Preventing Dementia A Major Challenge

New Report Offers Little Hope In Battle Against Neurodegenerative Disease

By Sharon Begley, STAT

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

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

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

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

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

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

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

prevent Alzheimer's disease

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

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

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

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

Neurodegenerative Disease News via STAT

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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

Alzheimer’s Disease Influenced By Acidity

pH Level Might Deter, Slow Progression Of Alzheimer’s Disease

Prion diseases are scary, incurable and fatal. They first gained notoriety when cows became infected by prion proteins and, in turn, infected people. Fervor surrounding mad cow disease resulted in the U.S. banning imports of beef from the European Union for 15 years.

New research led by Michigan State University and published in the current issue of the Proceedings of the National Academy of Sciences, offers hope by showing how we might prevent prions from aggregating or growing into deadly diseases.

Lisa Lapidus, MSU professor of physics and astronomy, has pioneered a laser technique to advance her medical discoveries. The two-laser approach measures the speed at which proteins rearrange before beginning to clump, or aggregate — the critical beginning of many neurodegenerative diseases.

Alzheimer's disease diagnosis

“While prion’s transmission method is quite unusual, the process of protein clumping is quite common in a number of diseases, such as Alzheimer’s and Parkinson’s disease,” said Lapidus, who published the paper with Kinshuk Raj Srivastava, former postdoctoral fellow at MSU. “We’ve discovered that there is a ‘dangerous middle range,’ a speed that individual proteins rearrange in which clumping happens fastest. We were also able to find a way to bump the proteins out of the danger zone and reduce the chances of clumping from happening.”

Bumping proteins out of the danger zone could help advance research on prion diseases, such as fatal familial insomnia and kuru in humans, mad cow disease, and chronic wasting disease in deer.

What these prion diseases have in common, the team discovered, is the key speed changer of pH. Using the protein from a hamster, a mammal with a history of suffering from prion diseases, the team found that prion-related protein chains reconfigure slowly at neutral pH, thus avoiding the sticky middle speeds.

However, at low pH, the scientists found the protein rearranged in the dangerous middle range, confirming that prions thrived and grew when pH levels were low. To further prove this middle regime is really dangerous, they compared the speed of hamster at low pH to rabbit, an animal that doesn’t get prion disease. Rabbit prion was much faster than hamster.

“If rearrangement is fast, when two chains come into contact, they can rearrange rapidly enough to avoid making interactions that lead to clumping,” Lapidus said. “When moving slow, neither chains will have sticky patches exposed. But when the rearrangements are happening at the same speed as the random collisions between two proteins, then clumping can occur more quickly.”

Taking the research one step further, Lapidus and her team decided to see if any drugs could move hamster prions out of this danger zone. Lapidus proved that astemizole is effective in speeding up protein self-interactions even further and preventing prion clumping.

Astemizole was once used to treat allergies, but it was pulled from the market due to rare but sometimes fatal side effects. The antihistamine, however, also has shown promise in some Alzheimer’s research.

This research didn’t directly examine disease transmission, but future research could tackle this and help understand how proteins rearranging in the danger zone can be recruited by an existing clump of protein.

Alzheimer’s Disease Prevention and Treatment Update via

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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

Together We Can Prevent Alzheimer’s Disease.

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:

Pomegranate Seeds Treat Neurodegenerative Disease

Alzheimer’s Disease Treated With Antioxidant

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

Alzheimer's disease prevention tips

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

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

Alzheimer's disease treatment

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

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

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

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

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

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New Drug Offers Promise Against Alzheimer’s Disease

Treatment Purges Plaque Deposits Within Brain

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

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

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

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

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

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

Alzheimer's disease treatment

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

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

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

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

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

Prions and Alzheimer's disease

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

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

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

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

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

caregivers Alzheimer's disease

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

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

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

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

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

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

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

Alzheimer’s Disease News via

Caregivers Overwhelmed By Alzheimer’s Disease

eBook Offers Vital Tips For Caregivers, Patients

Neurodegenerative disease is the fastest-growing cause of death in the world. There are no vaccines to prevent it or cure it. Prevention is our best hope and nutrition offers the only proven hope for those who have brain disease.

Alzheimer’s disease is a member of an aggressive family of neurodegenerative diseases known as transmissible spongiform encephalopathy (TSE). As the name implies, the disease is transmissible and extremely difficult to treat.

The good news is that with the truth, caregivers can safeguard themselves and others, while treating patients with targeted nutrition that helps treat the symptoms of Alzheimer’s disease. Targeted nutrition also offers promise in preventing brain disease.

A new book by researcher Gary R. Chandler sheds light on tips for aversion and treatment of Alzheimer’s disease and other forms of neurodegenerative disease. The most common forms of neurodegenerative disease include Alzheimer’s, Parkinson’s and Creutzfeldt-Jakob disease–the most aggressive and infectious of them all.

Prions and Alzheimer's disease

According to Nobel Prize Laureate Stanley Prusiner, they are all part of the same disease spectrum—prion disease. It’s also known as transmissible spongiform encephalopathy (TSE). The operative word is “transmissible.”

TSEs are caused by a deadly protein called a prion (PREE-on). Prion disease is unstoppable. The pathogen spreads through the bodily fluids and cell tissue of its victims. Blood, saliva, mucus, milk, urine and feces carry deadly prions from the victim. All tissue is infectious.

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 often become infectious long before they appear sick.

Prions kill everything in their path—man or beast. Prions are highly infectious and the bodies of victims become highly infectious long before they look or feel sick. Blood, milk, meat, urine, saliva, mucus, feces and other bodily fluids of victims are contagious.

According to research from Duke University, caregivers of someone with dementia are six times more likely to develop the condition themselves.

Even sophisticated healthcare systems have failed to grasp the severity of prion disease. Unfortunately, hospitals around the world have been sued for spreading CJD to innocent patients. Most health care systems are still misinformed and under-informed about the dangers that CJD patients pose to others. Therefore, these care facilities are exposing others and contributing to a global mismanagement problem.

Alzheimer's disease infectious disease

Only a decade ago, the idea that Alzheimer’s disease might be transmissible between people would have been laughed away. But scientists have now shown that tissues can transmit symptoms of the disease between animals. A new study published in the journal Nature raises additional concern about the transmissibility of Alzheimer’s disease between people.

Prion disease is a spectrum disease because of its many mutations and because some victims appear to have a genetic predisposition to resist the disease. 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 with infectious waste.

Alzheimer's disease research

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. 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.

Alzheimer’s diagnoses are wrong at least 20 percent of the time. 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.

infectious waste and food contamination

Although there are many causes and pathways contributing to prion disease, many pathways are being mismanaged around the globe. Not only are homes and hospitals exposed to the prion pathogen, so are entire sewage treatment systems. Wastewater treatment plants are prion incubators. Sewage sludge and wastewater pumped out spread the disease.

Caring For Someone With Alzheimer’s Disease

Nearly 15 million caregivers in the U.S. work with someone who has Alzheimer’s, and approximately 70 percent of Alzheimer’s patients are cared for by relatives and friends. In addition to the truth about transmissibility, these caregivers desperately need guidance on effective treatments. The search for cures has been a total washout.

Fortunately, targeted nutrition offers promise. Some foods increase your risk of contracting brain disease, while some foods help prevent it. Other foods offer the best hope for effective treatment. For example, the eBook explains how walnuts, coconut oil, olive oil, grapes, salmon and hundreds of other foods offer proven results to people with brain disease.

Alzheimer's disease Survival Guide

Order the eBook now and learn how to:

  • 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 us at risk.

treat Alzheimer's disease

Alzheimer’s Disease Research Targets Prions

More Evidence That Prions Cause Alzheimer’s Disease

ProMIS Neurosciences highlighted the growing mountain of research, which calls out Amyloid-beta and Tau prions (proteins), as the root cause for Alzheimer’s disease. The company released a white paper today compiling the scientific data as the basis for new treatments.

Prions and Alzheimer's disease

In the white paper, the company provided a concise overview of empirical evidence from a number of leading researchers, much of it recent, that supports the methodology of selectively targeting the prion variants of Amyloid-beta and Tau.

Amyloid-beta (Aβ) acts as a causative agent in the progression of Alzheimer’s disease. Researchers also have discovered that depletion of Aβ reversed cerebral amyloidosis and associated pathology in susceptible mice.

Other research points to the likelihood that prion-like oligomers of misfolded Aβ mediate neurotoxicity and progression of Alzheimer’s disease. In the Cleary et al 2004; Jin et al 2011 studies, scientists concluded that while the presence of Aβ plaque was the calling card of Alzheimer’s disease, the synaptic loss and neurodegenerative spread of the disease were primarily mediated by soluble oligomers of misfolded Aβ rather than plaque.

Alzheimer's disease research

Even more research contends that the progressive nature of Alzheimer’s disease comes from the formation and spread of Aβ prions. As found in the Khan et al 2014 study, the self-propagation of these Aβ prions follows the stereotypical progression of AD. The prion-like spread is well-documented in animal models.

A growing body of data also indicates that the selective targeting of Aβ prions offers distinct advantages over the broadly reactive Aβ antibodies currently in clinical testing. This specificity of Aβ prion neutralization is expected to increase efficacy by mitigating “target distraction.” This means that treating physicians can preserve normal Aβ function in the patient as well as decreasing the risk of edema and vascular adverse effects.

To achieve this precision medicine approach to Alzheimer’s therapy, ProMIS employed two proprietary computational discovery technologies, ProMIS™ and Collective Coordinates to predict regions of protein most likely to unfold based on thermodynamic stability. This means the company was able to identify six predicted disease-specific epitopes of Aβ prions that would act as homing beacons for antibody therapy. Antibodies have been raised from five of the epitopes and are currently undergoing screening and validation for prion-specific binding and functional activity.


Hallucinogen Offers Promise Against Alzheimer’s Disease

Neurogenesis A Possible Treatment For Alzheimer’s Disease

Scientists have discovered that a hallucinogenic substance from the Amazon stimulates the birth of new brains cells and could lead to treatment for neurodegenerative diseases such as Alzheimer’s disease.

The tea called ayahuasca, is also used a as traditional spiritual medicine in ceremonies in Peru. The Saint Pau Hospital Barcelona, which worked in collaboration with the Beckley Foundation and Spanish National Research Council in Madrid, has released the findings from a study investigating the potential of ayahuasca to promote neurogenesis – which is the development of new brain cells. The investigators believe that these findings will open up a new avenue of research that may help develop drugs to treat diseases, such as like Alzheimer’s, Parkinson’s and addiction.

Ayahuasca and Alzheimer's disease

Dr. Jordi Riba, lead investigator, presented preliminary data, at the Interdisciplinary Conference on Psychedelic Research in Amsterdam at the weekend. Results showed two compounds – harmine and tetrahydro harmine – which are found in the hallucinogenic tea, potently stimulated the transformation of stem cells into new neurons.

Amanda Feilding, director of the Beckley Foundation said: “The images from the Beckley/Saint Pau collaboration showing the birth of new neurons are very interesting and suggest that ayahuasca could lead to a new approach in the treatment of neurodegenerative conditions such as Alzheimer’s disease and Parkinson’s disease.”

Experts have believed for years that the brain doesn’t make neurons during adulthood. In the 1990s, research changed this finding, showing that new neurons are generated throughout adult life in two regions of the human brain: the area around the ventricles and in the hippocampus.

ayahuasca and Alzheimer's disease treatment

The hippocampus, which is thought to be the center of emotion and the autonomic nervous system, plays a key role in memory. Its function declines with age and in neurological disorders. Under normal conditions, the rate of the birth of new neurons is very low, and it cannot keep up with the rate of neural death that occurs in diseases such such as Alzheimer’s disease.

In the study, neural stem cells were isolated from the hippocampus of adult mice. The stem cells were grown in the lab and substances that are present in ayahuasca were added to the cultures and compared with a saline placebo. Scientists have described the results as impressive, with ayahuasca substances stimulating the transformation of stem cells into new neurons.

Dr. Riba has studied ayahuasca for 20 years. Ayahuasca is a potent hallucinogenic brew used by shamans in the Amazon for centuries for medical and spiritual purposes. Obtained from a mixture of jungle plants, its popularity around the world has hugely increased in recent years, as an aid to spiritual exploration, psychotherapy and healing.

Alzheimer’s Disease Treatments Update via

Prevent, Treat Alzheimer’s Disease With Smart Nutrition

Nutrition Delivers Effective Compounds To Brain

Alzheimer’s, Parkinson’s, ALS and other forms of brain disease are the fastest-growing causes of death in the world. Most forms of brain disease are preventable, transmissible and treatable with targeted nutrition. That’s the theme for a new book that shines light on the global epidemic of brain disease.

Alzheimer's disease treatment

According to Gary Chandler, author of Beat Brain Disease With Smart Food, 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.

Death rates from heart disease and cancer are dropping in most countries due to advances in nutrition, medicine and disease management. Meanwhile, neurodegenerative disease is spreading exponentially. In the U.S., deaths attributed to Alzheimer’s disease increased 71 percent from 2000 to 2013, while those attributed to heart disease decreased 14 percent. Experts suggest that the prevalence of brain disease will quadruple by 2050, if not sooner.

“Unfortunately, it appears that Alzheimer’s and Parkinson’s are just as infectious as Creutzfeldt-Jakob disease,” said Chandler. “Many industry practices are based upon a faulty risk assessment.”

The most common forms of neurodegenerative disease include Alzheimer’s, Parkinson’s, ALS and Creutzfeldt-Jakob disease–the most aggressive and infectious of them all. According to Nobel Prize Laureate Stanley Prusiner, they are all part of the same disease spectrum—prion disease. It’s also known as transmissible spongiform encephalopathy (TSE). The operative word is “transmissible.”

  • Women are contracting neurodegenerative disease at twice the rate of men;
  • Caregivers (spouses) are six times more likely to contract brain disease (most caregivers are women); and
  • People in Finland, Iceland, Sweden and the United States have the highest prevalence of Alzheimer’s disease.

Although there are many causes and pathways contributing to prion disease, many pathways are being mismanaged around the globe. Not only are homes and hospitals exposed to the prion pathogen, so are entire sewage treatment systems. Wastewater treatment plants are prion incubators. Sewage sludge and wastewater pumped out spread the disease.

infectious waste and food contamination

Sewage sludge, biosolids, and reclaimed wastewater are recycling prions from victims into our food and water supplies. 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. Avoiding prions in your food and water is a critical step in wellness. Unfortunately, it’s easier said than done.

Some foods increase your risk of contracting brain disease, while some foods help prevent it. Other foods offer the best hope for effective treatment. Most drugs offer no help at all. Drug companies are making billions selling placebos. Targeted nutrition is our best hope for prevention and treatment.

treat Alzheimer's disease

Preview and order the eBook now and learn how to:

  • 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.

Learn more about treating Alzheimer’s disease

Nutrition The Best Treatment For Alzheimer’s Disease

Only Six Drugs Approved To Treat Symptoms Of Alzheimer’s Disease

There are no cures for Alzheimer’s disease and similar forms of neurodegenerative disease. There are few effective treatments to alleviate the symptoms for Alzheimer’s disease.

Alzheimer's disease treatment

The good news is that there are several super foods that can help us avert Alzheimer’s disease in the first place. Other super foods effectively treat the symptoms of neurodegenerative disease, which can improve functioning and quality of life as the disease progresses. Walnuts are one of those super foods.

We will discuss many more nutritional treatments for Alzheimer’s disease in our upcoming documentary, Food For Thought. We also offer vital advice to caregivers, who have a 600% greater chance of contracting the disease than the average person. Learn why. 

Prions and Alzheimer's disease

Death rates from heart disease, cancer and other leading causes of death are dropping thanks to advances in medicine and disease management. Unfortunately, Alzheimer’s disease is the one glaring exception. Death rates from Alzheimer’s disease and related forms of neurodegenerative diseases are skyrocketing.

Neurodegenerative diseases are the fastest-growing cause of death today. If we had accurate mortality statistics, we would likely find that Alzheimer’s disease is already the leading cause of death. It will continue to spread around the world—to people of all ages.

There are many factors contributing to the global surge in Alzheimer’s disease. Age and genetics play a role, but it’s smaller than you realize. Due to mismanagement and misinformation, people from some regions of the world are at a higher risk than others. Finland, Iceland, Sweden and the United States have the highest rates in the world. These hot spots speak of an environmental disease not one driven by age and genetics. Women contract the disease at twice the rate of men. Why?

Alzheimer's disease prevention

Hope is on the horizon. These tips can help you and your loved ones beat and treat neurological disease. Prevention is the key.

Order the eBook now and learn how to:

  • 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.

We need your help to push for reforms that can stop the misinformation and mismanagement that are contributing to the global Alzheimer’s disease epidemic. Please contact us to find out how you can help. Write to Gary Chandler