Dr Tovar-Moll told Medscape Medical News. “This is not the same or common in any other congenital infection.”

In 10 percent of cases, Dr Tovar-Moll and her colleagues found that the baby’s head was a normal size at birth. However, she reported, “the brain inside was very abnormal. The MRI and ultrasound showed that they already had severe malformations — even more severe than those with a smaller head size at birth.”

It is incredibly important to look inside the brain because microcephaly is just one of the clinical signs for diagnosis, she added.

“Zika also causes neurologic damage that leads to paralysis in adults,” said Emerson de Melo Casagrande, MD, from the Federal Fluminense University in Niterói, Brazil.

“There are adults affected — who aren’t in the focus of the media — who were healthy people but aren’t now. Some of them will never recover,” he reported.

biosolids land application sewage sludge

Dr de Melo Casagrande presented results from a study that looked at adults, pregnant women, and newborns. He explained that the study got its start when the hospital began sending patients to radiology to rule out common diseases because serologic testing for Zika was not available.

The researchers were surprised by the effect the virus could have in adults. Of the 16 adults with acute neurologic syndromes sent to their lab, many presented with evidence of Guillain-Barré syndrome, its Miller Fisher variant, and Bickerstaff encephalitis. All three of the patients who presented with encephalomyelitis are now paralyzed.

“They were healthy and now they can’t move their arms or legs — that’s from Zika,” Dr de Melo Casagrande explained. Some patients recovered from the infection and others have sequelae in the face — they can work “and they have a life — but three people remain in the hospital.”

They don’t have the virus anymore, he pointed out, but it is still destroying their body as an autoimmune disease triggered by the infection. A previous infection could have had something to do with the strong reaction.

“We don’t know what makes it more severe in those patients, but we know we need to move the Zika conversation away from microcephaly alone,” said Dr de Melo Casagrande.

The problem in Brazil right now is that many hospitals cannot diagnose Zika because testing is not available. “They have a fast test for dengue because people can die from dengue,” he explained. “But if it’s not dengue, then you have to go home.”

Dr de Melo Casagrande said that his team expects to continue to use radiology to exclude other infections. All people should be wary of Zika, not just pregnant women. “It can be devastating for anyone,” he warned.

Brain Disease Update via http://www.medscape.com/viewarticle/872635

 

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Creutzfeldt-Jakob Disease Strikes Again In Maine

CJD Often Misdiagnosed As Alzheimer’s Disease

Maine Medical Center confirmed Friday that a patient treated at the hospital carried a rare, dangerous brain illness to which a “small number” of other patients may have been exposed, though the hospital called that risk “exceedingly low.”

The patient has Creutzfeldt-Jakob disease, or CJD, a degenerative brain disorder caused by an infectious type of protein, the hospital said in a statement. CJD is a form of prion disease, which is fatal.

Prions and Alzheimer's disease

Hospital officials suspected earlier this week that the patient, who was not identified for privacy reasons, carried the pathogen, based on an initial biopsy result. The National Prion Disease Pathology Surveillance Center at Case Western Reserve University in Cleveland confirmed the diagnosis on Friday, according to the statement.

“We are in the process of reaching out to the small number of patients who we think should be notified based on the details of their specific case,” Dr. Joel Botler, chief medical officer at MMC, said in the statement. “Our staff members have been fielding calls from patients who have legitimate concerns and questions about their care. Let me be clear, only a small number of patients who have had surgery at MMC have been exposed to any degree of risk, and that risk is exceedingly low approaching zero.”

CJD transmissible

Transmission of the disease in a hospital setting is “extremely rare,” with no confirmed cases in more than 20 years, the statement said.

Humans can contract prion disease from medical procedures, as the pathogen can survive on surgical tools and other equipment even after standard sterilization. Brain tissue from an infected patient potentially can infect subsequent patients before doctors know it’s there.

MMC is determining which patients were treated before the initial pathology report showing Creutzfeldt-Jakob disease and should be notified.

“While the hospital does track surgical equipment used in each case, the decision was made not to rely on tracking and instead make sure that any piece of equipment that could potentially be affected was treated,” Botler said in the statement. “Now that we know this case is confirmed, we can see that our response was 100 percent appropriate and that patients should feel confident in the safety of their care at Maine Medical Center.”

As a precaution, the hospital rescheduled approximately 150 elective surgeries Wednesday and Thursday while staff decontaminated surgical equipment and facilities in accordance with guidelines set by the U.S. Centers for Disease Control and Prevention, the hospital said.

Alzheimer's disease research

In the meantime, other Maine hospitals loaned equipment so MMC could perform emergency surgeries.

To treat metal instruments contaminated with prions, hospitals have to put them in an autoclave and heat the tools to 121 degrees Celsius for 30 minutes, according to CDC protocols. That’s much more than is required to kill bacteria and viruses.

But even that doesn’t always work. Prions can survive the superheating, though it does weaken them, according to a report in Scientific American.

Another reason why prion disease poses such a risk is that it has a long incubation period. The time between when a person is exposed to when they start feeling symptoms can range from months to years. That means a patient with the disease can arrive at the hospital and show no symptoms. It may not be until they’re on the operating table for another reason that doctors spot signs of trouble. Or the medical staff may spot no red flags at all, only to discover later that the patient was infected. In the meantime, other patients can be exposed to the contaminated tools and more.

infectious waste and food contamination

Prion disease is distinct from other infectious diseases in that it’s not caused by a bacteria, virus or fungus but by abnormal proteins called prions. They can cause other proteins in the brain to fold abnormally, essentially leaving the organ full of holes like a sponge. That brain damage leads to memory impairment, dementia, personality changes and difficulty moving, among other symptoms. The incurable disease usually progresses very quickly and is always fatal, according to the CDC.

Prion disease refers to a family of progressive disorders that affect humans and animals. The most common form of it among humans is Creutzfeldt-Jakob disease, which can arise spontaneously, for no known reason. A variant form of it is caused by eating meat from cattle infected with another prion disease, bovine spongiform encephalopathy, also known as mad cow disease. (Editor’s Note: In deer, elk, moose and reindeer, prion disease has been dubbed chronic wasting disease. It’s time to put the species-specific names aside. A deadly prion is a deadly prion.)

CJD is rare, estimated to affect about one out of every million people worldwide each year, according to the World Health Organization. About 250 cases are diagnosed each year in the U.S. but thousands of other cases are suspected to go undiagnosed and misdiagnosed.

In 2014, a Kennebunk woman who worked as a nurse at Maine Medical Center died from Creutzfeldt-Jakob disease, according her family.

Sandi Kennedy CJD

And in 2013, 15 people in New Hampshire, Massachusetts and Connecticut were warned that they may have been exposed to the disease through potentially contaminated medical equipment.

Editor’s Note: 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 on the same disease spectrum—prion disease. It’s also known as transmissible spongiform encephalopathy (TSE). The bodily fluids of TSE victims are infectious and deadly. This infectious waste is now an environmental nightmare.

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. It’s not known which patients with brain disease become infectious or when, but both CJD and Alzheimer’s patients are being mismanaged. The most savvy neurologists won’t touch patients with these symptoms because of the risks. They are making diagnoses from across the room. Unfortunately, caregivers aren’t warned accordingly.

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

Experts claim that at least 25 percent of Alzheimer’s diagnoses are not Alzheimer’s disease. Millions of misdiagnoses are actually CJD, which is further up the prion spectrum. Millions of patients and caregivers are being misinformed, misguided and exposed to an aggressive prion disease. Misdiagnosis and misinformation regarding prion disease is a matter of life and death.

Infectious Disease News via http://bangordailynews.com/2016/11/11/news/state/case-of-rare-infectious-brain-illness-confirmed-at-maine-med/?ref=comments

Posted in Alzheimer's Disease Diagnosis, Creutzfeldt-Jakob Disease, Infectious Disease, Prion Disease | Tagged , , , | Leave a comment

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

Posted in Alzheimer's Disease, Alzheimer's Disease Diagnosis, Alzheimer's Disease Prevention, Alzheimer's Disease Research, Alzheimer's Disease Treatment | Tagged , , , | Leave a comment

Urine Test Can Diagnose Creutzfeldt-Jakob Disease

Prions Fueling A Public Health Disaster

Urine can be used to test for Creutzfeldt-Jakob disease. Unfortunately, it also is a pathway that spreads prion disease among mammals.

infectious waste and food contamination

The Medical Research Council team is working on a simple test. They claim that their prototype test still needs honing before it could be used routinely. Currently there is no easy test available for this rare but fatal brain condition. Instead, doctors have to take a sample of spinal fluid or brain tissue, or wait for a post-mortem after death. What they look for is tell-tale deposits of abnormal proteins called prions, which cause the brain damage.

Building on earlier US work, Dr. Graham Jackson and colleagues, from University College London, have now found it is also possible to detect prions in urine. This might offer a way to diagnose CJD rapidly and earlier, they say, although there is no cure.

CJD is a rare, but fatal degenerative brain disorder caused by abnormal proteins called prions that damage brain cells. In the 1990s it became clear that a brain disease could be passed from cows to humans (it can also be passed from humans to other mammals). Since then, officials have kept a close check on how many people have become sick or died from CJD. There is no known cure.

Prions and Alzheimer's disease

The study looked at urine samples from 162 people. Of these:

  • 91 were healthy controls
  • 34 had neurological disease that was not thought to be caused by CJD
  • 37 had a diagnosis of CJD (20 of these were sporadic CJD)

The urine test gave no “false-positive” results – meaning it did not falsely suggest there was CJD in any of the patients known not to have the disease. But it was less reliable when it came to detecting actual cases. It accurately detected just under half of the sporadic CJD patients and even fewer of the vCJD patients. The researchers hope they will be able to improve the test further so it can reliably detect all types of CJD.

“Although there is currently no cure for this disease, an accurate and early diagnosis is extremely important for patients and their families, said Dr. Jackson. “In the future, as trials of potential therapies become available, the earlier a patient can be diagnosed the more effective any treatment is likely to be. This test could be a critical step forward.”

Editor’s Note: Prion disease is a spectrum disease that includes Alzheimer’s disease, Creutzfeldt-Jakob disease, Parkinson’s disease, Huntington’s disease, mad cow disease, chronic wasting disease and is likely a contributing factor in the global rise in autism. Victims are infectious long before they exhibit symptoms. Misinformation and mismanagement of sewage and wastewater are contributing to the global epidemic in neurodegenerative disease. As more people get the disease, the waste stream becomes even deadler. It’s time to regulate wastewater streams, including biosolids, as infectious waste and it’s time to enforce the Bioterrorism Preparedness and Response Act of 2002.

Neurodegenerative News via http://www.bbc.com/news/health-37541550?post_id=10153608943738725_10154203430888725

Posted in Creutzfeldt-Jakob Disease, Diagnosis, Disease Transmission, Infectious Disease, Prion Disease, Sewage Sludge | Tagged , , , | Leave a comment