Study Finds Way to Reverse Alzheimer’s

 

Did your incompetent? doctor DO NOTHING with this earlier research?

NAD (4 posts to May 2014)

Has your incompetent board of directors not fired your doctor yet? Is 10+ years of incompetence not enough to prove incompetence?

Study Finds Way to Reverse Alzheimer’s

Summary: A new study challenges the long-held belief that Alzheimer’s disease cannot be reversed. Researchers showed that a severe drop in NAD+—a core energy molecule—drives Alzheimer’s pathology in both human brains and mouse models.

Restoring proper NAD+ balance with the drug P7C3-A20 not only prevented disease in at-risk mice but also reversed advanced pathology, repairing brain damage and fully restoring cognitive function. The findings point to a major shift in how Alzheimer’s may be treated, suggesting that recovery—not just slowing decline—could one day be achievable.

Key Facts

• Central NAD+ Failure: Human and mouse Alzheimer’s brains showed a dramatic loss of NAD+, impairing essential cellular functions.
• Reversal Achieved: Restoring NAD+ balance repaired pathology and fully recovered cognition even in mice with advanced disease.
• New Treatment Pathway: The targeted drug P7C3-A20 restored healthy NAD+ levels without the dangers linked to over-the-counter NAD+ boosters.

Source: University Hospital Cleveland Medical Center

For over a century, Alzheimer’s disease (AD) has been considered irreversible. Consequently, research has focused on disease prevention or slowing, rather than recovery.

Despite billions of dollars spent on decades of research, there has never been a clinical trial of a drug for AD with an outcome goal of reversing disease and recovering function.

Now, a research team from University Hospitals, Case Western Reserve University, and the Louis Stokes Cleveland VA Medical Center has challenged this long-held dogma in the field. They tested whether brains already badly afflicted with advanced AD could recover.

The study, led by Kalyani Chaubey, PhD, from the Pieper Laboratory, published today in Cell Reports Medicine.

Through studying diverse preclinical mouse models and human AD brains, the team showed that the brain’s failure to maintain normal levels of a central cellular energy molecule, NAD+, is a major driver of AD, and that maintaining proper NAD+ balance can prevent and even reverse the disease.

NAD+ levels decline naturally across the body, including the brain, as people age. Without proper NAD+ balance, cells eventually become unable to execute critical processes required for proper functioning and survival.

In this study, the team showed that the decline in NAD+ is even more severe in the brains of people with AD, and that this also occurs in mouse models of the disease.

While AD is a uniquely human condition, it can be studied in the laboratory with mice that have been engineered to express genetic mutations that cause AD in people. The researchers used two of these models.

One line of mice carried multiple human mutations in amyloid processing, and the other mouse line carried a human mutation in the tau protein.

Amyloid and tau pathology are two of the major early events in AD, and both lines of mice develop brain pathology resembling AD, including blood-brain barrier deterioration, axonal degeneration, neuroinflammation, impaired hippocampal neurogenesis, reduced synaptic transmission, and widespread accumulation of oxidative damage.

These mice also develop severe cognitive impairments that resemble what is seen in people with AD.

After finding that NAD+ levels in the brain declined precipitously in both human and mouse AD, the research team tested whether preventing the loss of brain NAD+ balance before disease onset, or restoring brain NAD+ balance after significant disease progression, could prevent or reverse AD, respectively.

The study was based on their previous work, published in Proceeding of the National Academy of Sciences USA, showing that restoring the brain’s NAD+ balance achieved pathological and functional recovery after severe, long-lasting traumatic brain injury.

They restored NAD+ balance by administering a now well-characterized pharmacologic agent known as P7C3-A20, developed in the Pieper lab.

Remarkably, not only did preserving NAD+ balance protect mice from developing AD, but delayed treatment in mice with advanced disease also enabled the brain to fix the major pathological events caused by the genetic mutations. Moreover, both lines of mice fully recovered cognitive function.

This was accompanied by normalized blood levels of phosphorylated tau 217, a recently approved clinical biomarker of AD in people, providing confirmation of disease reversal and highlighting a potential biomarker for future clinical trials.

“We were very excited and encouraged by our results,” said Andrew A. Pieper, MD, PhD, senior author of the study and Director of the Brain Health Medicines Center, Harrington Discovery Institute at UH.

“Restoring the brain’s energy balance achieved pathological and functional recovery in both lines of mice with advanced Alzheimer’s. Seeing this effect in two very different animal models, each driven by different genetic causes, strengthens the idea that restoring the brain’s NAD+ balance might help patients recover from Alzheimer’s.”

Dr. Pieper also holds the Morley-Mather Chair in Neuropsychiatry at UH and the CWRU Rebecca E. Barchas, MD, DLFAPA, University Professorship in Translational Psychiatry. He serves as Psychiatrist and Investigator in the Louis Stokes VA Geriatric Research Education and Clinical Center (GRECC).

The results prompt a paradigm shift in how researchers, clinicians, and patients can think about treating AD in the future.

“The key takeaway is a message of hope – the effects of Alzheimer’s disease may not be inevitably permanent,” said Dr. Pieper. “The damaged brain can, under some conditions, repair itself and regain function.”

Dr. Chaubey further explained, “Through our study, we demonstrated one drug-based way to accomplish this in animal models, and also identified candidate proteins in the human AD brain that may relate to the ability to reverse AD.”

Dr. Pieper emphasized that currently available over the counter NAD+-precursors have been shown in animal models to raise cellular NAD+ to dangerously high levels that promote cancer.

The approach in this study, however, uses a pharmacologic agent (P7C3-A20) that enables cells to maintain their proper balance of NAD+ under conditions of otherwise overwhelming stress, without elevating NAD+ to supraphysiologic levels.

“This is important when considering patient care, and clinicians should consider the possibility that therapeutic strategies aimed at restoring brain energy balance might offer a path to disease recovery,” said Dr. Pieper.

This work also encourages new research into complementary approaches and eventual testing in patients, and the technology is being commercialized by Cleveland-based company Glengary Brain Health, co-founded by Dr. Pieper.

“This new therapeutic approach to recovery needs to be moved into carefully designed human clinical trials to determine whether the efficacy seen in animal models translates to human patients,” Dr. Pieper explained.

“Additional next steps for the laboratory research include pinpointing which aspects of brain energy balance are most important for recovery, identifying and evaluating complementary approaches to Alzheimer’s reversal, and investigating whether this recovery approach is also effective in other forms of chronic, age-related neurodegenerative disease.” 

Key Questions Answered:

Q: What did researchers discover about NAD+ in Alzheimer’s disease?

A: They found that a severe decline in NAD+ is a major driver of Alzheimer’s pathology, disrupting energy balance and damaging key brain systems.

Q: Can restoring NAD+ actually reverse advanced Alzheimer’s effects?

A: Yes. In two distinct Alzheimer’s mouse models, restoring NAD+ balance repaired structural and functional brain damage and fully restored cognitive performance.

Q: Why is P7C3-A20 different from common NAD+ supplements?

A: Over-the-counter NAD+ precursors can push NAD+ to unsafe levels, but P7C3-A20 helps the brain maintain proper NAD+ balance under stress without causing harmful elevations.

Editorial Notes:

• This article was edited by a Neuroscience News editor.
• Journal paper reviewed in full.
• Additional context added by our staff.

About this Alzheimer’s disease research news

Author: Ansley Kelm
Source: University Hospitals Cleveland Medical Center
Contact: Ansley Kelm – University Hospitals Cleveland Medical Center
Image: The image is credited to Neuroscience News

Original Research: Open access.
“Pharmacologic reversal of Alzheimer’s disease in mice reveals potential therapeutic nodes in human brain” by Kalyani Chaubey et al. Cell Reports Medicine

FIRST ON CNN: Fighting early-stage Alzheimer’s with intensive lifestyle changes works, study finds

 Will your competent? doctor get this for prevention of your upcoming dementia? NO? So, you DON'T have a functioning stroke doctor, do you?

The reason you need dementia prevention: 

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.

3. A 20% chance in this research.   July 2013. 

FIRST ON CNN: Fighting early-stage Alzheimer’s with intensive lifestyle changes works, study finds

8 min read

Scroll back up to restore default view.

Brain scan from one of Dr. Richard Isaacson’s Alzheimer’s patients who has shown an improvement in brain volume. - CNN

As her memory faded from Alzheimer’s disease in her late 50s, Tammy Maida began to lose track of her life. Car keys, eyeglasses and her purse disappeared multiple times a day. Key characters in novels she was reading were forgotten. Groceries were left in the garage. Keeping the books for the family’s businesses became impossible.

“I honestly thought I was losing my mind, and the fear of losing my mind was frightening,” Maida told CNN Chief Medical Correspondent Dr. Sanjay Gupta in the 2024 CNN documentary “The Last Alzheimer’s Patient.”

After 20 weeks in a randomized clinical trial designed to drastically change her diet, exercise, stress levels and social interactions, Maida’s cognition improved. She was able to read and recall novels and correctly balance spreadsheets again. A blood test even found levels of amyloid, a hallmark of Alzheimer’s disease, were retreating in her brain, according to the study published in June 2024.

“I’m coming back. It was really good — like I was prior to the disease being diagnosed,” Maida, now 68, told a researcher on the study. “An older but better version of me.”

Due to her cognitive improvement, Tammy Maida (left) and her husband Paul enjoy biking together again. - CNN

Maida’s cognition showed additional improvement, however, after she completed a total of 40 weeks of intensive lifestyle changes, said principal investigator Dr. Dean Ornish, a clinical professor of medicine at the University of California, San Francisco, and creator of the Ornish diet and lifestyle medicine program.

Ornish gave a study update on Tuesday at the 2025 Alzheimer’s Association International Conference in Toronto.

While not everyone in the 26-person interventional group benefited, 46% showed improvement in three of four standardized tests, he said, including one that measures changes in memory, judgment and problem-solving as well as the ability to function at home, practice hobbies and practice personal hygiene.“An additional 37.5% of people showed no decline in cognition during those 40 weeks,” Ornish said. “Thus, over 83% of patients improved or maintained their cognition during the five-month program.”

The new findings mirrored those of other studies on lifestyle interventions, he said, including the recent US POINTER study, the largest clinical trial in the United States to test moderate lifestyle interventions over two years in people who are at risk but do not yet have Alzheimer’s disease.

“Our study complements these findings by showing, for the first time, that more intensive lifestyle changes may often stop or even begin to reverse the decline in cognition in many of those who already have Alzheimer’s disease, and these improvements often continue over a longer period of time,” Ornish told CNN.

And unlike available medications for Alzheimer’s, he added, lifestyle changes have no side effects, such as bleeding and swelling in the brain that may occur with the newest class of drugs.

EmblemHealth, a New York-based insurance company, announced Tuesday that it will be the first health insurer to cover the Ornish lifestyle medicine program for patients who have early-stage Alzheimer’s disease.

‘Eat well, move more, stress less and love more’

The lifestyle intervention Ornish created — which he calls “eat well, move more, stress less and love more” — has been tested before. In 1990, Ornish showed for the first time in a randomized clinical trial that coronary artery disease could often be reversed with nothing more than diet, exercise, stress reduction and social support.

The US Centers for Medicare and Medicaid Services, or CMS, declared in 2010 that Ornish’s program for reversing heart disease was an “intensive cardiac rehabilitation” and that it would be eligible for reimbursement under Medicare.

Additional research has shown the same four-part program can lower blood sugars and heart disease risk in patients with diabetes, reduce prostate cancer cell growth, improve depression and even lengthen telomeres, the protective caps of chromosomes that are worn away by aging.

During the Ornish intervention, one group of people consumed a strict vegan diet, did daily aerobic exercise, practiced stress reduction and engaged in online support groups. The rest of the participants were in a control group and were asked to not make any changes in their daily habits.

Therapists led hour-long group sessions three times a week in which participants were encouraged to share their feelings and ask for support. Meditation, deep breathing, yoga and other ways to reduce stress took up another hour every day. The program also encouraged participants to prioritize good-quality sleep.

Supplements were provided to everyone in the intervention group, including a daily multivitamin, omega-3 fatty acids with curcumin, coenzyme Q10, vitamin C and B12, magnesium, a probiotic, and Lion’s mane mushroom.

In addition to online strength training led by a physical trainer, people in the intervention attended hour-long video classes on vegan nutrition hosted by a dietitian. Then, to ensure a vegan diet was followed, all meals and snacks for both participants and their partners were delivered to their homes.

Complex carbs found in whole grains, vegetables, fruits, tofu, nuts and seeds made up most of the diet. Sugar, alcohol and refined carbs found in processed and ultraprocessed foods were taboo. While calories were unrestricted, protein and total fat made up only some 18% of the daily caloric intake — far less than the typical protein intake by the average American, Ornish said.

Working harder pays off

People in the intervention group who put the most effort into changing their lifestyle have the most improvement in their cognition, said Ornish, founder and president of the nonprofit Preventive Medicine Research Institute and coauthor of “Undo It! How Simple Lifestyle Changes Can Reverse Most Chronic Diseases.”

“There was a statistically significant dose-response relationship between the degree of adherence to our lifestyle changes and the degree of improvement we saw on measures of cognition,” Ornish said.

The 25 people in the study’s original 20-week control group — who did not receive the intervention — had shown further cognitive decline during the program. They were later allowed to join the intervention for 40 weeks and significantly improved their cognitive scores during that time, Ornish said.

It all makes sense, said co-senior study author Rudy Tanzi, an Alzheimer’s researcher and professor of neurology at Harvard Medical School in Boston.

“If you picture a brain full of damage as a sink full of water, when you just turn off the tap, it takes a long time for that sink to slowly drain, right?” Tanzi told CNN in 2024. “If you want the amyloid to go down in 20 weeks, as we found on one blood test, you’re going to need a Roto-Rooter.”

Additional blood testing may offer insights

In the 2024 study, a blood test called plasma Aβ42/40 showed a significant improvement in the original intervention group. Aβ42/40 measures the level of amyloid in the blood, a key symptom of Alzheimer’s.

Tests that measure amyloid in different ways, however, did not show improvement, Dr. Suzanne Schindler, an associate professor of neurology at Washington University School of Medicine in St. Louis who specializes in blood biomarkers told CNN at the time.

There was no significant change in a test for amyloid called p-tau 181, considered to be a superior measure of Alzheimer’s risk, said Schindler, who was not involved in the study. Nor was there any change in glial fibrillary acidic protein, or GFAP, another blood biomarker that seems to correlate reasonably well with Alzheimer’s disease.

“If one of these markers improves, you typically see all of them improve, so the fact they did not makes me wonder whether this effect is real,” Schindler said. “If they were to repeat the study with a much larger population for a longer period of time, perhaps more change could be seen.”

Over the complete 40-week program, however, a number of people in the intervention group did continue to improve their Aβ42/40 scores, according to the study update.

“Changes in amyloid — as measured as the plasma Aβ42/40 ratio — occur before changes in tau markers such as p-tau 218, so this is not surprising after only 40 weeks,” Ornish said.

For Ornish, who has watched members of his family die from Alzheimer’s disease, the study’s results are important for one key reason — hope.

“So often when people get a diagnosis of dementia or Alzheimer’s, they are told by their doctors that there is no future, ‘It’s only going to get worse, get your affairs in order.’ That’s horrible news and is almost self-fulfilling,” Ornish said.

“Our new findings empower patients who have early-stage Alzheimer’s disease with the knowledge that if they make and maintain these intensive lifestyle changes, there is a reasonably good chance that they may slow the progression of the disease and often even improve it,” he said.

“Our study needs to be replicated with larger, more diverse groups of patients to make it more generalizable,” Ornish said. “But the findings we reported today are giving many people new hope and new choices — and the only side effects are good ones.”

Get inspired by a weekly roundup on living well, made simple. Sign up for CNN’s Life, But Better newsletter for information and tools designed to improve your well-being.

Efficacy and safety of lanabecestat for treatment of early and mild Alzheimer disease: The amaranth and daybreak-ALZ randomized clinical trials

You might very well need this, assuming your doctor is up-to-date on stroke research and is creating protocols to prevent your dementia. Also assumes your doctor even knows of your need for this.

Your chances of getting dementia.

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

5. Parkinson’s Disease May Have Link to Stroke March 2017

 

Efficacy and safety of lanabecestat for treatment of early and mild Alzheimer disease: The amaranth and daybreak-ALZ randomized clinical trials

JAMA — Wessels AM, Tariot PN, Zimmer JA, et al. | February 17, 2020

Advertisement

Researchers investigated whether lanabecestat slows the progression of Alzheimer disease (AD) compared with placebo in patients with early AD (mild cognitive impairment) and mild AD dementia. They performed two multicenter, global, double-blind studies at 257 and 251 centers in 15 and 18 countries or territories, respectively. AMARANTH included 2,218 randomized participants, of whom 539 individuals completed the study. DAYBREAK-ALZ included 1,722 (30.2%) randomized participants, of whom 76 individuals completed the study. In all, the researchers found that although lanabecestat was generally well tolerated, it did not slow cognitive or functional decline in individuals with early or mild AD dementia.

Read the full article on JAMA

Flickering Light Convinces Brain Proteins to Fight Alzheimer’s Disease

Did your stroke hospital and doctors going do one damn thing when this came out a year ago to see this gets tested in humans? Or will they sit with their heads up their asses sucking on their thumbs waiting for SOMEONE ELSE TO SOLVE THE PROBLEM? 

 

Flashing Light, Sound Restore Memory in Alzheimer's Mice Flashing Light, Sound Restore Memory in Alzheimer's Mice March 2019

 

Are you willing to try this even without human research? What is the downside?

The latest here which your stroke hospital will also ignore. Do you prefer your incompetency NOT KNOWING, or NOT DOING?

Flickering Light Convinces Brain Proteins to Fight Alzheimer’s Disease

Building upon a significant 2016 study that established a link between flickering light and Alzheimer’s treatment, researchers at Georgia Tech have now tapped into the brain chemistry behind the light’s effectiveness.
The original study, authored by Annabelle Singer when she was a professor at MIT, discovered that light flickering at 40 Hz entices brain immune cells—called microglia—to purge amyloid beta plaque, which have long been linked to the onset of Alzheimer’s Disease. The 40 Hz frequency stems from the observation that brains of Alzheimer's patients suffer early on from a lack of gamma, moments of gentle, constant brain waves that activate neuron activity. Its most common frequency is around 40 Hz—making that number the perfect target. (It’s worth nothing that, in an unrelated 2016 study, research connected gamma to working memory, a function key to train of thought.)
In the current study, Singer and colleagues in her Georgia Tech lab exposed healthy mice to light pulsing at 40 Hz and saw a surge of cytokines, accompanied by phosphoproteins. According to the researchers, the surging cytokines hinted at a connection with microglial activity, and in particular, the cytokine Macrophage Colony-Stimulating Factor (M-CSF). Since the phosphoproteins showed up first—about 15 minutes into the flickering of the light—the researchers hypothesize the proteins actually triggered the release of the cytokines at about the 1-hour mark.
“The vast majority of cytokines went up, some anti-inflammatory and some inflammatory, and it was a transient response,” said Georgia Tech’s Levi Wood, who co-led the study. “Often, a transient inflammatory response can promote pathogen clearance; it can promote repair.”
Interestingly, while the study was conducted on mice, the results are directly related to an undergoing human clinical trial at Emory University.
"I'll be running samples from mice in the lab, and around the same time, a colleague will be doing a strikingly similar analysis on patient fluid samples," said Kristie Garza, graduate research assistant in the Singer Lab and the study's first author.
In future studies, the researchers plan to look for a causal connection between a surge of cytokines and microglia activation. Additionally, based on results from stimuli intended as controls, the researchers may examine additional light frequencies—especially 20 Hz.
“At 20 Hz, cytokine levels were way down. That could be useful, too. There may be circumstances where you want to suppress cytokines,” said Singer. “We're thinking different kinds of stimulation could potentially become a platform of tools in a variety of contexts like Parkinson's or schizophrenia. Many neurological disorders are associated with immune response.”

Alzheimer’s disease may be combated by improving blood vessel health in the brain

You will need this. Ask your doctor for EXACT PROTOCOLS that improve cerebral blood vessel health. 

Your chances of getting dementia.

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

5. Parkinson’s Disease May Have Link to Stroke March 2017

 

Alzheimer’s disease may be combated by improving blood vessel health in the brain

A build-up of amyloid-beta in the brain is, by theory, a possible cause of Alzheimer’s disease among older adults. In a recent study, a team of researchers determined how such accumulation could be prevented and even treated.
According to the study, published in the peer-reviewed journal Neuron, improving blood vessel health in the brain may be a new route for combating the neurodegenerative disease.
The study focused on vasomotion, slow vessel pulsations associated with the clearance of substances from the brain, possibly affecting the accumulation of amyloid-beta. Such protein fragments are considered a hallmark sign for Alzheimer’s disease, based on countless studies targeting neurodegeneration.
For the study, researchers administered to rodents dextran, a fluorescently labeled carbohydrate, initiating imaging tests thereafter.
Upon evaluating the findings, researchers quickly noticed something aberrant: Vasomotion was detrimental in clearing dextran from the brain. Also, vessel pulsations were inhibited and clearance rates abated in rodents with cerebral amyloid angiopathy.
“Vasomotion correlated with paravascular clearance of fluorescent dextran from the interstitial fluid,” Susanne van Veluw, co-author of the study, explained.
“Increasing the amplitude of vasomotion by means of visually evoked vascular responses resulted in increased clearance rates in the visual cortex of awake mice. Evoked vascular reactivity was impaired in mice with CAA, which corresponded to slower clearance rates.”
Overall, the findings bring new light on how maintaining healthy vasculature may be beneficial for patients with Alzheimer’s disease.
“Our findings highlight the importance of the vasculature in the pathophysiology of Alzheimer’s disease.”
“If we direct therapeutic strategies towards promoting healthy vasculature and therefore improve clearance of amyloid-beta from the brain, we may be able to prevent or delay the onset of Alzheimer’s disease in the future.”

Seaweed-Based Drug Approved for Alzheimer's in China

What is your doctor and stroke hospital doing to ensure this gets tested for our use? NOTHING? Then have them fired. Or do they prefer you travel to China for medical interventions?  

You will need this because of these chances:

Your chances of getting dementia.

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

5. Parkinson’s Disease May Have Link to Stroke March 2017

Seaweed-Based Drug Approved for Alzheimer's in China

Oligomannate appears to affect gut microbiota, peripheral inflammation

by Judy George, Senior Staff Writer, MedPage Today November 4, 2019

A seaweed-derived oligomannate preparation (GV-971) received approval from China's National Medical Products Administration (NMPA) to treat mild to moderate Alzheimer's disease, Shanghai Green Valley Pharmaceuticals announced.
A phase III clinical trial of 818 patients with mild-to-moderate Alzheimer's disease showed that oligomannate improved cognition by week 4, showing a mean difference in ADAS-Cog 12 scores of 2.54 (P< 0.0001) between treatment and placebo arms with sustained efficacy until the end of 9 months of treatment, Green Valley said in a press release. The drug was well tolerated and adverse effects in each arm were comparable, the company added.
Full outcomes of the trial have not yet been published, but preclinical data reported in Cell Research showed that, in mice, sodium oligomannate changed gut microbiota, modulated peripheral and central inflammation, and was tied to changes in behavior and Alzheimer's-related pathology. In a commentary accompanying the preclinical study, David Holtzman, MD, of Washington University in St. Louis, and co-authors noted that "GV-971 decreases Aβ-related pathologies by reconditioning the gut microbiota, providing further evidence that gut-targeted interventions may serve as novel strategies to tackle Alzheimer's disease."
The mechanistic relationship between the microbiome and Alzheimer's remains unclear. Increasingly, researchers are looking at ways other organs may affect brain changes: altered liver enzymes have been linked to Alzheimer's disease and people who have had their appendix removed were shown to have a nearly 20% lower risk of Parkinson's disease.
The NMPA's decision marks the first novel drug approved globally for Alzheimer's disease since 2003, Green Valley said. The approval is conditional and will have monitoring for safety. The company plans a multinational phase III trial next year in the U.S, Europe, and Asia to support regulatory filings in other countries.

Researchers successfully reverse Alzheimer's disease in mouse model

Did your doctor followup on this with researchers to get this tested in humans? If not, incompetence reigns in your stroke hospital, beginning at the top with the stroke president and board of directors. Have them all fired.  Only 20 months old.

Researchers successfully reverse Alzheimer's disease in mouse model

by Rockefeller University Press

The brain of a 10-month-old mouse with Alzheimer's disease (left) is full of amyloid plaques (red) surrounded by activated microglial cells (green). But these hallmarks of Alzheimer's disease are reversed in animals that have gradually lost the BACE1 enzyme (right). Credit: Hu et al., 2018

A team of researchers from the Cleveland Clinic Lerner Research Institute have found that gradually depleting an enzyme called BACE1 completely reverses the formation of amyloid plaques in the brains of mice with Alzheimer's disease, thereby improving the animals' cognitive function. The study, which will be published February 14 in the Journal of Experimental Medicine, raises hopes that drugs targeting this enzyme will be able to successfully treat Alzheimer's disease in humans.

One of the earliest events in Alzheimer's disease is an abnormal buildup of beta-amyloid peptide, which can form large, amyloid plaques in the brain and disrupt the function of neuronal synapses. Also known as beta-secretase, BACE1 helps produce beta-amyloid peptide by cleaving amyloid precursor protein (APP). Drugs that inhibit BACE1 are therefore being developed as potential Alzheimer's disease treatments but, because BACE1 controls many important processes by cleaving proteins other than APP, these drugs could have serious side effects.
Mice completely lacking BACE1 suffer severe neurodevelopmental defects. To investigate whether inhibiting BACE1 in adults might be less harmful, Riqiang Yan and colleagues generated mice that gradually lose this enzyme as they grow older. These mice developed normally and appeared to remain perfectly healthy over time.
The researchers then bred these rodents with mice that start to develop amyloid plaques and Alzheimer's disease when they are 75 days old. The resulting offspring also formed plaques at this age, even though their BACE1 levels were approximately 50% lower than normal. Remarkably, however, the plaques began to disappear as the mice continued to age and lose BACE1 activity, until, at 10 months old, the mice had no plaques in their brains at all.
"To our knowledge, this is the first observation of such a dramatic reversal of amyloid deposition in any study of Alzheimer's disease mouse models," says Yan, who will be moving to become chair of the department of neuroscience at the University of Connecticut this spring.
Decreasing BACE1 activity also resulted in lower beta-amyloid peptide levels and reversed other hallmarks of Alzheimer's disease, such as the activation of microglial cells and the formation of abnormal neuronal processes.
Loss of BACE1 also improved the learning and memory of mice with Alzheimer's disease. However, when the researchers made electrophysiological recordings of neurons from these animals, they found that depletion of BACE1 only partially restored synaptic function, suggesting that BACE1 may be required for optimal synaptic activity and cognition.
"Our study provides genetic evidence that preformed amyloid deposition can be completely reversed after sequential and increased deletion of BACE1 in the adult," says Yan. "Our data show that BACE1 inhibitors have the potential to treat Alzheimer's disease patients without unwanted toxicity. Future studies should develop strategies to minimize the synaptic impairments arising from significant inhibition of BACE1 to achieve maximal and optimal benefits for Alzheimer's patients."

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Explore further

PET tracer gauges effectiveness of promising Alzheimer's treatment

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More information: Hu et al., 2018. J. Exp. Med. DOI: 10.1084/jem.20171831

Journal information: Journal of Experimental Medicine

Provided by Rockefeller University Press

Diet reverses Alzheimer’s-like symptoms in mice

You can't do this on your own, no human clinical research to back it up and no amounts or protocol to follow. 

Be very careful with green tea extract:

Herbal supplements linked to at least six Australian organ transplants since 2011, data shows  March 2016

Diet reverses Alzheimer’s-like symptoms in mice

• Download PDF Copy

Reviewed by Alina Shrourou, BScMar 7 2019

A diet containing compounds found in green tea and carrots reversed Alzheimer's-like symptoms in mice genetically programmed to develop the disease, USC researchers say.
Researchers emphasize that the study, recently published in the Journal of Biological Chemistry, was in mice, and many mouse discoveries never translate into human treatments. Nevertheless, the findings lend credence to the idea that certain readily available, plant-based supplements might offer protection against dementia in humans.
"You don't have to wait 10 to 12 years for a designer drug to make it to market; you can make these dietary changes today," said senior author Terrence Town, a professor of physiology and neuroscience at the Keck School of Medicine of USC's Zilkha Neurogenetic Institute. "I find that very encouraging."
What's more, the study supports the idea that combination therapy, rather than a single magic bullet, may offer the best approach to treating the 5.7 million Americans living with Alzheimer's. Combination treatment is already the standard of care for diseases such as cancer, HIV infection and rheumatoid arthritis.
For this study, the researchers took a look at two compounds: EGCG, or epigallocatechin-3-gallate, a key ingredient in green tea, and FA, or ferulic acid, which is found in carrots, tomatoes, rice, wheat and oats.
The researchers randomly assigned 32 mice with Alzheimer's-like symptoms to one of four groups with an equal number of males and females. For comparison, each group also contained an equal number of healthy mice. For three months, the mice consumed a combination of EGCG and FA, or EGCG or FA only, or a placebo. The dosage was 30 mg per kilogram of body weight--a dosage well-tolerated by humans and easily consumed as part of a healthy, plant-based diet or in the form supplements.

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Before and after the three-month special diet, scientists ran the mice through a battery of neuropsychological tests that are roughly analogous to the thinking and memory tests that assess dementia in humans. Of particular note was a maze in the shape of a Y, which tests a mouse's spatial working memory--a skill that humans use to find their way out of a building.
Healthy mice instinctively explore each arm of the Y maze, looking for food or a route to escape and entering the three arms in sequence more often than by chance alone. Impaired mice can't do this as well as their mentally healthy counterparts.
"After three months, combination treatment completely restored working memory and the Alzheimer's mice performed just as well as the healthy comparison mice," Town said.
How did it work? Town says one mechanism appeared to be the substances' ability to prevent amyloid precursor proteins from breaking up into the smaller proteins called amyloid beta that gum up Alzheimer patients' brains. In addition, the compounds appeared to reduce neuroinflammation and oxidative stress in the brain--key aspects of Alzheimer's pathology in humans.
Town said he and his lab will continue exploring combination treatment, with a focus on plant-derived substances that inhibit production of the sticky amyloid beta plaques.​

Source:

https://news.usc.edu/154890/alzheimers-like-symptoms-in-mice-reversed-with-special-diet/

Flashing Light, Sound Restore Memory in Alzheimer's Mice

Is your stroke hospital and doctors going to do one damn thing to see this gets tested in humans? Or will they sit with their heads up their asses sucking on their thumbs waiting for SOMEONE ELSE TO SOLVE THE PROBLEM? 

 

Flashing Light, Sound Restore Memory in Alzheimer's Mice Flashing Light, Sound Restore Memory in Alzheimer's Mice

 

An innovative light and sound stimulation therapy reduced the number of amyloid plaques found in the brains of laboratory mice with Alzheimer's disease, improving memory and cognitive function. Could an hour of light and sound a day keep Alzheimer's at bay in people?
Alzheimer's disease is a type of degenerative brain disease that causes memory loss and language problems. Over 5.8 million Americans are currently living with Alzheimer's disease, including one in 10 people age 65 or older, according to the Alzheimer's Association.
The disease is caused by the buildup of two proteins in the brain—amyloid beta and tau—that clump together to form plaques or neurofibrillary tangles that impair memory function.
The research was published March 14 in Cell.
The noninvasive treatment induces brain waves called gamma oscillations.
Alzheimer's patients have impairments in gamma-frequency oscillations. Although the exact function of these oscillations, which range from 25-90 hertz, is unknown, it's believed to contribute to attention perception and memory in the brain.
In 2016, Li-Huei Tsai, director of MIT's Picower Institute for Learning and Memory, and her team exposed laboratory mice that genetically predisposed to Alzheimer's disease to a light flickering at 40 hertz for one hour a day. They found that this treatment reduced the levels of tau and amyloid beta in visual cortex of the brain and stimulated the activity of debris-clearing immune cells.
For the current study, Tsai and her team sought to improve on these results. By adding sound stimuli, they hoped the treatment would be able to reach other brain regions.
They played a 40-hertz tone one hour a day for seven hours for laboratory mice predisposed to Alzheimer's disease. At the conclusion of the study, the mice had dramatically lowered levels of beta amyloid in the auditory cortex, which process sound, and the brain's memory center, the hippocampus.
The treated mice also displayed improvements in cognition when navigating a maze that required them to remember key landmarks.
Next, the researchers administered both light and sound together. This had an even greater effect than either one given alone. Amyloid plaques reduced throughout a greater part of the brain, including teh prefrontal cortex, where higher cognitive functions take place.
Preliminary safety tests for this type of brain stimulation have already been performed in healthy human subjects, although more research is needed to determine if the treatment will work in people with Alzheimer's disease.
"As our intervention is completely non-invasive, there is minimal safety concerns. We still need to conduct human trials to determine if this is effective," Tsai said.

Alzheimer’s Memory Loss Dramatically Reversed in Mice

So your doctors, stroke hospital and stroke association should followup with human research testing this out. That is the minimum a competent doctor, stroke hospital and stroke association should be doing.  But you already know that nothing will be done unless you do this testing yourself. Hope you don't die. You would be in good company;

10 Scientists Who Experimented on Themselves | Mental Floss

 

Alzheimer’s Memory Loss Dramatically Reversed in Mice

Mouse study reverses memory loss in mice with Alzheimer’s.

Memory loss caused by Alzheimer’s disease has been reversed in mice, reports a new study.
Alzheimer’s disease — the most common form of dementia –results from both genetic and environmental factors, and is currently untreatable.

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Scientists have discovered, though, that the disease interferes with electrical signalling in part of the brain responsible for memory.
Using techniques based on epigenetics, the researchers were able to reverse the memory loss.
Epigenetics involves how instructions contained in DNA are expressed in cells.
Professor Zhen Yan, the study’s first author, said:

“We have not only identified the epigenetic factors that contribute to the memory loss, we also found ways to temporarily reverse them in an animal model of AD.”

The scientists found that Alzheimer’s caused neurons in the frontal cortex to gradually lose glutamate receptors.
By inhibiting an enzyme, they were able to restore memory in mice.
Professor Yan said:

“When we gave the Alzheimer’s animals this enzyme inhibitor, we saw the rescue of cognitive function confirmed through evaluations of recognition memory, spatial memory and working memory.
We were quite surprised to see such dramatic cognitive improvement.
At the same time, we saw the recovery of glutamate receptor expression and function in the frontal cortex.”

While the drug only worked on the mice for one week, it is hoped the method can be refined to make it more powerful.
Epigenetics is powerful because it can target the effects of more than one gene, said Professor Yan:

“An epigenetic approach can correct a network of genes, which will collectively restore cells to their normal state and restore the complex brain function.
We have provided evidence showing that abnormal epigenetic regulation of glutamate receptor expression and function did contribute to cognitive decline in Alzheimer’s disease.
If many of the dysregulated genes in AD are normalized by targeting specific epigenetic enzymes, it will be possible to restore cognitive function and behavior.”

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The study was published in the journal Brain (Yan et al., 2019).