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.

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.

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.

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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.

 

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.

Preventing Dementia A Major Challenge

New Report Offers Little Hope In Battle Against Neurodegenerative Disease

By Sharon Begley, STAT

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

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

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

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

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

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

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

prevent Alzheimer's disease

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

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

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

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

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

Alzheimer's disease public relations firm

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

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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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/

Asians At Higher Risk For Dementia

DNA Analysis Reveals Key Genetic Mutations, Therapies

By Joana Fernandes, PhD

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

Alzheimer's disease research

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

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

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

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

Alzheimer's disease epidemic

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

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

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

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

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

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

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

Pomegranate Seeds Treat Neurodegenerative Disease

Alzheimer’s Disease Treatment Delivers Powerful Antioxidant

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

Alzheimer's disease prevention tips

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

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

Alzheimer's disease treatment

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

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

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

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

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

New Drug Offers Promise Against Alzheimer’s Disease

Treatment Purges Plaque Deposits Within Brain

A new drug that can treat Alzheimer’s disease is finally on the horizon after scientists proved they can clear the sticky plaques from the brain which cause dementia and halt mental decline. Hailed as the best news in dementia research for 25 years, the breakthrough is said to be a potential game changer for people with Alzheimer’s disease.

aducanumab treats Alzheimer's disease
Red areas represent plaque deposits targeted by aducanumab. Click to enlarge.

Scientists said they were amazed to find that patients treated with the highest dose of the antibody drug aducanumab experienced an almost complete clearance of the amyloid plaques that prevent brain cells communicating, leading to irreversible memory loss and cognitive decline.

Crucially they also found that after six months of the treatment, patients stopped deteriorating compared with those taking a placebo, suggesting that their dementia had been halted.

If shown to be effective in larger trials, the first drug to treat dementia could be available in just a few years.

“The results of this clinical study make us optimistic that we can potentially make a great step forward in treating Alzheimer’s disease,” said Prof Roger Nitsch, at the Institute for Regenerative Medicine at the University of Zurich. “In the high dose group the amyloid has almost completely disappeared. The effect size of this drug is unprecedented. Despite it being a small sample, there appeared to be a slowing of cognitive decline and functional decline. The group with a high degree of amyloid removal were basically stable. If we could reproduce this, it would be terrific.”

Alzheimer's disease treatment

Dr. Alfred Sandrock, from the Massachusetts-based biotech company Biogen, which is hoping to bring the drug to market, said: “This is the best news that we have had in 25 years and it brings new hope to patients with this disease.”

There are currently 850,000 people living with dementia in Britain, a figure that is expected to rise to one million by 2025 and two million by 2050. There are more than 50 million people battling the disease today. Despite a high death rate, the population of those afflicted with the disease is expected to soar over the next decade.

The most common kind of neurodegenerative disease is Alzheimer’s disease, but scientists have been unable to reach consensus about the cause of the condition, and despite more than 400 drug trials, nothing has been effective. Current treatments can reduce symptoms to some extent but doctors have nothing that can halt or slow progression of the disease.

Aducanumab is a treatment made up of antibodies, tiny y-shaped proteins that latch on to dangerous substances in the body, acting like flags, showing the immune system what to clear away.

Scientists tested various human immune cells with amyloid in a laboratory until they found one which produced an antibody that broke up the plaques. They then cloned it in large numbers for the new therapy, which is given intravenously just once a month.

Prions and Alzheimer's disease

In the trial, which was reported in the journal Nature, scientists tested varying levels of the drug over a year, as well as giving one group a placebo. They found that more amyloid was removed as the dose increased. Brain scans of those given the highest dose shown virtually no amyloid left at all.

The drug is likely to be most effective for patients in the very earliest stages of Alzheimer’s disease, or those who have not yet begun to show symptoms. Several universities are working on early blood tests for dementia which could pick the disease up a decade or more before the first physical signs appear.

Dementia experts and charities said that the breakthrough offered real hope for the future treatment of Alzheimer’s disease. There are now two large phase-three clinical studies taking place to further evaluate safety and efficacy on a total of 2,700 patients with early-stage Alzheimer’s disease and researchers are currently recruiting British participants.

“These results provide tantalizing evidence that a new class of drug to treat the disease may be on the horizon,” said Dr David Reynolds, chief scientific officer at Alzheimer’s Research UK.

“The findings suggest that aducanumab may slow memory and thinking decline in people with early Alzheimer’s and, although the analysis is only exploratory in this early trial, it paints a positive picture for ongoing trials with the drug.”

caregivers Alzheimer's disease

Encouragingly, this treatment also appeared to slow memory decline, demonstrating that amyloid formation is a direct or indirect cause of memory loss. This has been suspected for some time, but has never been proven in humans.

“These findings could be a game changer if the effects on memory decline can be confirmed in more extensive follow-on studies.”

The Alzheimer’s Society said the “most compelling” evidence from the trial was the fact that more amyloid was cleared when patients took higher doses of the drug.

Dr James Pickett, head of research at the charity, said: “No existing treatments for Alzheimer’s directly interfere with the disease process, and so a drug that actually slows the progress of the disease by clearing amyloid would be a significant step.

“While there were hints that it might have an effect on the symptoms of the disease, we need to see the results from further, larger research trials to understand whether this is the case. These larger trials are now under way, including in the UK, and due to finish in 2020.”

Prof Richard Morris, Professor of Neuroscience at the University of Edinburgh, said: “We cannot yet say we have a cure for Alzheimer’s, as this is only a first step … but the importance of this first step cannot be understated.

“Let’s keep our fingers crossed for success in the next steps.”

Alzheimer’s Disease News via http://www.telegraph.co.uk/science/2016/09/01/alzheimers-new-drug-that-halts-mental-decline-is-best-news-for-d/