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 skin, urine, feces, blood, mucus and saliva of each victim. Each victim becomes an incubator and a distributor of the Pandora-like pathogen. Victims are contagious long before they exhibit clinical symptoms.

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

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

wastewater treatment plant

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

Prion researcher Dr. Joel Pedersen, from the University of Wisconsin, found that prions become 680 times more infectious in certain soils. Pedersen also found that sewage treatment does not inactivate prions. Therefore, prions are lethal, mutating, migrating and multiplying everywhere sewage is dumped.

“Our results suggest that if prions enter municipal wastewater treatment systems, most of the agent would bond to sewage sludge, survive anaerobic digestion, and be present in treated biosolids,” Pedersen said.

joel pedersen prion research

“Land application of biosolids containing prions represents a route for their unintentional introduction into the environment. Our results emphasize the importance of keeping prions out of municipal wastewater treatment systems. Prions could end up in sewage treatment plants via slaughterhouses, hospitals, dental offices and mortuaries just to name a few of the pathways. The disposal of sludge represents the greatest risk of spreading prion contamination in the environment. Plus, we know that sewage sludge pathogens, pharmaceutical residue and chemical pollutants are taken up by plants and vegetables.”

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

biosolids land application sewage sludge

The U.S. Environmental Protection Agency (EPA) has confirmed that prions are in sewage and that there has been no way to detect them or stop them. As such, the EPA has never issued guidance on prion management within wastewater treatment plants. Unfortunately, the EPA’s risk assessment on sewage sludge and biosolids were prepared before the world of science knew about prions. The agency continues to cling to its antiquated sludge rule crafted back in the dark ages. It does, however, consider prions a “contaminant of emerging concern.” Meanwhile, its outdated risk assessments are promoting a public health disaster.

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

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

chronic wasting disease

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

mad cow disease

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

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

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

Do Prions Cause All Forms Of Neurodegenerative Disease

Deadly Proteins Link Creutzfeldt–Jakob Disease, Alzheimer’s, Parkinson’s

By Diana Kwon, Scientific American

In the human form of mad cow disease, called Creutzfeldt-Jakob, a person’s brain deteriorates—literally developing holes that cause rapidly progressing dementia. The condition is fatal within one year in 90 percent of cases. The culprits behind the disease are prions—misfolded proteins that can induce normal proteins around them to also misfold and accumulate.

Scientists have known that these self-propagating, pathological proteins cause some rare brain disorders, such as kuru in Papua New Guinea. But growing evidence suggests that prions are at play in many, if not all, neurodegenerative disorders, including Alzheimer’s, Huntington’s and Parkinson’s, also marked by aggregations of malformed proteins.

Prions and Alzheimer's disease

Until recently, there was no evidence that the abnormal proteins found in people who suffer from these well-known diseases could be transmitted directly from person to person. The tenor of that discussion suddenly changed this September when newly published research in the journalNature provided the first hint such human-to-human transmission may be possible. (Scientific American is part of Springer Nature.)

For the study, John Collinge, a neurologist at University College London, and his colleagues conducted autopsies on eight patients who died between the ages of 36 and 51 from Creutzfeldt-Jakob. All the subjects had acquired the disease after treatment with growth hormone later found to be contaminated with prions. The surprise came when the researchers discovered that six of the brains also bore telltale signs of Alzheimer’s—in the form of clumps of beta-amyloid proteins, diagnostic for the disease—even though the patients should have been too young to exhibit such symptoms.

Alzheimer's disease prevention and treatment

These observations suggest that the tainted hormone injections might have carried small amounts of beta-amyloid proteins that triggered the formation of more such proteins. Neither Alzheimer’s nor any known human prion diseases are contagious through direct contact. Yet human transmission of prion diseases has occurred through certain medical procedures and, in the case of kuru, cannibalism. The new study therefore raises the possibility that Alzheimer’s is a transmissible disease with an etiology akin to prion diseases.

The new finding is provocative, but experts advise caution in interpreting the results. For instance, neuroscientist John Trojanowski of the University of Pennsylvania points to the small size of the study and lack of direct evidence for transmission in support of causality. But if it is eventually shown that Alzheimer’s and other neurodegenerative diseases indeed share the same basic pathological pathway and mechanism, treatments could target one and all.

“Transmission may occur in only a small percentage of human cases,” says Claudio Soto, a professor of neurology at the University of Texas Health Science Center at Houston. “But the underlying principle is the most important thing that could lead to new opportunities for therapeutic interventions and diagnostics.” Investigators such as Soto and Collinge are working on ways to detect in body fluids the presence of small clumps of the transmissible proteins now thought to be involved in Alzheimer’s and other neurodegenerative diseases, which could represent a diagnostic advance.

Alzheimer's disease treatment

Such detection will likely be difficult. A study published online in September in the journal Nature Neuroscience by Mathias Jucker of the University of Tübingen in Germany and his colleagues required extremely sensitive methods to find minuscule clumps of beta-amyloid proteins, referred to as seeds, in mice brains. These seeds appear to be able to regain pathological properties even after six months of lying dormant. These possibly prion-like proteins might, therefore, exist in the brain long before symptoms develop, at levels too low to be found by routine tests.

One potentially prion-like protein may cause several diseases, according to a study published this summer by Nobel laureate Stanley Prusiner, who discovered prions in the 1980s. Prusiner and his colleagues found that a “strain” of alpha-synuclein—the misfolded protein involved in Parkinson’s—can cause a similar but rare neurodegenerative disease, called multiple-system atrophy. Understanding how variants of these disease-causing proteins differ in shape and how the particular configuration influences their pathogenic nature is destined to become a focus of future research.

“There’s evidence that both prions and beta-amyloid exist as different strains and have very different biological effects,” says Lary C. Walker of Emory University, who was involved in the Nature Neuroscience study. “I think understanding this will give us insight into what’s happening in disease.”

As the evidence increases, more scientists now suspect that prionlike processes probably underlie all neurodegenerative disorders. Prusiner expected the current change in thinking: in his 1997 Nobel Prize lecture, he predicted that the understanding of prion formation could “open new approaches to deciphering the causes of and to developing effective therapies for the more common neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis (ALS).”

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Alzheimer’s Research Shaping Prion Hypothesis

Proteins Link Most Neurodegenerative Disorders

Getting to the bottom of Alzheimer’s disease has been a rapidly evolving pursuit with many twists, turns and controversies. In the latest crook in the research road, scientists have found a new insight into the interaction between proteins associated with the disease. The report, which appears in the journal ACS Chemical Neuroscience, could have important implications for developing novel treatments.

Alzheimer's disease treatment

Witold K. Surewicz, Krzysztof Nieznanski and colleagues explain that for years, research has suggested a link between protein clumps, known as amyloid-beta plaques, in the brain and the development of Alzheimer’s disease, a devastating condition expected to affect more than 10 million Americans by 2050. But how they inflict their characteristic damage to nerve cells and memory is not fully understood. Recent studies have found that a so-called prion protein binds strongly to small aggregates of amyloid-beta peptides. But the details of how this attachment might contribute to disease — and approaches to treat it — are still up for debate. To resolve at least part of this controversy, Surewicz’s team decided to take a closer look.

treat Alzheimer's disease

Contrary to previous studies, they found that the prion protein also attaches to large fibrillar clumps of amyloid-beta and do not break them down into smaller, more harmful pieces, as once thought. This finding bodes well for researchers investigating a novel approach to treating Alzheimer’s disease — using prion-protein-based compounds to stop these smaller, toxic amyloid-beta pieces from forming, the authors conclude.


Alzheimer’s Disease Caused By Deadly Prions?

Editor’s Note: Many factors, including genetics, can contribute to the onset of Alzheimer’s disease. However, a deadly protein called a prion (PREE-on) also is contributing to the rapid spread of the disease. People and animals with prion disease are contagious and caregivers and family members are vulnerable to transmission. People with prion disease spread deadly and unstoppable prions through bodily fluids and cell tissue. Blood, saliva, mucus, urine, feces, milk and meat tissue from mammals with prion disease can spread the pathogen. Once an item is contaminated with prions, the item cannot be sterilized and the prions can be transmitted again and again forever. Using the drinking glass once used by a person with Alzheimer’s or CJD could prove fatal. Ask your local coroner about prions. Coroners will not touch the body of a person who died from a known prion disease. Unfortunately, most coroners and others don’t know that Alzheimer’s is part of the deadly prion family.

Nobel-Laureate One Of Many Proving Alzheimer’s Hypothesis

An infectious, self-replicating protein might be causing Alzheimer’s disease, a growing number of studies suggest. If correct, this idea could change how scientists view the condition, which affects 5.4 million Americans. A tiny seed of a dangerous protein could corrupt other harmless proteins, the theory goes, creating and unleashing a destructive army in the brain. And this process might not be restricted to Alzheimer’s disease.

Some researchers believe the spread of such proteins in the brain could explain other devastating disorders such as Parkinson’s, Huntington’s disease and amyotrophic lateral sclerosis. In Alzheimer’s, the possible infectious agent under scrutiny is a protein called amyloid-beta, best known as the main ingredient in the hulking, sticky gobs of plaque found in the brains of people with the disease. It turns out that A-beta probably causes damage long before it accumulates into these plaques. Smaller arrangements of A-beta, called oligomers, scramble brain messages and eventually kill nerve cells.

Prions and Alzheimer's disease

These oligomers, some scientists now believe, are infectious agents known as prions. Such self-replicating proteins, discovered 30 years ago by Stanley Prusiner of the University of California, San Francisco, are responsible for the brain-wasting Creutzfeldt-Jakob disease in people, scrapie in sheep and bovine spongiform encephalopathy in cattle. Over 20 years ago, Prusiner argued that something similar could be happening in Alzheimer’s and other brain diseases. In the last few years, he and others have turned up some evidence that his hunch could be right, and now more people are paying attention.

A-beta injected into half of a mouse’s brain slowly incites other A-beta molecules to accumulate, Prusiner and colleagues reported earlier this year (SN: 7/14/12, p. 5). And Swedish scientists caught A-beta jumping directly from nerve cell to nerve cell in rat and human cells in a dish, suggesting that the protein can follow neural connections in the brain.

Alzheimer's disease prevention and treatment

Still more evidence comes from a study on a particularly dangerous form of A-beta. In “vanishingly small” quantities, this form, called pyroglutamylated A-beta, can cause normal versions of A-beta to turn deadly, says study coauthor George Bloom of the University of Virginia. These proteins needed just 24 hours to kill half of mouse nerve cells tested in a dish (SN: 6/2/12, p. 18).

If the prion idea is right, then over many years a small, dangerous A-beta seed may cause harmless forms of A-beta to shape-shift into a destructive form of the protein. So far, there’s no direct evidence of this shift in people, but scientists are looking.

Thinking of Alzheimer’s as a prion disease could have big implications for treatment and prevention.


Alzheimer’s Caused By Many Factors, Pathways

Prion Pathogen Can Be Triggered Or Acquired

All causes of Alzheimer’s disease are not clear and it is likely that there are several causes. Alzheimer’s disease causes changes or deterioration in certain areas of the brain that control thinking, communication, and behavior. Some of the deterioration may be related to a loss of chemical messengers in the brain (neurotransmitters)-acetylcholine, in particular-that allow nerve cells in the brain to communicate properly.

Prions and Alzheimer's disease

It’s not clear why these changes in the brain occur, but they are a major focus of Alzheimer’s research. Although most people who have Alzheimer’s disease do not have a family history of the condition, you are at increased risk for the condition if a member of your family has it.

Some theories have suggested that metals, such as zinc or aluminum, play a role in Alzheimer’s disease. But research has not found much evidence to support these theories. Experts agree that there is no reason to leave zinc out of your diet or to avoid items that contain aluminum, such as cooking utensils or soda pop cans.

Alzheimer’s disease, Parkinson’s disease and other forms of neurodegenerative disease are collectively becoming the leading cause of death around the world. Alzheimer’s disease alone is killing 50-100 million people now. Millions more will contract the disease this year, while just as many will go undiagnosed and misdiagnosed. The vast majority of cases are preventable.