Category Archives: Alzheimer’s

Spermidine found to lengthen lifespan in mice and to promote cardiovascular health

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After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
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Original Article Here Via Medical Xpress

(Medical Xpress)—A large team of researchers with members from several Europeans countries and the U.S. has found that mice fed a compound called spermidine lived longer than ordinary mice and also had better cardiovascular heath. In their paper published in the journal Nature Medicine, the researchers describe experiments they carried out with the compound and mice, what they found and why they believe the compound might provide benefits for humans.

Prior research has found that ingestion of spermidine—which was first discovered in semen samples, hence its name—led to longer lifespans in simple organisms such as fruit flies, yeast and roundworms. In this new study, the researchers sought to find out if the same would prove true for more complex creatures.

The researchers chose mice as their target, feeding some groups water with spermidine mixed in, while other groups received plain water. After observing the rodents over the course of their lifespans, the researchers discovered that those who had been given spermidine lived longer than those who had not—even if the supplement was not given to them until middle age. Closer examination of the rodents revealed that those given the supplement also had better heart function and lower . They also found that rats fed a high-salt diet, which causes , had lower pressure readings when given spermidine.

Prior research had also suggested that the means by which spermidine extended lifespan was by inducing autophagy in heart cells, which is where cells naturally disable parts of themselves that are dysfunctional or no longer necessary. To find out if this might be the case for rodents, the researchers conducted the same experiments using that had a genetic defect that prevented autophagy from taking place and found that feeding them spermidine did not cause them to live longer or to have improved cardiovascular health, suggesting that autophagy may, indeed, be involved in the process.

The acknowledge that there is thus far little evidence that suggests humans might receive the same benefits from consuming the compound, but note that they did conduct a survey of approximately 800 people regarding their diets and found that those that reported eating foods that contained a fair amount of the compound (mushrooms, whole grains, aged cheese, etc.) had fewer cardiovascular disease symptoms including . They suggest a much larger study should be undertaken before any real conclusions can be made.

Explore further: Healthy ageing—longer healthspan with spermidine

More information: Tobias Eisenberg et al. Cardioprotection and lifespan extension by the natural polyamine spermidine, Nature Medicine (2016). DOI: 10.1038/nm.4222

Abstract
Aging is associated with an increased risk of cardiovascular disease and death. Here we show that oral supplementation of the natural polyamine spermidine extends the lifespan of mice and exerts cardioprotective effects, reducing cardiac hypertrophy and preserving diastolic function in old mice. Spermidine feeding enhanced cardiac autophagy, mitophagy and mitochondrial respiration, and it also improved the mechano-elastical properties of cardiomyocytes in vivo, coinciding with increased titin phosphorylation and suppressed subclinical inflammation. Spermidine feeding failed to provide cardioprotection in mice that lack the autophagy-related protein Atg5 in cardiomyocytes. In Dahl salt-sensitive rats that were fed a high-salt diet, a model for hypertension-induced congestive heart failure, spermidine feeding reduced systemic blood pressure, increased titin phosphorylation and prevented cardiac hypertrophy and a decline in diastolic function, thus delaying the progression to heart failure. In humans, high levels of dietary spermidine, as assessed from food questionnaires, correlated with reduced blood pressure and a lower incidence of cardiovascular disease. Our results suggest a new and feasible strategy for protection against cardiovascular disease.

Living forever as robot? Prototype lets humans upload their mind into mechanized ‘heads’

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After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
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Original Article Here

An Artificial Intelligence pioneer is embracing the controversial idea of uploading the memories, thoughts and feelings of a living person into a computer to create a Mind Clone or “second self.” The prototype for this new self is called ‘Bina-48’.

Entrepreneur Martine Rothblatt has created a new robotic head that she hopes, one day in the future, humans will be able to upload their minds into. Bina-48 is named after Rothblatt’s real-life wife, Bina Aspen, and serves as a proof-of-concept for the futuristic idea. The robot version is designed to carry on a conversation, with scientists hoping that these mind clones could give human owners a sort of artificial afterlife.

“I believe Mind Clones will be humanity’s biggest invention. The market opportunity is limitless,” Rothblatt told Bloomberg News. “Ultimately – just like we all want a smart phone, we all want a social media account – we are all going to want a Mind Clone. It will make everything in our life more useful, more valuable. It will give us twice as much time to do everything.”

Bena-48 was created five years ago as a digital replica uploaded with Bina Aspen’s thoughts, memories and feelings – all of which were broken down into computer code to create a digital version of her consciousness. Created by Hanson Robotics, Bina-48 can engage in conversation, answer questions and even have “spontaneous” thoughts that are derived from multimedia data in a “mindfile” created by the real Bina.

A similar mindfile is created when a person interacts on Twitter or Facebook and shares photos or blogs regularly – in essence, it’s a digital database of thoughts, memories, feelings and opinions. Mindware mimics the way the human brain supposedly organizes information, creates emotions and achieves self-awareness.

READ MORE: Bill Gates on AI doomsday: ‘I don’t understand why we aren’t concerned’

The proliferation of robots like Bina-48 may seem farfetched now, but Rothblatt is the woman who helped pioneered satellite radio as founder of Sirius and now oversees biotech innovation at United Therapeutics.

Mind Clone is a digital copy of your mind outside of your body,” said Rothblatt. “I think Mind Clone will look like an avatar on the screen, talking, instead of a robot version. Mind Clones are 10-20 years away.”

Am I talking about a law of physics here? Am I talking about defying gravity here? No. Am I talking about going faster than light? No. All I am doing here is talking about writing some good code.”

READ MORE: Elon Musk donates $10mn to stop AI from turning against humans

Companies such as eterni.me, Gordon Bell’s MyLifeBits, and Terasem’s Lifenaut are all pursuing Mind Clone to help a person’s personality, work and relationships survive after death.

Eterni.me is a proposed for-profit service that will reportedly offer immortality by creating “a virtual YOU, an avatar that emulates your personality and can interact with, and offer information and advice to your family and friends, even after you pass away.”

 

Drug Could Rejuvenate Aging Brain And Muscle Tissue

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Undergraduate at The University of Southern Indiana + More Years Less Tears + Your NeXt Computer
After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
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The ability of adult stem cells to renew themselves decline as we age, but researchers have discovered a small molecular drug that could ‘rejuvenate’ brain and muscle tissue. The study, published in the journal Oncotarget, successfully interrupted the activity of a growth factor in mice that has been previously shown to affect a stem cell’s ability to regenerate.

Previous research has shown that molecular changes in a stem cell microenvironment contributes to the tissues’ ability to repair damage and maintain homeostasis. Researchers found the transforming growth factor beta 1 (TGF-beta1) pathway to play a significant role in the aging of multiple stem cells. In the new study, researchers reduced TGF-beta1 activity by inserting genetic blockers into the brains of old mice. The results found tissue regeneration of stem cells to be ‘enhanced’ in old mice.

“Based on our earlier papers, the TGF-beta1 pathway seemed to be one of the main culprits in multi-tissue aging,” said co-author David Schaffer, director of the Berkeley Stem Cell Center and a professor of chemical and biomolecular engineering, in a statement. “That one protein, when upregulated, ages multiple stem cells in distinct organs, such as the brain, pancreas, heart and muscle. This is really the first demonstration that we can find a drug that makes the key TGF-beta1 pathway, which is elevated by aging, behave younger, thereby rejuvenating multiple organ systems.”

The research team injected a small molecule called Alk5 kinase inhibitor, which is known to reduce the influence of TGF-beta1, into the blood of old mice once a day for 11 days. Researchers found the small molecule had ‘perked up’ the stem cells’ ability to regenerate both brain and muscle tissue in old mice.

Researchers hope this research could result in effective treatments for combating multiple age-related degenerative disorders, which can have a range of debilitating effects

“The challenge ahead is to carefully retune the various signaling pathways in the stem cell environment, using a small number of chemicals, so that we end up recalibrating the environment to be youth-like,” Conboy said. “Dosage is going to be the key to rejuvenating the stem cell environment.”

Alzheimer’s – Glen Campbell – I’m not gonna miss you.

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Jonathon Fulkerson

Undergraduate at The University of Southern Indiana + More Years Less Tears + Your NeXt Computer
After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
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RB2015 Rejuvenation Biotechnology Conference Aug 19-21

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Jonathon Fulkerson

Undergraduate at The University of Southern Indiana + More Years Less Tears + Your NeXt Computer
After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
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RB2015

WHO ATTENDS

  • Academic Researchers
  • Pharmaceutical and Biotech Industry
  • Undergrad, Graduate and Post Doctorial Students
  • Nonprofits
  • Regulatory
  • Investors
  • The General Public

WHY ATTEND

  • Focused tracks covering three key elements of successful drug development: clinical review, therapeutic approaches, industry and policy
  • In depth examination of advances in tissue engineering and gene therapy
  • More interactivity – 6 hours of interactive discussion sessions and 17 hours of networking
  • Jobs Board – review and share the expertise needs of the industry’s leading research and development organizers
  • Understand and shape the scientific and investment opportunities of the new Rejuvenation Biotechnology Industry
  • Extended poster sessions
  • Back by popular demand – our opening evening’s entertainment will be Hal Sparks – Comedian, Actor and Musician.

Skin test may shed new light on Alzheimer’s and Parkinson’s diseases

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Jonathon Fulkerson

Undergraduate at The University of Southern Indiana + More Years Less Tears + Your NeXt Computer
After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
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Scientists have discovered a skin test that may shed new light on Alzheimer’s and Parkinson’s diseases, according to a study released today will be presented at the American Academy of Neurology’s 67th Annual Meeting in Washington, D.C., April 18 to 25, 2015.

The study showed that skin biopsies can be used to detect elevated levels of abnormal proteins found in the two diseases.

“Until now, pathological confirmation was not possible without a brain biopsy, so these diseases often go unrecognized until after the disease has progressed,” said study author Ildefonso Rodriguez-Leyva, MD, at Central Hospital at the University of San Luis Potosi in San Luis Potosi, Mexico. “We hypothesized that since skin has the same origin as brain tissue while in the embryo that they might also show the same abnormal proteins. This new test offers a potential biomarker that may allow doctors to identify and diagnose these diseases earlier on.”

For the study, researchers took skin biopsies from 20 people with Alzheimer’s disease, 16 with Parkinson’s disease and 17 with dementia caused by other conditions and compared them to 12 healthy people in the same age group. They tested these skin samples to see if specific types of altered proteins were found — ones that indicate a person has Alzheimer’s or Parkinson’s.

As compared to healthy patients and ones with dementia caused by other conditions, those with both Alzheimer’s and Parkinson’s had seven times higher levels of the tau protein. People with Parkinson’s also had an eight times higher level of alpha-synuclein protein than the healthy control group.

Alzheimer’s disease is ranked as the sixth leading cause of death in the United States, and 5.4 million Americans are currently diagnosed with Alzheimer’s disease. Parkinson’s disease affects one million Americans, with at least 60,000 new cases reported annually each year.

“More research is needed to confirm these results, but the findings are exciting because we could potentially begin to use skin biopsies from living patients to study and learn more about these diseases. This also means tissue will be much more readily available for scientists to study,” said Rodriguez-Leyva. “This procedure could be used to study not only Alzheimer’s and Parkinson’s, but also other neurodegenerative diseases.”

The study was supported by the National Council of Science and Technology of Mexico.


Story Source:

The above story is based on materials provided by American Academy of Neurology (AAN). Note: Materials may be edited for content and length.

Study Shows New Diet Lowers Risk of Alzheimer’s

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After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
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By Associate News Editor
Reviewed by John M. Grohol, Psy.D. on March 20, 2015    ~ 2 min read

Tracies Source

A new diet, known by the acronym MIND, has been found to significantly reduce a person’s risk of developing Alzheimer’s disease (AD), even when the diet is not strictly followed, according to new research published inAlzheimer’s & Dementia: The Journal of the Alzheimer’s Association.

The MIND  (Mediterranean-DASH Intervention for Neurodegenerative Delay) diet is a hybrid of the Mediterranean and DASH (Dietary Approaches to Stop Hypertension) diets, both of which have been found to reduce the risk of cardiovascular conditions, including hypertension, heart attack and stroke.

The diet was developed by nutritional epidemiologist Martha Clare Morris, Ph.D., of Rush University in Chicago, and her colleagues.

According to the study findings, the MIND diet was able to lower the risk of AD by as much as 53 percent in participants who strictly adhered to the diet, and by about 35 percent in those who followed it fairly well.

“One of the more exciting things about this is that people who adhered even moderately to the MIND diet had a reduction in their risk for AD,” said Morris, a Rush professor, assistant provost for Community Research, and director of Nutrition and Nutritional Epidemiology.

“I think that will motivate people.”

The diet is based on information accrued from years’ worth of past research about which foods and nutrients have positive and negative effects on the functioning of the brain over time. This is the first study to relate the MIND diet to Alzheimer’s disease.

For the study, the MIND diet was compared with the two other diets. People with high adherence to the DASH and Mediterranean diets also had reductions in AD — 39 percent with the DASH diet and 54 percent with the Mediterranean diet — but got insignificant benefits when they only loosely followed either diet.

The MIND diet labels 15 dietary components: 10 “brain-healthy food groups” — green leafy vegetables, other vegetables, nuts, berries, beans, whole grains, fish, poultry, olive oil, and wine — and five unhealthy groups such as red meats, butter and stick margarine, cheese, pastries, and sweets, and fried or fast food.

To follow the MIND diet, a person should eat at least three servings of whole grains, a salad and one other vegetable every day —  along with a glass of wine —  snack most days on nuts, eat beans every other day or so, eat poultry and berries at least twice a week, and eat fish at least once a week.

However, a person should limit consumption of the designated unhealthy foods, especially butter (less than one tablespoon a day), cheese, and fried or fast food (less than a serving a week for any of the three), to have a real shot at avoiding the devastating effects of AD, according to the study.

Berries are the only fruit included in the MIND diet. “Blueberries are one of the more potent foods in terms of protecting the brain,” Morris said, and strawberries have also performed well in past studies of the effect of food on cognitive function.

AD, which takes a devastating toll on cognitive function, is not unlike heart disease in that there appear to be “many factors that play into who gets the disease,” including behavioral, environmental and genetic components, Morris said.

“With late-onset AD, with that older group of people, genetic risk factors are a small piece of the picture,” she said. Research has shown that what we eat may play a significant role in determining who gets AD and who doesn’t, Morris added.

The findings also suggest that the longer a person adheres to the MIND diet, the less risk a person will have of developing AD. “You’ll be healthier if you’ve been doing the right thing for a long time,” Morris added.

Source: Rush University Medical Center

ULTRASOUND RESTORES MEMORY TO MICE WITH ALZHEIMER’S

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After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
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Alzheimer's Brain National Institute of Aging

Alzheimer’s Brain
National Institute of Aging

A PET scan of the brain of a patient with Alzheimer’s Disease (Original Source Here)

Using ultrasound waves targeted at the brain, a team of Australian researchers has restored memory to mice with Alzheimer’s disease.

More than 5 million Americans have Alzheimer’s disease, a degenerative condition that causes memory loss, behavioral changes, confusion, and disorientation. Scientists still don’t know what causes it, but they do know some of the factors that might work together to trigger the disease.

Doctors can sometimes tell if someone has Alzheimer’s because of the buildup of a plaque called amyloid-β. Over time, it seems, the brain of an Alzheimer’s patient becomes less efficient at breaking up these clumped-together proteins that can inhibit the communication between brain cells.

Researchers have been trying to find ways to break up the plaque in order to restore memory and speed up slowing brain functions. But they face a challenge because of the blood-brain barrier, a layer of tightly bound cells that separates the blood, water and other chemicals that are inside the brain from those outside it. Though this barrier wears down as a person ages, it’s still extremely difficult to penetrate, so most drugs designed to break up neural plaques don’t even reach the brain. The researchers needed to find a non-invasive way to work through the barrier without causing damage.

Over the course of several weeks, the Australian team sent ultrasound waves–sound waves that move at a much higher frequency than humans can hear–at the mice’s brains. They found that the ultrasound stimulates a particular kind of cell in the brain, called microglia, which work as the brain’s immune system, attacking things that shouldn’t be there. With more of these cells in action, the researchers found that the amount of plaque was dramatically reduced in 75 percent of mice that received the treatment. Analyses over the subsequent weeks showed that the treated mice performed better on memory and spatial recognition tests.

When the ultrasound was combined with an injection of microbubbles, it created a temporary opening in the blood-brain barrier that didn’t impair brain function. While the researchers aren’t sure if that will affect the plaque buildup, it might make it easier to administer pharmaceuticals designed to fight the plaque.

The researchers hope to test their technique on sheep with Alzheimer’s before turning to humans.

Their work was published today in Science Translational Medicine.

Memory loss associated with Alzheimer’s reversed for first time

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After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
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Original Source Here

Patient 1 had two years of progressive memory loss. She was considering quitting her job, which involved analyzing data and writing reports, she got disoriented driving, and she mixed up the names of her pets.

Patient 2 kept forgetting once-familiar faces at work, forgot his gym locker combination and had to have his assistants constantly remind him of his work schedule.

Patient 3’s memory was so bad that she used an iPad to record everything, then forgot her password. Her children noticed she commonly lost her train of thought in mid-sentence, and often asked them if they had carried out the tasks that she mistakenly thought she had asked them to do.

— “Reversal of cognitive decline: A novel therapeutic program,” UCLA/Buck Institute, 2014

Since it was first described over 100 years ago, Alzheimer’s disease has been without an effective treatment.

That may finally be about to change: In the first, small study of a novel, personalized and comprehensive program to reverse memory loss, nine of 10 participants, including those described above, displayed subjective or objective improvement in their memories beginning within three to six months.

Six patients had discontinued working or had been struggling at their jobs at the time they joined the study; all were able to return to their jobs or continue working with improved performance, and their improvements have been sustained. (The patient in treatment the longest has been receiving the therapy for two-and-a-half years.)

Among the 10 were patients with memory loss associated with Alzheimer’s disease, amnestic mild cognitive impairment or subjective cognitive impairment (in which the patient reports cognitive problems). One patient who had been diagnosed with late stage Alzheimer’s did not improve.

The study was conducted Dr. Dale Bredesen of the UCLA Mary S. Easton Center for Alzheimer’s Disease Research and the Buck Institute for Research on Aging. It is the first to suggest that memory loss in patients may be reversed — and improvement sustained — using a complex, 36-point therapeutic program that involves comprehensive diet changes, brain stimulation, exercise, sleep optimization, specific pharmaceuticals and vitamins, and multiple additional steps that affect brain chemistry.

The findings are published in the current online edition of the journal Aging.

Bredesen, UCLA’s Augustus Rose Professor of Neurology, director of the Easton Center and the paper’s author, said the findings are “very encouraging,” but he added that the results are anecdotal, and a more extensive, controlled clinical trial is needed.

No single drug has been found to stop or even slow the progression of Alzheimer’s, and drugs have only had modest effects on symptoms. “In the past decade alone, hundreds of clinical trials have been conducted for Alzheimer’s, without success, at an aggregate cost of over $1 billion,” said Bredesen, who also is a professor at the Buck Institute.

Although other chronic illnesses such as cardiovascular disease, cancer and HIV have been improved through the use of combination therapies, comprehensive combination therapies have not been explored for Alzheimer’s and other memory disorders. However, over the past few decades, genetic and biochemical research has revealed an extensive network of molecular interactions involved in the development of Alzheimer’s.

“That suggested that a broader-based therapeutic approach, rather than a single drug that aims at a single target, may be feasible and potentially more effective for the treatment of cognitive decline due to Alzheimer’s,” Bredesen said.

While extensive preclinical studies in numerous other laboratories have identified single pathogenic targets for potential intervention, in human studies, such single target therapeutic approaches have not borne out. But, said Bredesen, it’s possible that addressing multiple targets within the network underlying Alzheimer’s may be successful even when each target is affected in a relatively modest way. “In other words,” he said, “the effects of the various targets may be additive, or even synergistic.”

The uniform failure of drug trials in Alzheimer’s influenced Bredesen’s desire to better understand the fundamental nature of the disease. His laboratory has found evidence that Alzheimer’s stems from an imbalance in nerve cell signaling. In the normal brain, specific signals foster nerve connections and memory making, while balancing signals support memory loss, allowing irrelevant information to be forgotten. But in people with Alzheimer’s, the balance of these opposing signals is disturbed, nerve connections are suppressed and memories are lost.

That finding is contrary to the popular belief that Alzheimer’s is caused by the accumulation of sticky plaques in the brain. Bredesen believes the amyloid beta peptide, the source of the plaques, has a normal function in the brain, as part of a larger set of molecules that promote signals that cause nerve connections to lapse. Thus, the increase in the peptide that occurs in Alzheimer’s shifts the balance in favor of memory loss.

Bredesen therefore thought that, rather than a single targeted agent, the solution might be a multiple-component system approach, in line with the approach for other chronic illnesses.

“The existing Alzheimer’s drugs affect a single target, but Alzheimer’s disease is more complex. Imagine having a roof with 36 holes in it, and your drug patched one hole very well,” he said. “The drug may have worked, and a single hole may have been fixed, but you still have 35 other leaks, and so the underlying process may not be affected much.”

Bredesen’s approach is personalized to the patient, based on extensive testing to determine what is affecting the brain’s plasticity signaling network. In the case of the patient with the demanding job who was forgetting her way home, her therapy consisted of some, but not all, of the components of Bredesen’s program, including:

  • eliminating all simple carbohydrates, gluten and processed food from her diet, and eating more vegetables, fruits and non-farmed fish
  • meditating twice a day and beginning yoga to reduce stress
  • sleeping seven to eight hours per night, up from four to five
  • taking melatonin, methylcobalamin, vitamin D3, fish oil and coenzyme Q10 each day
  • optimizing oral hygiene using an electric flosser and electric toothbrush
  • reinstating hormone replacement therapy, which had previously been discontinued
  • fasting for a minimum of 12 hours between dinner and breakfast, and for a minimum of three hours between dinner and bedtime
  • exercising for a minimum of 30 minutes, four to six days per week

Bredesen said the program’s downsides are its complexity and that the burden falls on patients and caregivers to follow it. In the study, none of the patients was able to stick to the entire protocol. Their most common complaints were the diet and lifestyle changes, and having to take multiple pills each day.

The good news, though, said Bredesen, are the side effects: “It is noteworthy that the major side effects of this therapeutic system are improved health and an improved body mass index, a stark contrast to the side effects of many drugs.”

The results suggest that memory loss may be reversed and improvement sustained with the therapeutic program, but Bredesen cautioned that the results need to be replicated.

“The current, anecdotal results require a larger trial, not only to confirm or refute the results reported here, but also to address key questions raised, such as the degree of improvement that can be achieved routinely, how late in the course of cognitive decline reversal can be effected, whether such an approach may be effective in patients with familial Alzheimer’s disease, and last, how long improvement can be sustained,” he said.

Cognitive decline is a major concern of the aging population. Alzheimer’s affects approximately 5.4 million Americans and 30 million people globally. By 2050, without effective prevention and treatment, an estimated 160 million people globally would have the disease, including 13 million Americans, which could potentially bankrupt the Medicare system. Unlike several other chronic illnesses, the incidence of Alzheimer’s is on the rise; recent estimates suggest that it has become the third leading cause of death in the U.S. behind cardiovascular disease and cancer.

Multiple entities provided support for the study, including the National Institutes of Health (AG16570, AG034427 and AG036975). The complete list is included in the paper.