A simple blood test reliably detects signs of brain damage in people on the path to developing Alzheimer’s disease – even before they show signs of confusion and memory loss, according to a new study from Washington University School of Medicine in St. Louis and the German Center for Neurodegenerative Diseases in Germany.
The findings may one day be applied to quickly and inexpensively identify brain damage in people with not just Alzheimer’s disease but other neurodegenerative conditions such as multiple sclerosis, traumatic brain injury or stroke. The findings also indicate that deadly proteins are found in blood, which further confirms the transmissibility of neurodegenerative disease via a blood transfusion from an infected donor.
“This is something that would be easy to incorporate into a screening test in a neurology clinic,” said Brian Gordon, PhD, an assistant professor of radiology at Washington University’s Mallinckrodt Institute of Radiology and an author on the study. “We validated it in people with Alzheimer’s disease because we know their brains undergo lots of neurodegeneration, but this marker isn’t specific for Alzheimer’s disease. High levels could be a sign of many different neurological diseases and injuries.”
The test detects neurofilament light chain, a structural protein that forms part of the internal skeleton of neurons. When brain neurons are damaged or dying, the protein leaks out into the cerebrospinal fluid that bathes the brain and spinal cord and from there, into the bloodstream.
Finding high levels of the protein in a person’s cerebrospinal fluid has been shown to provide strong evidence that some of their brain cells have been damaged. But obtaining cerebrospinal fluid requires a spinal tap, which many people are reluctant to undergo. Senior author Mathias Jucker, PhD, a professor of cellular neurology at the German Center for Neurodegenerative Diseases in Tübingen, along with Gordon and colleagues from all over the world, studied whether levels of the protein in blood also reflect neurological damage.
To find out whether protein blood levels could be used to predict cognitive decline, the researchers collected data on 39 people with disease-causing variants when they returned to the clinic an average of two years after their last visit. The participants underwent brain scans and two cognitive tests: the Mini-Mental State Exam and the Logical Memory test. The researchers found that people whose blood protein levels had previously risen rapidly were most likely to show signs of brain atrophy and diminished cognitive abilities when they revisited the clinic.
“It will be important to confirm our findings in late-onset Alzheimer´s disease and to define the time period over which neurofilament changes have to be assessed for optimal clinical predictability,” said Jucker, who leads the DIAN study in Germany.
All kinds of neurological damage can cause the neurofilament light protein to spill out of neurons and into blood. Protein levels are high in people with Lewy body dementia and Huntington’s disease; they rise dramatically in people with multiple sclerosis during a flare-up and in football players immediately after a blow to the head.
A commercial kit – very similar to the one used by the authors – is available to test for protein levels in the blood, but it has not been approved by the FDA to diagnose or predict an individual’s risk of brain damage. Before such a test can be used for individual patients with Alzheimer’s or any other neurodegenerative condition, researchers will need to determine how much protein in the blood is too much, and how quickly protein levels can rise before it becomes a cause for concern.
“I could see this being used in the clinic in a few years to identify signs of brain damage in individual patients,” said Gordon, who is also an assistant professor of psychological & brain sciences. “We’re not at the point we can tell people, ‘In five years you’ll have dementia.’ We are all working towards that.”
Neurodegenerative disease has been surging around the world for the past 30 years. It’s the fastest-growing cause of death and it will soon be the leading cause of death.
Alzheimer’s disease alone is taking the lives of 50-100 million people around the world now. The epidemic is more severe in some countries than others. As millions die, even more will be diagnosed. Millions more are suffering in silence with a misdiagnosis or no diagnosis. No one really knows the scope of the epidemic. Unfortunately, one of the common threads is the mishandling of infectious waste. A variety of factors can trigger neurodegenerative disease, including genetics, head trauma and neurotoxins.
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, Parkinson’s disease and other brain diseases are transmissible. They also are being misdiagnosed and undiagnosed at an alarming rate. Deadly, self-replicating proteins appear to be one of the common threads.
At $236 billion a year, Alzheimer’s disease is already the most expensive disease in the United States. The disease saw a 15.7 percent jump over 2014 numbers–the largest increase of all major causes of death. It accounted for 108,227 documented deaths (and thousands more of undiagnosed and undocumented ones) in the U.S. alone in 2015. A similar pattern is emerging around the globe–some regions much more than others.
In the U.S., nearly one in every five Medicare dollars is spent on people with Alzheimer’s disease or another dementia.
Prions (PREE-ons) are a deadly and unstoppable form of protein that migrates, mutates, multiplies and kills with unparalleled efficiency. Prions cause fatal neurodegenerative disease in humans and other mammals by converting the cellular version of prion protein into a toxic form that erodes the brain and body. Prion disease often is described as a wasting disease that causes a loss of body mass and brain mass.
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 and prion disease. President Obama awarded Prusiner the National Medal of Science in 2010 to recognize the importance of his research.
Prion disease also is known as transmissible spongiform encephalopathy (TSE). The operative word is “transmissible.” Prusiner claims that all forms of TSE are caused by infectious prions.
“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 adds to the evidence about the transmissibility of Alzheimer’s disease between people. A second study by the same scientist in early 2016 supports the claim. Meanwhile, there is absolutely no evidence to the contrary. Even wildlife and sea mammals are contracting brain disease from people because of the dumping of infectious waste on farms, ranches and forests. Yes, research has found that plants/crops grown in infectious prions uptake those prions and become infectious.
TSE is a spectrum disease that varies in severity and symptoms. It depends on which region of the brain is impacted first and by what prion mutation. Few cases are identical in terms of symptoms and diagnoses. When the presenting symptom is memory loss, the diagnoses flow along the following chart.
In humans, the prion spectrum includes Alzheimer’s disease, Parkinson’s disease and an extremely aggressive version known as Creutzfeldt-Jakob disease. The difference between these diseases is very slight and often indistinguishable to neurologists. For example, millions of people have the severe form of Alzheimer’s disease, which is known as Creutzfeldt-Jakob disease (CJD). CJD is clearly a prion disease. According to neuroscientists Dr. Laura Manuelidis, at least 25 percent of Alzheimer’s disease diagnoses 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 across the U.S. and many other nations. Within the continuum of care, some treat it as an infectious disease, while others don’t.
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 prion disease. Millions of people with prion disease have exposed us all to their infectious waste thanks to misinformation, mismanagement and negligence.
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.
Prion disease is highly contagious, incurable and fatal. Despite all of the smoke and mirrors, prion disease is prion disease. It’s killing more and more mammals, including humans, every year. The hype about species barriers is ridiculous, reckless and irresponsible.
Victims should be quarantined because prions are in the urine, feces, blood, saliva, mucus, skin and cell tissue of all victims–all human byproducts that are washed, dumped, or flushed down sinks and toilets. One can assume that the waste is extra infectious when it comes from funeral homes, nursing homes, hospitals, dental offices, veterinarians, slaughterhouses and some laboratories.
Wastewater treatment plants are collecting points for prions from infected humans. The sewage treatment process can’t stop prions from migrating, mutating and multiplying before being discharged into the environment where they can kill again. Wastewater treatment plants are spreading infectious waste far and wide because they are incapable of stopping prions. As such, all by-products and discharges from wastewater treatment plants are infectious waste, which are contributing to the global epidemic of neurodegenerative disease among humans, wildlife and livestock.
The U.S. Environmental Protection Agency (EPA) has confirmed that prions are in sewage and that there has been no way to detect them or stop them. As such, the EPA has never issued guidance on prion management within wastewater treatment plants. Unfortunately, the EPA’s risk assessment on sewage sludge and biosolids were prepared before the world of science knew about prions. The agency continues to cling to its antiquated sludge rule crafted back in the dark ages. It does, however, consider prions a “emerging contaminant of concern.” Meanwhile, its outdated risk assessments are promoting a public health disaster. The neurotoxins found in sewage, including heavy metals, also are contributing to the global spike in autism, which follows the same timing and trajectory as the spike in neurodegenerative diseases.
“Since it’s unlikely that the sewage treatment process can effectively deactivate prions, adopting measures to prevent the entry of prions into the sewer system is advisable,” said the Toronto Department of Health, November 2004.
Once unleashed on the environment, prions remain infectious. They migrate, mutate and multiply as they infect crops, water supplies, wildlife, livestock, sea mammals and humans. According to prion researcher Joel Pedersen at the University of Wisconsin, prions in soil become up to 680 times more infectious. From there, they migrate, mutate and multiply. It’s a real world version of Pandora’s Lunchbox.
“Our results suggest that if prions enter municipal wastewater treatment systems, most of the agent would bond to sewage sludge, survive anaerobic digestion, and be present in treated biosolids,” Pedersen said. “Land application of biosolids containing prions represents a route for their unintentional introduction into the environment. Our results emphasize the importance of keeping prions out of municipal wastewater treatment systems.”
Pedersen also found that sewage treatment does not inactivate prions. Therefore, prions are lethal, mutating, migrating and multiplying everywhere sewage is dumped.
The risk assessments prepared by the U.S. EPA for wastewater treatment and sewage sludge are flawed and current practices of recycling this infectious waste is fueling a public health disaster. Many risks are not addressed, including prions and radioactive waste. They don’t mention prions or radiation because there is no answer. Most nations are making the same mistake. We’re dumping killer proteins on crops, parks, golf courses, gardens, ski areas, school grounds and beyond. Wind, rain and irrigation spread these contaminants and many more throughout our communities and watersheds.
Failure to account for known risks is negligent. Crops for humans and livestock grown in sewage sludge absorb prions and become infectious. We’re all vulnerable to neurotoxins and right now due to widespread denial and mismanagement. It’s time to stop the land application of sewage sludge (LASS) in all nations. Safer alternatives exist.
Gary Chandler is a prion expert. He is the CEO of Crossbow Communications, author of several books and producer of documentaries about health and environmental issues around the world. Chandler is connecting the dots to the global surge in neurodegenerative disease, including Alzheimer’s disease, Parkinson’s disease, Creutzfeldt-Jakob disease, chronic wasting disease and other forms of prion disease. The scientific name for prion disease is transmissible spongiform encephalopathy. The operative word is “transmissible.” Even the global surge in autism appears to be related.