New 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

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

Prevent Alzheimer’s Disease.

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

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

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:

Ken Stabler Added To Growing List Of CTE Victims

Brain Disease Found In Former Quarterback

By John Branch, New York Times

Shortly before he died in July, the former NFL quarterback Ken Stabler was rushed away by doctors, desperate to save him, in a Mississippi hospital. His longtime partner followed the scrum to the elevator, holding his hand. She told him that she loved him. Stabler said that he loved her, too.

Ken Stabler CTE

“I turned my head to wipe the tears away,” his partner, Kim Bush, said recently. “And when I looked back, he looked me dead in the eye and said, ‘I’m tired.’ ”

They were the last words anyone in Stabler’s family heard him speak.

“I knew that was it,” Bush said. “I knew that he had gone the distance. Because Kenny Stabler was never tired.”

The day after Stabler died on July 8, a victim of colon cancer at 69, his brain was removed during an autopsy and sent to scientists in Massachusetts. It weighed 1,318 grams, or just under three pounds. Over several months, it was dissected for clues, as Stabler had wished, to help those left behind understand why his mind seemed to slip so precipitously in his final years.

On the neuropathologist’s scale of 1 to 4, Stabler had high Stage 3 chronic traumatic encephalopathy, or CTE, the degenerative brain disease believed to be caused by repeated blows to the head, according to researchers at Boston University. The relationship between blows to the head and brain degeneration is still poorly understood, and some experts caution that other factors, like unrelated mood problems or dementia, might contribute to symptoms experienced by those later found to have had CTE.

CTE and football players

Stabler, well known by his nickname, the Snake, is one of the highest-profile football players to have had CTE. The list, now well over 100 names long, includes at least seven members of the Pro Football Hall of Fame, including Junior Seau (above), Mike Webster and Frank Gifford.

Frank Gifford CTE

Few, if any, had the free-spirited charisma of Stabler, a longhaired, left-handed quarterback from Alabama who personified the renegade Oakland Raiders in the 1970s. Stabler was the NFL’s most valuable player in 1974 and led the Raiders to their first Super Bowl title two seasons later. He ended his 15-year NFL career with the New Orleans Saints in 1984.

“He had moderately severe disease,” said Dr. Ann McKee, chief of neuropathology at the V.A. Boston Healthcare System and a professor of neurology and pathology at Boston University School of Medicine, who conducted the examination. “Pretty classic. It may be surprising since he was a quarterback, but certainly the lesions were widespread, and they were quite severe, affecting many regions of the brain.”

Quarterbacks are provided more protection from hits than most football players, but they still take wicked blindside hits. An offensive line’s purpose is, in part, to protect the quarterback, and leagues like the NFL have special rules to discourage severe blows to players in the most important position on the field.

CTE brain

But Stabler’s diagnosis further suggests that no position in football, except perhaps kicker, is immune from progressive brain damage linked to hits to the head, both concussive and subconcussive.

Stabler is the seventh former NFL quarterback found to have had CTE by Boston University, which says it has found CTE in 90 of the 94 former NFL players it has examined, including the former Giants safety Tyler Sash, who died at 27 in September and whose diagnosis was made public last week.

On Wednesday, the family of another Super Bowl quarterback, Earl Morrall, told The New York Times that Morrall was found to have Stage 4 CTE after his death in 2014 at age 79.

Alzheimer's disease prevention

Order the eBook now. The nutritional advice should be beneficial to all forms of neurodegenerative disease:

  • Avoid neurotoxins in food, water and the circles of life;
  • Prevent brain disease with targeted nutritional guidance;
  • Effectively treat brain disease with nutritional therapies. It’s the most logical and comprehensive nutritional advice available for neurological disease; and
  • Keep caregivers safe. Misinformation and misdiagnoses are putting them at risk.

Read The Full Story About CTE


Alzheimer’s Disease Surging Across Scandinavia

Sewage Sludge Contaminating Food, Water

Alzheimer’s disease is the fastest-growing cause of death in the world. People living across Scandinavia have some of the highest prevalence of the disease in the world.

At least 50 million people already have Alzheimer’s disease and other forms of dementia. It’s vastly undiagnosed and misdiagnosed. According to the Alzheimer’s Association, doctors are withholding millions of additional diagnoses in the United States, so we don’t know the extent of the epidemic in America, but the incidence likely rivals Finland.

Alzheimer's disease and caregivers

According to recent studies, Finland has the highest incidence of Alzheimer’s disease in the world. Iceland and Sweden aren’t far behind. It could be that Finland is doing a better job of screening, diagnosing and offering honest assessments.

What can we learn from these regional variations? What are the common threads that can help us unravel the causes of neurological disease?

Alzheimer’s/Dementia Deaths/100K

1.   Finland                     34.9
2.  Iceland                      25.1
3.  United States           24.8
4.  Sweden                     21.5
5.  Netherlands             21.4
6.  Switzerland              20.0
7.  Cuba                           19.6
8.  Chile                          19.6
9.  Andorra                     19.4
10.  Spain                        18.7
11.  Norway                     18.6
12.  Uruguay                   17.5
13.  Denmark                  17.4
14.  United Kingdom    17.1
15.  France                      16.6

Although there are many causes of Alzheimer’s disease and related neurological diseases, the Baltic Sea region is a microcosm worth studying. The Baltic Sea is one of the most polluted bodies of water on the planet. Much of the pollution originates upstream and on land, but tons of it are dumped directly in the sea.

biosolids land application contaminates food water

It’s infectious waste. Raw sewage and sewage sludge. Waste from morgues, hospitals, nursing homes, slaughter houses, veterinarians and the homes of millions of people who have brain disease and other infectious diseases. This infectious waste is being dumped on open land as fertilizer. It’s contaminating food, water, air and more in most countries.

The Problem With Prions

In order to understand the threat, one must understand the dynamics of this neurological disease. Alzheimer’s disease, for example, is a member of an aggressive family (spectrum) of neurodegenerative diseases known as Transmissible Spongiform Encephalopathy (TSE)The operative word is “transmissible.”

Prions and Alzheimer's disease

TSEs include Alzheimer’s disease, Creutzfeldt-Jakob disease, Parkinson’s, Huntington’s, mad cow disease and chronic wasting disease in deer. Few, if any, mammals are immune. There is no cure. There is no species barrier. 

TSEs are caused by a deadly protein called a prion (PREE-on). Prion disease is unstoppable and the pathogen spreads through the bodily fluids and cell tissue of its victims. Prions are in the blood, saliva, urine, feces, mucus, and bodily tissue of its victims, including skin.

“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).”

Prions linger in the environment infinitely because they defy all attempts at sterilization and inactivation. They spread uncontrollably within victims and within the environment. They know no borders. Unlike radiation, however, prions do not deplete themselves. Unlike cancer, there is no cure. Prions migrate, mutate, multiply and kill with unparalleled efficiency. Each victim becomes an incubator and a distributor of the unstoppable pathogen.

“The (human) brain diseases caused by prions include Alzheimer’s, Parkinson’s, Huntington’s, amyotrophic lateral sclerosis (Lou Gehrig’s disease), and other disorders known as frontotemporal dementias,” said Nobel Laureate Stanley Prusiner, who earned a Nobel Prize in Physiology in 1997 for discovering deadly prions.

prion disease spectrum

Prion disease is a spectrum disease because of its many mutations and genetic resistance. Some prions can kill people within weeks of exhibiting clinical symptoms, while others can take years. Others may not fall victim to the disease, but can still carry the pathogen internally and externally. Victims become infectious long before they appear sick. Their bodily fluids proceed to contaminate the world around them.

Since prion disease is a spectrum disease, doctors can’t tell the difference between Alzheimer’s disease and CJD. It’s a process of elimination and a shot in the dark.

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

According to neuroscientists Dr. Laura Manuelidis, at least 25 percent of Alzheimer’s diagnoses are not Alzheimer’s disease. These misdiagnoses are actually CJD, which is further up the prion spectrum. CJD, without dispute, is extremely infectious to caregivers and loved ones. 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.

The only definitive diagnosis comes with an autopsy, which rarely happens with neurological disease (concerns over deadly contamination). All doctors are guessing with each diagnosis based on the severity of the symptoms. This problem also complicates the search for accurate statistics about the size and scope of the epidemic.

Unfortunately for caregivers and family members, the protocol for patient care and caregiver safety are vastly different for Alzheimer’s patients and CJD patients. The double standards put many stakeholders at risk. It’s reckless to try to distinguish between prion diseases on the spectrum. In other words, treat people with Alzheimer’s disease as though they have CJD. Assume the worst and hope for the best. A deadly prion is a deadly prion.

biosolids land application sewage sludge

The Sewage Tsunami

Although there are many causes and pathways contributing to the prion disease epidemic, many pathways are being mismanaged. Thanks to sewage, biosolids, and reclaimed sewage water, we’re recycling the prion pathogen that causes Alzheimer’s and CJD right back into our food and water. Every sewage system in the world has been used by someone, if not millions, of people with Alzheimer’s disease and Creutzfeldt-Jakob disease. Sewage systems are now prion incubators and distributors. Sewage sludge, wastewater, biosolids and other byproducts are highly lethal.

Thanks to more and more people dying from TSEs, and thanks to more and more sewage mismanagement, we’re dumping deadly pathogens on farms, parks, golf courses and school grounds. Rain and irrigation spread the prions throughout our communities, watersheds and into our oceans. Winds carries prion-laced dust into our communities, schools, offices and homes.

Dumping tons of sewage from millions of people on land and at sea spreads the prion pathogen far and wide. It’s a case of Pandora’s lunchbox. We’re contaminating our food and water supplies with our own sewage.

Alzheimer's disease Finland Sweden Iceland
Sewage and other contaminants dumped in the Baltic Sea are essentially trapped, where they continue to contribute to prion contamination.

Now, back to our Baltic story. The Baltic Sea is positioned in Northern Europe and bordered by Sweden, Finland, Russia, Estonia, Latvia, Lithuania, Poland, northeastern Germany, and eastern Denmark and its numerous islands. It’s the source of food for millions of people. Its watersheds provide drinking water for hundreds of communities, not to mention livestock, throughout the region. Unfortunately, pollution is killing the Baltic Sea and residents of the region.

“This is one of the world’s most polluted oceans,” said Fredrik Wulff, a professor of marine systems ecology at Stockholm University. “Because it’s an almost closed body of water, everything that’s dumped here stays for decades.”

Baltic Sea pollution

The untreated waste from the Russian city of Kaliningrad is part of the problem. Kaliningrad dumps about 150,000 cubic meters of raw sewage from 450,000 people into the sea every day. Most other coastal cities throughout the region dump even higher quantities of sewage, although it’s treated slightly. These treated wastewater facilities might help reduce solids and nitrogen, but nothing stops a prion in sewage.

“Kaliningrad is a medieval city that pours its waste into the gutter,” said Aleksandra Korolyova, a Kaliningrad-based activist with the Russian group Ekozashchita (Environmental Protection). “It’s just a black torrent that pours out of the pipe directly into the lagoon, and the lagoon is part of the sea.”

Poland’s waste compounds the problem. It accounts for 30 percent of emissions into the Baltic Sea. Sweden and Russia each dump in about 12 percent. The sewage pollution impacts everything between the point of dumping and the sea, including codfish, herring, shellfish and the people who eat them. The streams, rivers and groundwater are likely contaminated forever with sewage and prions, not to mention other toxins and carcinogens.

The entire region is swimming in sewage. Prion pollution from sewage also impacts the beaches and the people who play on them. It contaminates clothing and shoes. It contaminates boats of all sizes. Prions don’t need the help of mismanaged sewage to find pathways back to humans. Toxins in mismanaged sewage are contributing to cancer, endocrine system disruption and many other health issues.

Leaders in Alzheimer’s disease, Finland and Sweden dump their sewage into rivers and lakes, which is contaminating waterways and communities, while exposing families to various toxins and pathogens, including Pandora-like prions. This mismanagement is exposing millions of people, wildlife and livestock to the prion epidemic.

Towns and cities across the European Union are required to collect and treat their urban wastewater under the Urban Wastewater Treatment Directive. In 2006, the European Commission took Finland and Sweden to the European Court of Justice for failing to ensure proper treatment of urban wastewater in a significant number of towns and cities. In 2010, Finland and Sweden again were cited for failing to install the proper infrastructure for collecting and treating urban wastewater. Unfortunately, sewage treatment of any sort doesn’t stop a prion, but sewage mismanagement is obviously an issue in the region and in these two countries, which are afflicted with abnormally high rates of neurodegenerative disorders.

“Finland and Sweden are rightly concerned about the state of the Baltic Sea. They can help make it healthier by improving their own wastewater treatment,” said EU Environment Commissioner Stavros Dimas.

cruise ships and sewage Baltic SeaCruise Ship Sewage Dumped At Sea

Cruise ships in the region also dump their sewage in the Baltic Sea. Last year, 261 international cruise ships pulled to port just in Helsinki. It’s legal to discharge untreated wastewater in international waters, as long as it is done at least twelve kilometers from the nearest coast. Finnish cruise lines stopped dumping wastewater in the Baltic in 2007.

In addition, Baltic countries generate about 3.5 million tons of dry sewage sludge every year. In the past, it was dumped in a variety of ways, including at sea. Sludge dumped into the Baltic has polluted the sea forever. Additional wastewater and sewage runoff just adds fuel to the fire.

Adding to the insanity, sewage sludge has been used in agriculture throughout the Baltic Sea Region for at least 40 years. It is used as a fertilizer. Unfortunately, crops and grass uptake prions and become infectious. The Netherlands, Belgium and Switzerland have forbidden or restricted the agricultural disposal of sewage sludge. They incinerate it. Finland and Norway, however, dump sludge on green areas of all sorts.

Europe alone spends more than 2.2 billion euros every year getting rid of sewage sludge. About 60 percent of it goes toward agriculture and landscaping applications. Disposing of it safely would cost billions more. The same goes for every nation on the planet. It’s better to protect corporate profits than people or the planet?

Sewage mismanagement is not limited to the Baltic Sea region. Virtually every coastal city in the world dumps sewage in the sea. Boston, for example, dumps about 500 million gallons of sewage off the coast of Cape Cod every day. Many more cities dump it in rivers, streams and on crops. Cattle graze on it. Thanks to the creative marketing of biosolids, kids play on it and gardeners are using this death dust at home.

People, wildlife, marine life and livestock around the world are caught in the crossfire. Failure to address these issues will cost billions of lives. The body count is already in the millions.

Alzheimer's disease treatment

Whales Are Bioindicators Of Neurological Disease In Iceland

Iceland is a different case study in sewage management and diet. It’s obviously not impacted by the problems of the Baltic Sea, but it could still serve as a canary in a coal mine.

First of all, Iceland is smart enough to not put sewage sludge on its farmlands. It disposes of it in landfills. Unfortunately, if these landfills aren’t capped and lined like a nuclear waste dump, water will leach through the prion pathogens and contaminate groundwater.

The main sources of sewage in Iceland are residential areas, fish processing, livestock, slaughtering, dairy industries, aquaculture, textile industries, tanning plants and some heavy industries. Both the industrial and domestic sewage is usually disposed through the same drainage into the sea. The majority of sewage in Iceland is released untreated into the ocean where it impacts coastal waters, fish, shellfish and waterfowl. It also could be impacting whales and dolphins. Even if the sewage were treated, the deadly prions would survive the process.

Hafnarfjordur, for example, is located on the coast just southwest of Reykjavik on the southwest coast of Iceland. The city of about 21,000 people has four sewage outlets that discharge directly into the bay where people fish, boat, golf and swim. Any sewage that escapes the bay is then driven up the western coast by the currents of the North Atlantic. Pardon my French, but it’s the equivalent of pissing into the wind. The damage done by sewage to Iceland’s coastal waters are well documented. Do you think that it’s contributing to the nation’s high rate of Alzheimer’s deaths? Do you think it’s a good idea to dump sewage where you eat and drink?

Neurological Disease In Whales

Whale meat also is a likely pathway that could be contributing to high rates of neurological disease in Nordic and Baltic nations. Whales and dolphins are vulnerable to prion disease. At least one dolphin has been found with prion disease, but testing is severely lacking. Since dietary factors are clearly linked to neurological disease, studying the correlation between diet and disease can help illuminate the prion problem.

As stated before, Alzheimer’s (and other diseases on the prion spectrum) are extremely high in the region. Pioneering research found that Parkinson’s patients on the Faroe Islands have consumed about six times more whale meat and blubber than their neighbors who don’t have the disease.

Maria Skaalum Petersen is working to shed light on the connection between sick seas, sick whales and the people who consume them. Petersen is a researcher in the Department of Occupational and Public Health in the Faroe Islands health service. One of her projects has included a comparison of the prevalence of Parkinson’s disease (part of the TSE spectrum) in the Nordic countries.

whale meat and neurological disease
Maria Skaalum hit the tip of an iceberg by connecting the consumption of pilot whales to neurological disease.

She found that Parkinson’s disease is twice as prevalent on the Faroe Islands as in Norway and other Nordic countries. A traditional diet on the Faroe Islands typically includes pilot whale meat.

Predators, including some whales, are high on the food chain. Animals that consume predators are consuming the toxic build-up from every animal ever consumed. Therefore, these predators (and the people who consume them) often serve as an excellent indicator of the health of an entire ecosystem, including prion contamination.

Not all whales are created equal, though. The whale meat sold in Norway and Iceland is mostly from minke whales, a species that has a diet much lower in the food chain. This means they do not accumulate as many contaminants or prions as pilot whales. This means that the risks associated with whale meat is slightly less for the people in Norway. However, as you recall from the chart above, Norway still has a fairly high rate of neurological disease.

eating pilot whales causes Parkinson's disease

“The Faroe Islanders eat pilot whales, while Norwegians eat baleen whales. Pilot whales have teeth and primarily eat fish and squid, which puts them higher on the food chain,” Petersen says.

Baleen whales feed by filtering zooplankton and krill into their mouths as they swim. Eating lower on the food chain lowers their prion exposure, but it doesn’t make them immune to the prion problem. More importantly, this study indicates that there is prion accumulation in whales–some more than others. It indicates that prions are in our oceans and onward upstream. It indicates that prions are in our food and water supplies and reckless sewage management is contributing to the problem. It reminds us of the hazards associated with wastewater reuse, sewage sludge disposal and biosolids in our communities and watersheds.

Prions have already left Pandora’s box. It’s easy to spot areas of mismanagement. If we fail to connect the dots and react soon enough, it won’t matter. What can we learn from the Baltic Sea, Iceland, the Faroe Islands and whales? Prions are building up in the environment and in mammals now. Eating infected mammals spreads the disease up the food chain.

public relations firm Alzheimer's disease

Crossbow Communications specializes in issue management and public affairs. Call 602-999-7204 (USA) or write to Gary Chandler to join our campaign and coalition for truth and reform.

Alzheimer’s Disease Taking Omar Sharif

Sharif Latest Victim Of Global Epidemic

Legendary actor Omar Sharif is battling Alzheimer’s disease, his agent Steve Kenis confirmed. He said that the 83-year-old actor was resting at his home in Egypt. No additional details were provided about the 83-year-old actor or his care. His son, Tarek Sharif, revealed the diagnosis just a few days earlier.

Omar Sharif Alzheimer's disease

“It’s difficult to determine what stage it’s at. It’s obvious he’ll never improve and it will get worse. He still knows he’s a famous actor. The loss of memory affects above all specific things, details like when he was in a specific place or who he acted with in a specific film,” Tarek El-Sharif told El Mundo.

“He remembers, for example, that it was Doctor Zhivago but he’s forgotten when it was filmed. He can talk about the film but he forgets its name or he calls it something else instead like Lawrence of Arabia.”

Sharif began his career in the 1950s. His role in Lawrence of Arabia in 1962 earned him two Golden Globe awards and an Academy Award nomination for Best Supporting Actor. He also played the lead role in Doctor Zhivago in 1965, which earned him another Golden Globe. He also starred in Funny Girl with Barbara Streisand in 1968.

Alzheimer’s Diagnoses Withheld From Millions Of Patients

Withholding Alzheimer’s Diagnosis Raises Concerns Over Malpractice, Collusion

More than 50 million people around the world have a terminal diagnosis of Alzheimer’s disease. Alzheimer’s and related neurological disease is rapidly becoming the leading cause of death around the globe. Thanks to a new report from the Alzheimer’s Association, those numbers grew exploded overnight.

Alzheimer's disease treatment

The Alzheimer’s Association’s new report raises many scathing questions over ethics, treatment, malpractice, denial of care and mismanagement. The report found that just 45 percent of Medicare patients diagnosed with Alzheimer’s disease were informed of the diagnosis by their physician. By contrast, more than 90 percent of Medicare patients with cancer said they were informed by their doctor.

“What we found is really shocking,” says Beth Kallmyer, vice president of constituent services for the Alzheimer’s Association. “This is reminiscent of what happened in the 1960s and 1970s with cancer. But that’s changed now, and it really needs to change for Alzheimer’s disease as well.”

For years, the association received complaints from family members who say that doctors are reluctant to reveal an Alzheimer’s diagnosis, Kallmyer says. So the association decided to investigate by studying medical records and survey results from Medicare recipients.

To make sure that Alzheimer’s patients hadn’t simply forgotten, the group also looked at Medicare survey responses from family members and other caregivers. The result wasn’t much better: Just 53 percent said a doctor told them of the patient’s diagnosis.

The report also found that patients with advanced Alzheimer’s disease were more likely to receive the diagnosis than people in the early stages of the disease. Doctors often blame the time constraints of short appointments. Or, it could be part of a culture of cost containment, risk management and denial in care.

“It’s difficult to disclose a diagnosis of a fatal brain disease in just a few minutes,” said Keith Fargo, director of scientific programs at the Alzheimer’s Association. “It’s also hard for doctors to tell patients they have a fatal disease that can’t be cured. And doctors often fear the emotional reaction an Alzheimer’s diagnosis can cause. By the time people are diagnosed with Alzheimer’s disease they are already losing cognitive functions. That’s distressing. Not knowing why is confusing and frightening.”

Alzheimer’s Disease Diagnosis Not A Precise Science

Let’s refresh our memories on some critical facts about Alzheimer’s disease diagnoses. It’s far from precise. In fact, it’s impossible to diagnose Alzheimer’s disease without an autopsy (which doesn’t happen). After the process of elimination, doctors can only guess at which neurological disease to diagnose.

This is where it gets complicated. Unfortunately, Alzheimer’s disease is a member of an aggressive family of neurodegenerative diseases known as Transmissible Spongiform Encephalopathy (TSE)Again, the operative word is “transmissible.” Related diseases are killing wildlife and livestock. Unfortunately, the TSE epidemic represents an environmental nightmare. The outbreak threatens every mammal on Earth.

TSEs include Alzheimer’s disease, Creutzfeldt-Jakob disease, Huntington’s disease, and Parkinson’s disease. TSEs also include mad cow disease and chronic wasting disease in deer. Few, if any, mammals are immune. There is no cure and there is no species barrier.

TSEs are caused by a deadly proteins called prions (PREE-on). Prion disease is unstoppable and the pathogen spreads through bodily fluids and cell tissue. Prions linger in the environment, homes, hospitals, nursing homes, dental offices, restaurants and many other places infinitely. They migrate, mutate, multiply and kill with unparalleled efficiency. Prions defy all attempts at sterilization and inactivation. Victims of the disease can spread the disease even further via bodily fluids and cell tissue. Victims often are contagious long before they appear sick.

What does all of this background have to do with an Alzheimer’s disease diagnosis? Doctors can’t tell the difference between any of the human forms of prion disease. They basically read the wind, flip a coin and diagnose the patient’s symptoms as Alzheimer’s disease, Creutzfeldt-Jakob disease (CJD) or Parkinson’s disease. It would better serve the public to stop the name game and use the most common term–prion disease. All patients should trigger the same protocol in care and safeguards to the public.

Prions and Alzheimer's disease

“The (human) brain diseases caused by prions includes Alzheimer’s, Parkinson’s, Huntington’s, amyotrophic lateral sclerosis (Lou Gehrig’s disease), and other disorders known as frontotemporal dementias,” said Nobel Laureate Stanley Prusiner, who earned a Nobel Prize in Physiology in 1997 for discovering deadly prions.

Safeguard Protocols For Prion Disease Not Uniform

Unfortunately, the protocol for patient care is vastly different for CJD and related prion diseases. That’s a mistake. CJD is handled with the respect that a prion disease demands. Alzheimer’s disease is not. Hospitals, doctors and even coroners handle CJD with a wide berth, if at all. Unfortunately, they fail to warn family members. Meanwhile, no one is talking about the transmissible aspect of Alzheimer’s disease. That’s another mistake.

With this background in mind, let’s get back to the issue of doctors withholding information about patients. What does this pattern of activity suggest:

  1. The size of the epidemic is much larger than estimates, which means that it will spread even faster. The latest estimates claim about 45 million people globally who are battling Alzheimer’s disease today. It’s been commonly estimated that two-thirds of cases are undiagnosed. This new report suggests that it could be much higher. Alzheimer’s was already the fifth-highest cause of death in the world. If more than half of the cases are going undiagnosed, neurological disease could already top the list.
  2. Ethical issues abound. Withholding information, even if only suspicions, can delay treatment and humane care. It also can put caregivers in harms way with a sense of false security (given the transmissibility of the disease and the precautions that should be given to caregivers).
  3. Malpractice issues abound. This knife cuts both ways. Doctors could be withholding opinions to avoid malpractice issues over misdiagnosis. Plus, the protocols for patient care and caregiver precautions are vastly different between Alzheimer’s disease and CJD. Since the diseases are handled differently, malpractice issues over misdiagnosis face doctors and hospitals.
  4. Many health experts have predicted that the global surge in dementia cases will bankrupt nations, states and insurance carriers that can’t dodge the bullet. What type of industry guidance is shaping this wave of denial in care? Are insurance companies urging doctors and hospitals to avoid the dicey waters of prion disease? Do insurance companies hope to avoid the murky waters and severe costs associated with patient care? Are governments trying to dilute the true size of the largest health threat on the planet today?
  5. Isn’t it time to offer safeguards and guidance to caregivers and family members to minimize the risk of exposure to deadly prions from patients fighting Alzheimer’s disease, CJD, Huntington’s, ALS and Parkinson’s diseases?
  6. Given the size and speed of this epidemic, isn’t it time to reconsider what we are doing with the infectious waste from millions of infected people around the world? Is it really a good idea to reuse their wastewater and sewage sludge (biosolids)? Is it a good idea to dump their sewage on our crops, golf courses, playgrounds and lawns or in our rivers and oceans? Hospitals dispose of anything that might have possibly been infected by prions. Sterilization is impossible. Therefore, prions in sewage cannot be stopped with wishful thinking. Prions migrate, mutate and multiply. Prions are an environmental nightmare that make radiation look like candy.

Alzheimer's disease research

As you can see, the new report from the Alzheimer’s Association sparks more questions than it answers. We seek allies in pursuit of truth and reforms. Please join us.

Please Read The Full Story At

Alzheimer’s Action Plans Not Strong Enough In U.S.

Alzheimer’s Association Offers Recommendations For Faster Progress

The U.S. Government has initiated a major effort to prevent and effectively treat Alzheimer’s disease by 2025. However, a workgroup of nearly 40 Alzheimer’s researchers and scientists says the research milestones in the U.S. Government’s National Plan to Address Alzheimer’s Disease must be broadened in scope, increased in scale, and adequately funded in order to make an impact on the Alzheimer’s epidemic.

Alzheimer's disease treatment

A series of proposals by the workgroup to enlarge and strengthen the Plan are published today in Alzheimer’s & Dementia: the Journal of the Alzheimer’s Association. According to the authors of the newly published article, who include U.S.-based academic and industry scientists across all disciplines of Alzheimer’s research, “Many prominent investigators believe the prospect of delaying the onset of disabling symptoms within a decade is an attainable goal, provided we can surmount several scientific, administrative, and most importantly, financial impediments.” The authors continue,

“Inadequate funding remains the single most important impediment to progress in achieving the research goal of the National Alzheimer’s Plan.”

There are more than 5 million Americans currently living with Alzheimer’s at a cost to the nation of $214 billion, according to the Alzheimer’s Association 2014 Alzheimer’s Disease Facts and Figures report. With Americans living longer than ever before, these numbers are set to soar to as many as 16 million people living with Alzheimer’s disease at an unsustainable cost to the nation of $1.2 trillion by 2050.

“We are a scant 11 years from the 2025 goal of the Plan, and we have no time to lose,” said Maria Carrillo, Ph.D., Alzheimer’s Association vice president of Medical and Scientific Relations and a co-author of the article. “We commend the U.S. National Institute on Aging for creating the original milestones that have been incorporated into the Plan, and for committing to revising these milestones regularly. Further, the NIA has created an excellent opportunity to update these milestones in conjunction with its Alzheimer’s Disease Research Summit to be held in February 2015. While our workgroup does not believe the milestones, as they currently stand, are sufficient to reach the 2025 goal, if the suggested updates are swiftly implemented and funded we believe prospects for being able to prevent and effectively treat Alzheimer’s by 2025 will increase dramatically.”

“This article is the voice of leading scientists recommending what needs to be incorporated into the Plan’s milestones now to prevent and effectively treat Alzheimer’s and other dementias,” said William Klunk, M.D., Ph.D., chair of the Alzheimer’s Association Medical and Scientific Advisory Council and a co-author of the article. “The suggested milestones outlined in the article identify significant increases in the scope and scale of Alzheimer’s research, which would bring Alzheimer’s research efforts more closely into line with the scale of activity needed to make substantial progress against other major diseases like Cancer and HIV/AIDS. The proposed revisions are meant to ensure that the National Alzheimer’s Plan’s milestones outline an adequate level of both the types and amount of research that are needed to achieve the 2025 goal.”

Klunk is a Distinguished Professor of Psychiatry and Neurology at the University of Pittsburgh School of Medicine in Pittsburgh, PA. He is also the Co-Director of the Alzheimer’s Disease Research Center at the University of Pittsburgh.

treat Alzheimer's disease

New Objectives For Alzheimer’s Research, Treatment, Prevention

The National Alzheimer’s Project Act (NAPA) was signed into law in 2011, calling for the development of the country’s first-ever National Plan to Address Alzheimer’s Disease. The Plan, released in 2012, outlined a set of initiatives to provide improved tools for doctors, assist caregivers and individuals with Alzheimer’s and other dementias, raise public awareness about the disease, and advance research. It set an aggressive research goal to “Prevent and Effectively Treat Alzheimer’s Disease by 2025.”

A variety of strategies were created, including identifying “research priorities and milestones.” The U.S. Department of Health and Human Services approved a set of interim milestones in 2013 to provide a roadmap toward achieving the Plan’s 2025 goal.

In June 2014, the Alzheimer’s Association convened an expert workgroup to evaluate the milestones, determine whether the field is on track to achieve them, recommend changes in the parameters of the milestones, identify unaddressed gaps, and recommend additional milestones to fill these gaps. The workgroup consisted of world-renowned experts in Alzheimer’s research and policy.

One goal of the workgroup was to stimulate thinking about the Plan milestones at the upcoming NIA Alzheimer’s Disease Research Summit to improve the dialoge about Alzheimer’s disease.

The recommendations from the Alzheimer’s Association suggest that Alzheimer’s disease research must be expanded in scale and scope, including:

  • More clinical trials, testing more drugs – and more non-drug strategies – against more targets, involving more people and more diverse populations, aimed at treating and preventing more types of symptoms.
  • More basic research to discover and validate additional biomarkers and uncover new therapeutic targets.
  • And a stronger research system and infrastructure with more data sharing and collaboration, conducted in a more interdisciplinary manner with increased emphasis on research to identify and translate effective treatments to medically accepted and widespread use.

The authors suggest revisions to a majority of the existing Plan milestones, and propose 25 new milestones. Those of greatest urgency and highest potential impact are in drug development, risk reduction, and new conceptual models of Alzheimer’s.

Alzheimer’s Treatments

Six current milestones focus on developing novel targets into effective treatments. The expert workgroup supported the overall goals of these milestones, but commented that history shows that only about 13 percent of new drugs make it from the preclinical stage to Phase III trials.

  • This suggests that to achieve the stated success criteria, approximately 23 drugs and/or targets would need to be identified, characterized, and validated. The current milestone only calls for six.
  • In fact, because novel targets need to be identified across many pathways and mechanisms (e.g., reducing amyloid, reducing inflammation) the workgroup suggests that, in reality, a much larger number – 60 – will likely need to be identified.
  • The expert workgroup recommends that the numbers and projected costs in these milestones be adjusted to more accurately reflect the reality of drug development.

Current milestones concerning the development of drugs against known targets call for initiation of three to six Phase II drug trials, at least two of which should be in asymptomatic subjects.

  • The workgroup says, “given the high attrition rate in Phase II trials to date, to achieve the success criteria … perhaps 12 or more trials will need to be initiated. … The milestone also calls for trials of agents against three to six therapeutic targets, so these trials will need to involve targets beyond amyloid.” These targets could include tau, inflammation, and nicotinic agonist receptors, according to the article.

Current milestones call for initiation of Phase III trials against at least three known targets, with at least one of these trials in asymptomatic, at risk subjects. Currently, four asymptomatic Phase III trials are already underway.

  • The authors suggest that the milestone be revised to reflect the large number of Phase III trials that will need to be initiated to achieve three successful trials, and that at least one trial should be of a symptomatic therapy.

Alzheimer’s Disease Prevention

Epidemiological studies have provided important information about the many possible exposures that influence the risk of developing Alzheimer’s and other dementias. These include genetic, vascular, psychosocial, dietary, and other lifestyle factors. The utility and importance of epidemiologic studies have been confirmed with the recent success reported at the 2014 Alzheimer’s Association International Conference of an early analysis of the Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER) multidomain prevention trial. All the factors used as part of the intervention in this trial—diet, physical exercise, cognitive training, social activities, and control of vascular risk factors—were identified through epidemiologic studies. However, more resources must be committed to epidemiological infrastructure and studies to fully harness the power of this methodology.

  • The expert workgroup calls for, among other things, a reframing of the Plan milestones to focus more broadly on risk issues and prevention of cognitive impairment and dementia across the entire lifespan. Studies generated to meet these milestones should be attentive to changing demographics and ethnic and racial shifts in the population, and should have harmonized data collection methods.
  • The workgroup further recommends the initiation of a large, multidomain prevention trial focused on modifiable risk factors in the United States to replicate the results of the FINGER trial in a larger, more diverse population.

New Alzheimer’s Treatment Models

Given that current approaches to treatment have not yet resulted in effective new therapies, strategies are needed to re-examine existing paradigms and consider new conceptual models of Alzheimer’s. The Alzheimer’s Association convened Research Roundtables in 2006 and 2012 to explore mechanisms other than the dominant amyloid hypothesis that may contribute to neurodegeneration in Alzheimer’s. Pathways identified that may offer additional therapeutic targets include those associated with aging, such as synaptic loss, decreased neurogenesis, cell death through internal mechanisms, and insulin resistance; and cell cycle events and other cellular processes such as inflammation, mitochondrial dysfunction, and alterations in various proteins.

Among the barriers to exploring these alternative hypotheses has been a lack of tools, infrastructure, and resources, especially for basic science and pre-clinical research. Recommended new research milestones for this area include:

  • Creation of several mechanisms for funding a substantial training and research program on the basic biology of aging, vulnerabilities and diseases of the brain and nervous system, and the biological underpinnings of “super-aging.”
  • Convening a “think tank” to reexamine conceptual models of Alzheimer’s disease.

Click here for more information on Alzheimer’s research and the National Alzheimer’s

AC/DC Founder Rocked By Brain Disease

Malcolm Young Leaves Band Because Of Dementia

The family of founding AC/DC guitarist Malcolm Young has confirmed the illness that forced the 61-year-old to quit the band because of dementia symptoms.

“Malcolm is suffering from dementia and the family thanks you for respecting their privacy,” they said in a statement, according to People magazine.

malcolm young AC/DC dementia

The group had previously announced in April that Young would be taking a break from the band and that it would be recording a new record without him. When AC/DC announced that it would be putting out the record, “Rock or Bust,” this fall, they confirmed that Young would not be returning to the band, “due to the nature of Malcolm’s condition.” They did not go into the specifics of the illness.

Young’s nephew, Stevie Young, played rhythm guitar in Malcolm’s stead on “Rock or Bust.” He will also be filling in for the elder Young on the group’s upcoming world tour in 2015. According to a family friend, the guitarist could no longer remember how to play AC/DC songs.

“If you were in the room with Malcolm and walked out, then came back in one minute later, he wouldn’t remember you. He has a complete loss of short-term memory,” according to an unnamed source.

Scottish-born brothers Malcolm and Angus Young formed AC/DC in 1973. The Australian band sold more than 200 million albums, with their 1980 record Back in Black their biggest-selling hit.

“We miss Malcolm, obviously,” AC/DC frontman Brian Johnson told Classic Rock in July at a time when the band was optimistic about the guitarist’s return. “He’s a fighter. He’s in the hospital, but he’s a fighter. We’ve got our fingers crossed that he’ll get strong again. … Stevie, Malcolm’s nephew, was magnificent, but when you’re recording with this thing hanging over you and your work mate isn’t well, it’s difficult. But I’m sure (Malcolm) was rooting for us.”


Alzheimer's disease treatment