PORTLAND, OR – Scientists at Oregon Health & Science University are working on a federally funded project that could turn the human eye into an early warning system for Alzheimer’s disease.
The five-year, $3.3 million award from the National Institutes of Health will support development of an experimental eye drop designed to detect a fluorescent signal from amyloid, a protein associated with Alzheimer’s. Used alongside a noninvasive retinal scanner, the approach could lead to a low-cost, widely accessible screening tool to identify the disease before symptoms appear.
“We’re looking for early-stage patients who don’t have symptoms,” said project leader Lei Wang, an assistant professor of biomedical engineering at OHSU. “The goal is to develop population-level screening involving a simple eye drop and a quick scan.”
The research is funded through a National Institute on Aging program for early-stage investigators, named for the late NIH scientist Stephen I. Katz. The project is considered high-risk, high-reward, but researchers say success could improve outcomes as new Alzheimer’s treatments work best in the earliest stages of the disease.
Alzheimer’s is typically associated with amyloid-beta and tau proteins that form plaques in the brain, contributing to cognitive decline. While brain imaging can detect amyloid, the tests are costly and not practical for routine screening.
Wang’s team aims to detect amyloid through the retina, which is directly connected to the brain and can be imaged noninvasively at cellular resolution. The researchers plan to develop a fluorescence-based molecule that could be delivered as an eye drop, making amyloid visible during a retinal scan.
“The retina is a neural sensory extension of the brain,” Wang said. “If we can detect a buildup of amyloid in the retina, it may be possible to flag early-stage Alzheimer’s among patients who aren’t yet experiencing any symptoms.”
The project brings together experts in chemistry, retinal imaging and neurology. Yifan Jian, an associate professor of ophthalmology and biomedical engineering at OHSU, will refine the ultrawide field fluorescence scanning technology to safely highlight amyloid in the retina.
If successful, the screening approach could be used in ophthalmology clinics rather than specialized medical centers, expanding access in both rural and urban areas. Patients flagged through retinal screening could then be referred to neurologists for further evaluation and brain imaging.
The research will first focus on developing and testing the fluorescent agent for safety and effectiveness in mouse models. Only after that would the project move toward human clinical trials.
“The long-term vision is something that is accurate, affordable and available in many communities,” Wang said. “Not only at large academic centers.”
Boston University researchers in a groundbreaking study found that those with CTE have a much higher chance of being diagnosed with dementia.
The largest study of its kind from the Boston University CTE Center reveals that the progressive brain disease chronic traumatic encephalopathy should be recognized as a new cause of dementia.
The BU researchers discovered that those with advanced CTE — who had been exposed to repetitive head impacts — had four times higher odds of having dementia.
“This study provides evidence of a robust association between CTE and dementia as well as cognitive symptoms, supporting our suspicions of CTE being a possible cause of dementia,” said Michael Alosco, associate professor of neurology at Boston University Chobanian and Avedisian School of Medicine.
“Establishing that cognitive symptoms and dementia are outcomes of CTE moves us closer to being able to accurately detect and diagnose CTE during life, which is urgently needed,” added Alosco, who’s the co-director of clinical research at the BU CTE Center.
The researchers studied 614 brain donors who had been exposed to repetitive head impacts, primarily contact sport athletes.
By isolating 366 brain donors who had CTE alone, compared to 248 donors without CTE, researchers found that those with the most advanced form of CTE had four times increased odds of having dementia.
The four times odds are similar to the strength of the relationship between dementia and advanced Alzheimer’s disease pathology, which is the leading cause of dementia.
Dementia is a clinical syndrome that refers to impairments in thinking and memory, in addition to trouble with performing tasks of daily living like driving and managing finances. Alzheimer’s disease is the leading cause, but there are several other progressive brain diseases listed as causes of dementia that are collectively referred to as Alzheimer’s disease related dementias (ADRD).
With this new study, the authors argue that CTE should now also be formally considered an ADRD.
The study also reveals that dementia due to CTE is often misdiagnosed during life as Alzheimer’s disease, or not diagnosed at all. Among those who received a dementia diagnosis during life, 40% were told they had Alzheimer’s disease despite showing no evidence of Alzheimer’s disease at autopsy. An additional 38% were told the causes of their loved one’s dementia was “unknown” or could not be specified.
In addition, this study addressed the controversial viewpoint expressed by some clinicians and researchers that CTE has no clinical symptoms. As recently as 2022, clinicians and researchers affiliated with the Concussion in Sport Group meeting, which was underwritten by international professional sports organizations, claimed, “It is not known whether CTE causes specific neurological or psychiatric problems.”
Alosco said, “There is a viewpoint out there that CTE is a benign brain disease; this is the opposite of the experience of most patients and families. Evidence from this study shows CTE has a significant impact on people’s lives, and now we need to accelerate efforts to distinguish CTE from Alzheimer’s disease and other causes of dementia during life.”
As expected, the study did not find associations with dementia or cognition for low-stage CTE.
The BU CTE Center is an independent academic research center at the Boston University Avedisian and Chobanian School of Medicine. It conducts pathological, clinical and molecular research on CTE and other long-term consequences of repetitive brain trauma in athletes and military personnel.
The timing of your sleep patterns could be linked to increased dementia risk, according to a new study.
Each person’s circadian rhythm, often defined as the body’s internal 24-hour clock, keeps the body operating on a healthy pattern of sleeping and waking. It also affects other systems in your body, according to Cleveland Clinic.
While most people’s circadian rhythms are automatically regulated, things like light levels can throw them off balance.
People with strong circadian rhythms are usually able to stick to regular times for sleeping and activity, even with schedule or season changes, experts say.
With a weaker circadian rhythm, light and schedule changes are more likely to disrupt the body clock, leading to shifts in sleep and activity patterns.
Older adults with weaker daily activity rhythms were more likely to develop dementia over the following years.(iStock)
The new study, published in the journal Neurology, sought to explore whether these disruptions play a role in dementia risk among older adults.
Researchers from the Academy of Neurology monitored more than 2,000 people for an average of 12 days to track their rest and rhythm activities.
“A novel aspect of our study is that we derived circadian rhythms from a chest-worn ECG patch that is commonly used clinically,” lead study author Wendy Wang, Ph.D., of the Peter O’Donnell Jr. School of Public Health at UT Southwestern Medical Center in Dallas, told Fox News Digital.
The participants’ average age was 79, and none had dementia at the time of the study. They were divided into three groups based on the strength of their circadian rhythms.
In the group with the strongest rhythms, 31 of 728 people developed dementia, compared to 106 of 727 people in the group with the weakest rhythms.
Chest-worn ECG patches monitored patients’ circadian rhythm in the new study.(iStock)
After adjusting for factors such as age, blood pressure and heart disease, researchers found that people in the weakest rhythm group had nearly 2.5 times the risk of dementia.
The researchers identified a possible “U-shaped” association between the stability of the sleep-wake cycle and dementia, noting that people with consistently low activity levels may have less stable circadian rhythms.
People whose activity peaked at 2:15 p.m. or later had a 45% higher risk of dementia compared to those whose activity peaked earlier in the day. About 7% of people in the earlier peak group developed dementia, compared to 10% in the later peak group.
The study did have some limitations. Data on sleep disorders, such as obstructive sleep apnea or sleep-disordered breathing, were not available. Wang noted that more research is needed to understand the possible link.
With a weaker circadian rhythm, light and schedule changes are more likely to disrupt the body clock, leading to shifts in sleep and activity patterns.(iStock)
The researcher also recommended that people maintain a strong circadian rhythm that is “well-aligned” with the 24-hour day.
“People with strong circadian rhythms often follow regular sleep and activity times,” she said.
“However, it’s important to note that our research does not prove that irregular circadian rhythms cause dementia, only that an association was observed.”
Khloe Quill is a lifestyle production assistant with Fox News Digital. She and the lifestyle team cover a range of story topics including food and drink, travel, and health.
The presence of beta amyloid and tau proteinsare hallmark signs of Alzheimer’s. Amyloid can begin to accumulate in the spaces between neurons as early as one’s 30s, potentially affecting communication between brain cells. As amyloid deposits grow, they can lead to a rapid spread of abnormal tau proteins, which form tangles inside brain cells, thus killing them.
“Physical activity may help slow the buildup of tau — the protein most closely linked to memory loss — and delay cognitive decline in people with early Alzheimer’s,” said lead study author Dr. Wai-Ying Wendy Yau, a neurologist and memory disorders physician scientist at Massachusetts General Hospital in Boston.
Cognitive decline was delayed by an average of three years for people who walked 3,000 to 5,000 steps per day, and by seven years in individuals who walked 5,000 to 7,500 steps per day, Yau said in an email.
While the research is informative, relying on a specific number of steps per day to prevent Alzheimer’s is too simplistic, said neurologist Dr. Richard Isaacson, director of research at the Institute for Neurodegenerative Diseases in Florida. He was not involved in the study.
“I get really cautious about catchy numbers like walking 5,000 or 7,000 steps,” said Isaacson, who conducts studies on cognitive improvement in people who are genetically at risk for Alzheimer’s disease.
“If someone has excess body fat, if someone has prediabetes, if someone has high blood pressure, just walking a certain number of steps won’t be enough,” he said. “Everyone needs their own individualized plan.”
No decline in beta amyloid
The study was small — only 296 people between the ages of 50 and 90 — but researchers used objective measures, which improved the reliability of the 14-year study published Monday in the journal Nature Medicine.
“The strength of this research is the combination of serial highly specialized scans that measure amyloid and tau deposition in the brain, with cognitive assessments and baseline step count. This is unique,” said Masud Husain, a professor of neurology and cognitive neuroscience at the University of Oxford’s medical science division, in a statement. He was not involved in the study.
Steps were measured by pedometer; participants underwent yearly cognitive testing for an average of nine years; and everyone received a PET (or positron-emission tomography)scan at the beginning of the study to measure levels of amyloid and tau. A smaller group received a follow-up PET scan at the end of the study.
While tau buildup slowed by between three and seven years for people who walked up to 7,500 steps per day, people who were sedentary had a significantly faster buildup of tau proteins and more rapid declines in cognition and daily functioning, the study found.
An unusual finding was the lack of a relationship between physical activity and a decline in beta amyloid, which appears before tau.
“Instead, for a given amount of elevated amyloid burden, higher step counts were associated with slower accumulation of tau, which largely explained the relationship with slower cognitive decline,” said Yau, who is also an instructor at Harvard Medical School.
Because the study was only observational, it cannot show a direct cause and effect, Yau said. However, such studies reinforce existing knowledge that what is good for the heart — such as walking, stress reduction, quality sleep and a plant-based diet — is good for the brain, experts say.
“We’ve known for years that mice which exercise on their little wheels have about 50% less amyloid in their brains,” Isaacson said. “While we need more research in people, I’m convinced exercise on a regular basis reduces amyloid buildup and improves cognition.”
An enhanced version of vitamin K could help reverse brain damage from Alzheimer’s disease, a study has found.
Alzheimer’s and many other neurodegenerative diseases are marked by a loss of brain neurons. While most medications treat only the symptoms, researchers from the Department of Bioscience and Engineering at Shibaura Institute of Technology in Japan set out to determine whether a new approach could replace the lost cells.
Vitamin K is an essential nutrient that aids with blood clotting, bone health and other important functions in the body, according to the National Institutes of Health.
While it has been shown to support brain protection and neuron creation, the natural forms of vitamin K — including menaquinone-4 (MK-4) — might not be powerful enough to effectively treat neurodegenerative diseases, experts say.
An enhanced version of vitamin K could help reverse brain damage from Alzheimer’s disease, a study has found.(iStock)
To boost its potency, researchers from the Department of Bioscience and Engineering at Shibaura Institute of Technology in Japan developed new, stronger forms of the vitamin.
They did this by creating 12 new versions of vitamin K and combining it with retinoic acid, an active metabolite of vitamin A that helps brain cells grow and develop.
In lab tests, the new lab-made versions of vitamin K were about three times more effective than natural vitamin K at helping immature brain cells develop into neurons, according to study co-lead Associate Professor Yoshihisa Hirota.
Vitamin K is an essential nutrient that aids with blood clotting, bone health and other important functions in the body.(iStock)
The new vitamin K compound was also shown to successfully cross the blood-brain barrier in animal tests.
Another important benefit, the researchers noted, is that the new molecules retained the same benefits of vitamin K and vitamin A while showing stronger brain-cell activity.
The findings were published in the journal ACS Chemical Neuroscience.
The new vitamin K compound was also shown to successfully cross the blood-brain barrier in animal tests. (iStock)
“Since neuronal loss is a hallmark of neurodegenerative diseases such as Alzheimer’s disease, these analogues may serve as regenerative agents that help replenish lost neurons and restore brain function,” Hirota said in a press release.
Looking ahead, the research team plans to test the new compounds in animal and human studies, in hopes that this could lead to a new approach for slowing or repairing brain degeneration for patients with neurodegenerative diseases.
“A vitamin K-derived drug that slows the progression of Alzheimer’s disease or improves its symptoms could not only improve the quality of life for patients and their families, but also significantly reduce the growing societal burden of healthcare expenditures and long-term caregiving,” Hirota added.
Melissa Rudy is senior health editor and a member of the lifestyle team at Fox News Digital. Story tips can be sent to melissa.rudy@fox.com.
Some dolphins found stranded on beaches may have ended up their because they suffer from a form of Alzheimer’s disease linked to toxins in the water.
This is the conclusion of a study led by researchers from Florida’s Hubbs-SeaWorld Research Institute, who suspect that—just like some adult humans with dementia are occasionally found wandering far from their homes—dolphins may become similarly disoriented when suffering from Alzheimer’s.
Their findings, published in the journal Communications Biology, point to chronic exposure to toxins produced by microorgansims known as cynobacteria—which are frequently found in freshwater, estuarine and marine waters—as a possible trigger.
The cyanobacterial toxin β-N-methylamino-L-alanine (BMAA), as well as its isomers 2,4-diaminobutyric acid (2,4-DAB), and N-2-aminoethylglycine (AEG), have been found to be extremely toxic to neurons.
BMAA triggers Alzheimer’s-like neuropathology and cognitive loss in experimental animals. These toxins can be biomagnified as they accumulate up the food chain in the marine ecosystem towards top predators like dolphins.
The resarcher’s study, which involved 20 common bottlenose dolphins stranded in the Indian River Lagoon in eastern Florida during the summer cyanobacterial bloom season, identfied markers of Alzheimer’s disease.
The duration of cyanobacterial blooms is increasing due to climate change and nutrient pollution from agricultural runoff and sewage discharges. Cyanobacterial-laden waters have often been released down the St. Lucie River from Lake Okeechobee into the Indian River Lagoon, intensifying exposure risks even in humans.
“Since dolphins are considered environmental sentinels for toxic exposures in marine environments, there are concerns about human health issues associated with cyanobacterial blooms,” said paper author and neuropathologist Dr. David Davis of the University of Miami said in a statement.
Studies of villagers on the island of Guam show that chronic dietary exposure to cyanobacterial toxins are associated with misfolded tau proteins and amyloid plaques characteristic of Alzheimer’s disease.
“Among Guam villagers, exposure to cyanobacterial toxins appeared to trigger neurological disease,” explained Dr. Paul Alan Cox, of the Brain Chemistry Labs in Jackson Hole, in a statement.
In 2024, Miami Dade County had the highest prevalence of Alzheimer’s disease in the United States.
“Although there are likely many paths to Alzheimer’s disease, cyanobacterial exposures increasingly appear to be a risk factor,” adds Dr. Davis.
Do you have a tip on a science story that Newsweek should be covering? Do you have a question about dolphins? Let us know via science@newsweek.com.
Reference
Noke Durden, W., Stolen, M. K., Garamszegi, S. P., Banack, S. A., Brzostowicki, D. J., Vontell, R. T., Brand, L. E., Cox, P. A., & Davis, D. A. (2025). Alzheimer’s disease signatures in the brain transcriptome of Estuarine Dolphins. Communications Biology, 8(1), 1400. https://doi.org/10.1038/s42003-025-08796-0
This isn’t the first time Bill Gates has poured money into Alzheimer’s research. Arun Sankar/AFP via Getty Images
More than 7 million Americans are currently living with Alzheimer’s disease—a figure expected to rise as life expectancies increase. To help accelerate progress, Bill Gates and a coalition of partners are backing a new A.I. competition designed to spur breakthroughs in Alzheimer’s and related dementia research.
Unveiled today (Aug. 19) by the Alzheimer’s Disease Data Initiative (AD Data Initiative), the competition will award a $1 million prize to a team that successfully utilizes agentic A.I. to develop innovative solutions. The resulting tools will be made publicly available through the AD Data Initiative’s online research environment.
“The Alzheimer’s Insights A.I. Prize is our call to the global innovation system to act with urgency,” said Niranjan Bose, interim executive director of the AD Data Initiative, in a statement. “A.I. has the potential to revolutionize the pace and scale of dementia research—providing an opportunity we cannot afford to miss out on, especially with so many lives at risk,” added Bose, who also serves as managing director for health and life sciences at Gates Ventures, the family office funding the competition.
For Gates, the mission is deeply personal. He helped launch the AD Data Initiative in 2020, just months after his father died at age 94 from the disease. “We are closer than ever before to a world where no one has to watch someone they love suffer from this awful disease,” said Gates in a Father’s Day post this year, calling for faster progress in Alzheimer’s research.
How can A.I. help?
Alzheimer’s is a particularly complex disease, with multiple potential causes and a web of biological pathways that have long stymied researchers. Agentic A.I. is well-suited to tackling these challenges because it can autonomously analyze large amounts of data and catch insights that human researchers might miss, according to the AD Data Initiative.
Beyond data analysis, A.I. could also transform the very nature of Alzheimer’s research. “A.I. is opening the door for a shift from reactive to predictive research—identifying novel biomarkers of early disease patterns, optimizing clinical trial designs, and revealing unexpected opportunities for drug creation and repurposing,” said Gregory Moore, senior advisor at both Gates Ventures and the AD Data Initiative, in a statement.
Over the years, Gates has poured billions into public health initiatives via his charitable foundation. But his Alzheimer’s work has largely come from his personal fortune, which currently stands at around $118.3 billion. His donations include a $50 million gift to support novel treatments, another $50 million toward clinical trials and early detection and $30 million to create an initiative focused on improving diagnostics.
Now, with the new competition, Gates is widening the call for innovation. Applications open today for A.I. and machine learning engineers, computational biomedicine experts, tech companies, clinical specialists and Alzheimer’s researchers. Semi-finalists will be announced in December, with finalists competing next March at the Alzheimer’s Disease and Parkinson’s Disease Conference in Copenhagen.
Eli Lilly & Co.’s Alzheimer’s treatment was cleared in the US as the second drug to slow progression of the mind-robbing disease that afflicts 6 million Americans.
It’s a big win for Lilly and its investors, who have been eagerly anticipating the drug since it showed promise in clinical trials more than three years ago. Called Kisunla, the medicine endured a number of regulatory delays on the road to approval. It will compete with Eisai Co.’s Leqembi, which has been available for sale in the US since early 2023.
Shares of Indianapolis-based Lilly closed down 0.8% Tuesday in New York. The stock had surged more than 50% so far this year before today amid rapid growth of weight-loss and diabetes sales. Shares of Eisai partner Biogen Inc. fell 1.3%
The Alzheimer’s drug will cost $32,000 in the first year of treatment, Lilly said. That’s slightly more than the $26,500 annual price for Leqembi for a person of average size. But doctors can stop the treatment if brain plaques — the toxic material that the drug removes — fall to minimal levels, which they did in many people in trials after about a year.
Lower costs
That means that the total out-of-pocket treatment cost of the drug could sometimes be less than other amyloid drugs, Lilly said. In Leqembi’s main approval trial, patients were treated for a full 18 months. The Eisai and Lilly products are both infusions that remove toxic amyloid from the brains of Alzheimer’s patients. They only modestly slow the disease and are approved only for people with early-stage Alzheimer’s, a minority of the total patient population with the disease. Side effects of both include brain swelling and brain bleeding.
Brain swelling or bleeding occurred in 36% of patients on Lilly’s drug in the company’s main study, and produced symptoms in 6% of them, according to the drug’s label. Regular scans are required to monitor for these effects. Lilly’s drug has a potential convenience advantage since it’s infused every four weeks, compared with every two for Leqembi.
Less frequent dosing and the potential to stop treatment are “a really big deal,” Howard Fillit, co-founder of the Alzheimer’s Drug Discovery Foundation, said in an interview before the approval.
Series of delays
Lilly faced a series of delays bringing Kisunla to the market. In early 2023, the FDA refused to give the drug accelerated approval based on early trial results, telling the company it wanted to wait for a late-stage trial. When Lilly submitted that data, the FDA needed more time to review it. Then earlier this year, the agency decided late in the review process to convene a day-long hearing to review the drug’s safety and efficacy.
A panel of outside advisers to the FDA voted unanimously in favor of the drug on June 10. “There’s a lot of emotion in the hallways today,” Anne White, president of Lilly Neuroscience, said in an interview before the approval. “We have portraits up on our walls of family members to remind us why we’re doing what we’re doing.”
Once considered integral to Lilly’s future, Alzheimer’s has been overshadowed by the company’s GLP-1 medicines that aid in weight loss, a market expected to reach $130 billion a year by the end of the decade, according to analysts at Goldman Sachs.
Sales of Alzheimer’s drugs are also expected to grow significantly. Bloomberg Intelligence analysts see sales surging to $13 billion by 2030 from about $250 million this year.
“Having multiple treatment options is the kind of advancement we’ve all been waiting for — all of us who have been touched, even blindsided, by this difficult and devastating disease,” said Joanne Pike, CEO of the Alzheimer’s Association, in a statement. The nonprofit has pushed hard for approval and broad insurance coverage for amyloid-lowering drugs.
Leqembi’s rollout by Eisai and partner Biogen Inc. has been slowed by logistical issues, reimbursement uncertainties and complicated safety testing requirements. Medicare, the US health program for the elderly, didn’t routinely cover the treatments until recently, and hospital neurology programs weren’t set up to perform the monitoring required to use the drugs.
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Editor’s note: CNN Chief Medical Correspondent Dr. Sanjay Gupta is a practicing neurosurgeon and best-selling author on brain health. “The Last Alzheimer’s Patient” premieres on “The Whole Story with Anderson Cooper” on Sunday, May 19, at 8 p.m. ET/PT on CNN and streams on MAX on June 18.
Preventive neurologist Dr Richard Isaacson stared at the numbers on the fax in astonishment. Blood biomarkers of telltale signs of early Alzheimer’s disease in the brain of his patient, 55-year-old entrepreneur Simon Nicholls, had all but disappeared in a mere 14 months.
“I had to catch my breath. It was a complete shock: The blood tests on his brain had normalized,” said Isaacson, director of research at the Institute for Neurodegenerative Diseases in Boca Raton, Florida.
Dr. Richard Isaacson, left, discusses test results with Simon Nicholls, participant No. 34 in his clinical trial. – CNN
Was this stunning result the work of some new miracle drug designed to combat dementia? Not at all. This is a story of old-fashioned grit and determination.
“Simon was on a mission, as if the Grim Reaper was peering over his shoulder. He was going to kick ass and take names,” Isaacson said.
Nicholls reduced his risk of developing Alzheimer’s via lifestyle changes recommended by Isaacson, including diet, exercise, reducing stress and optimizing sleep, along with a few strategically chosen supplements and medications prescribed by his cardiologist.
“I was very worried,” Nicholls told CNN Chief Medical Correspondent Dr. Sanjay Gupta in his new documentary, “The Last Alzheimer’s Patient,” which is airing on “The Whole Story with Anderson Cooper.”
“I have a 3-year-old son and an 8-year-old son. It’s really important for me, as I get older, to try and be there for them in the future,” he said. “There are many [changes] in lifestyle you can do to hopefully push the disease backwards and give yourself more time, which is all we need until we find a cure.”
CNN Chief Medical Correspondent Dr. Sanjay Gupta, left, interviews Simon Nicholls for his documentary “The Last Alzheimer’s Patient.” – CNN
Unlucky genes
When it came to genetics and dementia, Nicholls had drawn the short straw. He carried two copies of the APOE4 gene, one from each parent, which may increase the risk of developing Alzheimer’s at least tenfold.
“Sadly, my mum passed away from what we think is Alzheimer’s in her 70s,” Nicholls said. “For the last 10 years of her life, she just sat in a chair, rocking, while on about 14 medications. I’d much rather have a longer health span and then just go quickly.”
Not everyone with one or even two copies of APOE4 develops Alzheimer’s, however, creating a tantalizing opportunity. Can a person diminish their genetic risk for Alzheimer’s via lifestyle and various medical interventions, especially if started early, before too much damage is done?
Isaacson, who also has a family history of Alzheimer’s, believes the answer is yes. He began the first US clinic devoted to Alzheimer’s prevention in New York City in 2013 before moving his program to Florida in 2021. His research has shown that following a dozen or more lifestyle interventions, when practiced 60% or more of the time, can improve cognitive function, especially in women.
Isaacson, second from right, calls in a team of specialists from nearly every profession to discuss each case. – CNN
“I don’t use the term ‘reverse.’ I don’t know what reverse means when it comes to the field of Alzheimer’s,” Isaacson said. “But the results we’ve seen with Simon and some other patients in our research are extremely exciting.”
How the heart and the brain are intertwined
Alzheimer’s isn’t the only pathway to a life of dwindling memory and the inability to think, plan and interact with loved ones.
Vascular dementia, the second most common type of dementia after Alzheimer’s disease, can be caused by atherosclerosis, a buildup of plaque in the arteries that can lead to heart attacks, stroke, blood clots and more, all of which can further damage the body and brain.
Poor hearts and their consequences can run rampant in a family over generations, a fact Nicholls knew all too well.
“My whole family had endless heart attacks, resulting in my grandfather on my mother’s side dying around age 50,” he said. “My mother had three heart attacks, the first at age 50, then a triple bypass before she went on to develop dementia.”
Simon Nicholls reads with his 3-year-old son, Sylver, at his home in Miami. – CNN
Carrying an APOE4 gene further increases the risk for heart disease as well as dementia, experts say.
“My sister had three heart attacks, and when I was 40, I was told that I had atherosclerosis, with a ridiculously massive coronary artery calcium score of like 1,500 and occlusions in about 96% of my arteries.” A normal coronary artery calcium score is zero.
For a man in the prime of his life, the news was crushing. Doctors tried to use lifestyle changes and statins to reverse the plaque buildup but finally resorted to surgery, opening three of Nicholls’ arteries with stents. He also began using an injectable drug called evolocumab, designed to boost the liver’s ability to remove “bad” low-density lipoprotein, or LDL, from the body.
‘It was time to turn to my brain’
Slowly, Nicholls’ heart condition began to improve, but the bad news didn’t end there. A brain scan found telltale signs of vascular damage in Nicholls’ brain, which occurs when the tiniest blood vessels are starved of oxygen.
“The doctors said I had too many white matter lesions. I told myself that since I now had my heart more or less under control, it was time to turn to my brain,” Nicholls said.
In January 2023, Nicholls became participant No. 34 in a novel clinical trial at Isaacson’s Florida center. The trial is designed to uncover cognitive risk factors and counter them with a personalized plan of attack. (Full disclosure: I am participant No. 20 in the same trial; you can read about my experience here.)
“The overall goal of the study is democratize access to preventive neurology care by eventually using at-home blood testing to cost-effectively reach the most people,” Isaacson said.
As part of the trial, Nicholls underwent a battery of tests, including a unique blood test that can track levels of amyloid, tau and otherhallmark biomarkers for Alzheimer’s disease and other degenerative conditions. Deposits of amyloid can begin accumulating in the brain decades before symptoms begin, even in a person’s 30s and 40s.
“Simon’s first test came back with a score of 70. Anything over 58 was positive for amyloid in the brain,” Isaacson said. “The results backed up the amyloid PET scan Simon had taken in 2019, where I could see the plaque in his brain.”
10,000 steps a day: ‘I’m very consistent’
Nicholls needed to loose weight, so he began taking tirzepatide (the active ingredient in the medications Mounjaro and Zepbound), one of the newer injectable drugs that suppress appetite by stimulating hormones that control blood sugar levels.
At the same time, Nicholls was encouraged to step up his physical activity by incorporating strength training three times a week while adding 45 to 60 minutes a day of zone 2 exercise, in which you briskly walk, ruck, jog or cycle at 60% to 70% of your heart rate.
“I love going for a walk every morning at sunrise for an hour and a half with a podcast. I get in 10,000 steps or more every day. I’m very consistent,” Nicholls said. “I also do a very slow full-body workout with weights three times a week for an hour’s time.”
“When I first saw Simon, he had a bit of a middle, like most guys in their 50s,” Isaacson said. “When I saw him at nine weeks, I did a double take. He was totally buff, ripped even.
“Within those nine weeks, he had lost 21 pounds, about 80% of that fat, and put on muscle, which was excellent,” Isaacson added. “I almost didn’t recognize him.”
The weight loss and increased muscle mass lowered Nicholls’ fasting blood sugar levels, ending his march toward diabetes, while some tweaks to his cholesterol medications further optimized his good and bad cholesterol numbers.
In August 2023, it was time to repeat the blood test for amyloid. By then, the company that administers the tests had added a measurement for tau, another key hallmark sign of Alzheimer’s, frontal lobe dementia and Lewy body disease.
“Simon’s amyloid probability score on the new APS2 test had dropped to 53, which was phenomenal,” Isaacson said. “But he was still positive, as anything between 48 and 100 is considered to reflect a high probability of amyloid brain plaques on a brain scan.”
Within six months, Nicholls had dropped the levels of amyloid in his blood from 70 to 53. – CNN/Dr. Richard Isaacson
‘Turn on the screws’
Now that the big concerns of cholesterol, insulin, diet, exercise and fat mass were addressed, it was time “to turn on the screws,” Isaacson said, with personalized recommendations based on Nicholls’ biology.
“We optimized Simon’s omega-3 fatty acid levels, which is especially important for people with APOE ε4, as they need more omega-3. We also added B complex vitamins to control elevated homocysteine in his blood,” Isaacson said. “However, we would not give B complex vitamins to anyone who did not have higher homocysteine levels.”
Elevated homocysteine, which is an amino acid used by the body to make protein, is a risk factor for brain atrophy, cognitive impairment and dementia. A September 2010 randomized controlled trial found that supplementation slowed brain atrophy in people with mild cognitive impairment.
In the meantime, Nicholls, an avid researcher who loves to read medical journals, was adding some interventions of his own.
“I have steam and sauna rooms in my home, I do a lot of that. I love it,” he said. “I’ve tried cold water plunges, and I have lists of things to do I get from podcasts, from walking to sleeping to gratitude to yoga to sleep routines.
“But there’s one thing I do that Dr. Isaacson doesn’t agree with: I get stem cell injections twice a year,” Nicholls added. “Sadly, I have arthritis in my hands, and that definitely feels better when I use stem cells, and I like to think they may be helping my brain, as well.”
With business around the world, Nicholls is a frequent flyer with “terrible sleep” due to jet lag and insomnia. “I’m also a worrier type of person,” he confessed.
Adding a sleep medication approved for insomnia helped, “but Simon really needs to tackle his sleep by improving his sleep hygiene with a more regular sleep schedule,” Isaacson said.
An unbelievable result
On Halloween 2023, the next APS2 score arrived. Amazingly, Nicholls had reduced the amount of amyloid and tau in his blood to 40: He was testing negative in blood for signs of Alzheimer’s.
Shocked and amazed, Isaacson remained skeptical. “I was very cautious. You know, promise not to overpromise. I needed to retest.”
Both the October and December 2023 blood tests showed Nicholls was negative for amyloid and tau in his blood. – CNN/Dr. Richard Isaacson
A few days before Christmas, the repeat test results arrived. When it too was a negative finding of 40, Isaacson decided to tell Nicholls in person.
“Dr. Isaacson drove all the way from Boca Raton to Miami excited, very happy,” Nicholls said. “We walked on a beach together, and we were ecstatic that we’d actually been able go from positive to negative for amyloid.”
Although Nicholls is ecstatic about the improvements, he’s also very humble about his efforts to improve his health.
“I’m really not all that compliant. To comply is just horrendously difficult, right? Of course I want to have a beer or a hamburger or something stupid. I love gummy bears and eating crappy food,” he said.
“It’s helped that I have some great doctors to help me, but to be honest, my biggest motivator are my children,” Nicholls added. “I’d love to see my sons get married and have their own kids, and to do that, I have to put in the work to stay the way I am now.”
Simon Nicholls and his 8-year-old son, Salvadore. – Courtesy Simon Nicholls
Even lower amyloid levels and a larger hippocampus
It appears Nicholls is well on his way toward that goal. In March, his APS2 score had dropped to 25, an unbelievably low number.
Not only was Nicholls blood negative for amyloid and tau, the test suggested that his brain amyloid might be normal, with no distinguishable signs of the disease. The only way to definitively prove this, however, would be to repeat his amyloid PET scan, Isaacson said.
Simon Nicholls’ March blood tests showed that his brain had continued to improve. – CNN/Dr. Richard Isaacson
“What really drove his score down was the amyloid value,” Isaacson said. “It normalized at .101, which is like crazy good. That’s not matter for discussion; for amyloid, .1 or above is normal.”
Even more startling: Brain volume scans showed that the hippocampus, the tiny seahorse-shaped organ responsible for memory, had actually grown in volume in Nicholls’ brain since he started the intervention.
In early Alzheimer’s stages, the hippocampus loses tissue rapidly and then atrophies as the disease progresses.
A brain volume image showing the increased size of Nicholls’ hippocampus. – CNN/Dr. Richard Isaacson
Despite these amazing outcomes, Isaacson remains cautious. After all, this is one person, and similar findings have not been been replicated in a larger, more controlled sample and published in a peer-reviewed journal.
“I don’t believe in the term ‘reverse’ because I don’t know what will happen if the person stops doing the intervention,” Isaacson said. “I also don’t know if the brain might normalize for a short period of time and then, five years later, catch up. Until I have more data, I don’t think that reverse is the right word.”
That doesn’t stop his wonder at the results and his gratitude to Nicholls for his continuing dedication to the study and the personalized interventions.
“I still can’t believe it. I’d seen this before, but only in people who are taking anti-amyloid medications,” Isaacson said. “When you work your entire career and are told by everyone, ‘It’s not possible to do this,’ and then you see it — well, I’m still humbled and amazed.”
Consider joining Isaacson’s latest online clinical trial, designed to provide cognitive assessments and personalized advice via smartphones. People over 21 who meet certain criteria can sign up for the study at Retain Your Brain.
The National Institute on Agingcurrently supports nearly 500 active clinical trials on Alzheimer’s disease and related dementias. For information, go here.
TROY, N.Y. (NEWS10) — Rensselaer Polytechnic Institute researchers will start working on a new approach to treating and preventing genetic diseases like Alzheimer’s. They received a grant from the National Institutes of Health to fund this research.
“A delivery mechanism that works within the body itself could be a game changer,” said William Lawler, a doctoral student at RPI, who is working on the project.
These researchers will search for ways to get around the immune system’s ability to destroy the gene therapy if it sees the new technology as a threat. They will also attempt to use systems in the human body to their advantage, like our own intercellular mail delivery system, to try and treat these genetic diseases.
“Currently, gene editing tools, such as CRISPR, can only treat cells that have been removed from the body and processed in the lab. That limits the kinds of cells and conditions that can be treated,” Lawler said. “Our goal is to develop a technology that, once in the body, will correct the genetic mutations in brain cells linked to Alzheimer’s disease.”
Hope is on the horizon for millions of Alzheimer’s disease patients as scientists develop a new target for Alzheimer’s treatment: the immune system.
Alzheimer’s affects roughly 5.8 million Americans, according to the Centers for Disease Control and Prevention (CDC). The progressive disease is the most common form of dementia and is associated with memory loss and cognitive decline in regions of the brain involved in thought, memory and language.
Scientists believe that Alzheimer’s is caused by the abnormal buildup of proteins in and around the brain cells, but exactly what triggers this is still unclear.
Today, there is no known cure for Alzheimer’s. However, new medications may offer relief to patients and slow the disease’s progression. And our body’s immune system can help with this.
“There are many approaches that are in various stages of development that target the immune system, which is now known to play a key role in Alzheimer’s disease,” Todd Golde, a professor of pharmacology, chemical biology and neurology at Emory University, told Newsweek.
One particularly exciting approach involves the use of antibodies that can target and bind to the abnormal protein clumps that form in the brain. “This results in clearance or reduction of [the protein clumps],” Golde said.
Golde and colleague Allan Levey have summarized this approach in a recently published perspective in the journal Science.
Precisely what mediates this interaction is still unknown, but Golde said that the brain’s private squad of immune cells may play an important role. These cells, called microglia, are found exclusively in the brain and central nervous system and can engulf problematic proteins and infectious particles like bacteria. Therefore, researchers believe that the antibodies may act as little molecular flags to signal to the microglial cells that a mess needs cleaning up—a mess in the form of an Alzheimer ‘s-associated protein clump.
Based on clinical trials, these antibodies offer a very promising avenue for future treatments.
“These treatments slow decline in the very earliest symptomatic stages of Alzheimer’s disease on average by about 25 to 30 percent over 18 months of treatment,” Golde said. “Notably, the antibodies show quite remarkable impacts on amyloid deposits [aka the protein clumps] themselves.”
Unlike previous therapies designed to ease symptoms and boost cognitive function, Golde said that these antibodies represent the first therapies capable of altering the course of the disease.
“Having a disease-modifying therapy (like this) is in some ways a game changer for Alzheimer’s disease, as it says that we can alter the course of this devastating disease and slow it down,” Golde said. “This is just a start, and that either improved versions of these therapies, other types of disease-modifying therapies, or combination therapies will likely in the future lead to treatments with bigger impacts, halting or preventing disease.”
Artist’s impression of a nerve cell surrounded by antibodies. Antibody treatments may be the future of Alzheimer’s therapy. peterschreiber.media/Getty
Two of the antibodies used in these trials have already been FDA approved; the third is expected to be approved in 2024. However, care still needs to be taken over their use.
“Because of potential for side effects, the need to treat patients early in the symptomatic phase of the disease in individuals [and] the fact that they are currently given through multiple IV infusions and require careful monitoring, there are some barriers to widespread use [of these antibodies],” Golde said. “Indeed, there is appropriate caution among most clinicians to ensure that the right patients most likely to benefit from these therapies are treated.”
Golde stresses that, while these results are fascinating, we are still a long way from effectively treating Alzheimer’s.
“Though this represents an initial success, huge unmet medical need remains,” he said. “We need continuing investment in the public and private sectors to ensure that we can meet that need and build off this initial, but limited, success.”
Is there a health issue that’s worrying you? Do you have a question about Alzheimer’s? Let us know via health@newsweek.com. We can ask experts for advice, and your story could be featured on Newsweek.
Uncommon Knowledge
Newsweek is committed to challenging conventional wisdom and finding connections in the search for common ground.
Newsweek is committed to challenging conventional wisdom and finding connections in the search for common ground.
The eastern and southeastern United States have the highest prevalences of Alzheimer’s dementia, according to new research released Monday at the Alzheimer’s Association International Conference in Amsterdam.
The study, by researchers at Rush Medical College in Chicago, includes county-level estimates of Alzheimer’s rates among adults age 65 and older in all 3,142 U.S. counties.
In November of 1901, a young German psychiatrist and neuroanatomist, Alois Alzheimer, found what appeared to be misfolded proteins forming sticky clumps, or plaques, between the neurons in the brain tissue of a patient who had died from dementia. Inside the neurons he found threadlike twists, called neurofibrillary tangles, of another protein. Eventually these plaques and tangles came to define the disease named after him: Alzheimer’s disease.
By the mid 1980s, these strange proteins had been identified as beta-amyloid proteins, and by the 1990s it was widely accepted that an excess of these proteins caused the formation of the plaques, which in turn caused the disease. The tangles, which turned out to be malformed strands of a protein called tau, were thought to be a result of the amyloid plaques. For the past 30 years, the bulk of research on Alzheimer’s, and most of the efforts to find a cure, have been based on the amyloid hypothesis.
However, after decades of research based on this hypothesis, drug trials have mostly struck out. No drug tested has produced meaningful improvement in the symptoms of the disease. Even drugs that reduce amyloid levels in the brain haven’t done what really matters: improve the lives of people with Alzheimer’s disease.
In January of this year, a new Alzheimer’s drug, lecanemab, was approved by the FDA even after the deaths of several trial participants raised questions about the drug’s safety. Safety issues aside, lecanemab is far from a cure. It did not stop the progression of the disease, and it reduced cognitive decline by only a small amount. “It’s a small step in the right direction,” says Donald Weaver, MD, PhD, clinical neurologist and Alzheimer’s researcher at the University of Toronto, “not a big stride.”
Are We in a Rut?
These disappointing results have led many researchers to ask if the amyloid hypothesis needs rethinking. Marissa Natelson Love, MD, is a neurology researcher at the Heersink School of Medicine at the University of Alabama at Birmingham. Natelson Love has focused her research on anti-amyloid therapies based on the amyloid hypothesis and is recruiting patients for further studies on lecanemab. Still, she says, “Every time we have a meeting, someone asks, ‘Are we on the wrong track?’” Perhaps, as Weaver once put it, Alzheimer’s research is in an “intellectual rut.”
There’s a reason science sometimes gets in these ruts. Science is a slow, accretive process that builds upon work — often decades of work — that came before.
Researchers complete PhDs on a particular topic, then go on to be postdocs in the lab of an established scientist in the same area. Soon there’s an entire body of researchers with years of training and experience in one approach to a given problem, explains Michael Strevens, PhD, philosopher of science at New York University. “There’s a protocol, what you might call a recipe book, for doing the science. Whereas with a new, untested hypothesis, no one has yet written the recipe book.” This isn’t laziness, but momentum. Like a giant ocean liner, research can’t turn on a dime. When it comes to Alzheimer’s, the momentum is mostly behind the amyloid hypothesis. The roles of other processes in the course of the disease, such as inflammation, prior infections, or autoimmune illness, have gotten short shrift.
Still, we shouldn’t throw the baby out with the bathwater. The problem may not be with the amyloid hypothesis, but with the specific drugs being tested. Maybe researchers just haven’t found the right drug. Or maybe these are the right drugs and they’re just being given at the wrong time; it could be that in order to be successful, anti-amyloid treatments need to start long before symptoms appear.
Another possibility is that the selection of trial participants has not been ideal. Until the past decade or so, Alzheimer’s couldn’t be definitively diagnosed until after death. “If we go back and look at the autopsies from previous Alzheimer’s disease studies,” says Natelson Love, “not everyone in the study actually had Alzheimer’s.” Not only might that explain why a particular trial was unsuccessful, but it could also have a downstream effect on future research. If researchers were unknowingly testing a potential Alzheimer’s treatment on patients who didn’t have Alzheimer’s, that data would be flawed — and later research that drew on it could be flawed, too.
New techniques make it possible to diagnose Alzheimer’s before death. Imaging tests like MRI can rule out other reasons for memory loss; specialized PET scans can detect beta-amyloid plaques and tau proteins. Cerebrospinal fluid can now be tested for biomarkers of amyloid and tau, and though not yet widely available, some new blood tests can detect the presence of amyloid. While these techniques are not enough to diagnose the illness alone, they are making it much easier to confirm it in living patients.
Traffic Jams in the Brain
New approaches to studying amyloid plaques might also change the trajectory of Alzheimer’s research. Rather than just trying to rid the brain of plaques and tangles, researchers are now investigating the biological pathways that created them in the first place. As Scott Small, MD, director of the Alzheimer’s Disease Research Center at Columbia University, put it, “One of the reasons there’s been such frustration is because we haven’t yet fully understood what’s fundamentally broken in Alzheimer’s, what’s fundamentally wrong. If you don’t know what’s fundamentally broken, you can’t fix it.”
Though Small says he has great respect for the amyloid hypothesis, he agrees that clearing plaques, while beneficial, results in only “subtle slowing of cognitive decline.” If you want to have a meaningful impact on the illness, he says, you need to get to the actual source of the pathology by addressing the cellular biology of the disease. He and his colleagues are pursuing that approach, looking for the source of the problem at the cellular level and trying to discover what is happening inside neurons to create the problems between neurons.
Small and others are seeking the source of the problem in endosomes, organelles inside cells that regulate the movement of proteins. Proteins on their way out of the endosomes get blocked, creating what Small calls “traffic jams,” eventually leading to the buildup of amyloid and tau proteins and thus to Alzheimer’s. They’re working on therapies that would unjam endosomes.
Meanwhile, a variety of other approaches to the problem are gaining traction. Weaver’s lab in Toronto is working on the hypothesis that Alzheimer’s disease is an autoimmune disorder in the brain. The hypothesis is that amyloid is not an abnormal protein, but a normal component of the brain’s immune system, produced in response to bacterial infections. The problem, as with all autoimmune illnesses, is that something goes wrong with the immune system, causing it to attack the body’s own tissues; in this case, the amyloid confuses healthy brain cells with infectious bacteria and attacks brain cells instead of or along with the bacteria. The result, of course, is Alzheimer’s disease. Because the drugs used to treat autoimmune illness in other parts of the body do not have a therapeutic effect in the brain, Weaver and colleagues are researching drugs that target the immune pathways specifically in the brain.
Other researchers are looking into possible connections between infections and the inflammation associated with Alzheimer’s. Kristen Funk, PhD, a neuroimmunologist at the University of North Carolina, Charlotte, studies how the body’s inflammatory response to viral infections, such as herpes simplex and viral encephalitis, affects cognition and might be linked to the development of Alzheimer’s.
Some evidence suggests that Alzheimer’s could be a metabolic disorder, much like type 2 diabetes. In fact, some researchers have called Alzheimer’s “diabetes of the brain” or “type 3 diabetes.” Insulin resistance in the brain can lead to inflammation and oxidative stress, and eventually to amyloid plaques and Alzheimer’s. Bolstering this theory are findings that some diabetes drugs may reduce the risk of Alzheimer’s.
Alzheimer’s takes a long time to develop. The damage to the brain that eventually results in the disease can begin 20 or even 30 years before memory loss or other symptoms. In a way, that’s a cause for hope: if we could only figure out how to stop it or slow it down, we’d have so much time to do it. Epidemiological studies, studies that look at who gets Alzheimer’s and when, offer some hints about prevention. Those studies suggest that although the end result is amyloid plaques in the brain, the disease could actually be caused by a number of factors at once.
While genetics certainly plays a role, some of those risk factors are modifiable: obesity, diabetes, cardiovascular disease, high cholesterol, high blood pressure, hearing loss, and depression are some known ones.
As more evidence suggests that modifying those risk factors can prevent — or at least reduce the risk — of Alzheimer’s, many researchers are looking at what they call a multimodal approach to prevention. Lifestyle interventions, like an improved diet and more exercise, reduce the risk of cardiovascular disease and diabetes. Existing medications that control blood pressure, cholesterol, and blood sugar, for example, become a key part of this approach to prevention. Something as simple as fitting a patient with hearing aids or addressing their loneliness and isolation might be effective as well.
The beauty of these interventions is that they’re mostly low risk. Treatments for the risk factors for Alzheimer’s have already been in constant use for years. They’re likely to be relatively inexpensive and are typically covered by Medicare and other insurance plans. Lecanemab, on the other hand, is expected to cost more than $25,000 per year.
“Who can afford that?” asks Weaver. “Is it going to be restricted to wealthy people in wealthy countries? Ultimately, I hope that somebody comes up with an agent which is cost-effective to produce, cost-effective to distribute, and therefore may actually have a global impact on this disease.”
Most researchers agree that the final answer will likely involve a combination of approaches. “I think, just like in cancer, [Alzheimer’s treatment] is eventually going to be a cocktail that will bolster people’s resilience to the breakdown of the nerve cells, as well as remove some of the things triggering it,” says Love.
Any real hope for a cure for Alzheimer’s likely rests not on any one hypothesis, but with the willingness of scientists to question themselves, each other, and their prior assumptions. That doesn’t mean the years spent with a laser focus on amyloid have been wasted. But researchers do agree that it’s time to look more closely not only at the amyloid paradigm, but also further afield, in the hope of finally making progress against this devastating illness.
Chris Hemsworth has announced that he will be taking a break from acting after receiving news that he has a heightened genetic risk of developing Alzheimer’s disease.
Hemsworth, 39, discovered this heightened genetic predisposition while undergoing tests for his Disney+ documentary series Limitless, which sees the Thor actor test his body and explore new ways to live longer and healthier.
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Hemsworth told Vanity Fair that the tests confirmed his “biggest fear.” The results weren’t a total surprise for him because the actor’s grandfather is currently being treated for Alzheimer’s.
“It’s not like I’ve been handed my resignation,” Hemsworth said in the interview, clarifying that he hasn’t been diagnosed with Alzheimer’s. “It’s not a pre-deterministic gene, but it is a strong indication.”
Hemsworth revealed that he was supposed to learn his genetic test results live on camera while filming Limitless, but one of the doctors on the show, Peter Attia, and series creator Darren Aronofsky, decided to tell him the news privately. Hemsworth was given the option of removing references to Alzheimer’s from the show but he said it was important to keep those parts in to increase awareness about Alzheimer’s prevention.
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“My concern was I just didn’t want to manipulate it and overdramatize it, and make it into some sort of hokey grab at empathy or whatever for entertainment,” he told Vanity Fair.
The Marvel star added that the benefit of knowing about this grim outlook is that he can work to prevent the onset of the disease.
“If you look at Alzheimer’s prevention, the benefit of preventative steps is that it affects the rest of your life,” Hemsworth told Vanity Fair. “It’s all about sleep management, stress management, nutrition, movement, fitness. It’s all kind of the same tools that need to be applied in a consistent way.”
Learning about his Alzheimer’s risk prompted Hemsworth to reflect on his family and career, telling Vanity Fair that he’s worried about missing out on important moments with his children. Hemsworth is married to fellow actor Elsa Pataky, with whom he has three kids.
“Before you know it, they’re 18 and they’ve moved out of the house, and I missed the window,” he said. “It really triggered something in me to want to take some time off. And since we finished the show, I’ve been completing the things I was already contracted to do.”
Hemsworth announced that he will be taking a break from acting after he finishes the press tour for Limitless.
“I’m going home and I’m going to have a good chunk of time off and just simplify. Be with the kids, be with my wife.”
Hemsworth will be on the silver screen again in George Miller’s new addition to the Mad Max franchise, Furiosa, which wrapped shooting earlier this month.
According to the Alzheimer Society of Canada, by the year 2050 more than 1.7 million Canadians are expected to be living with dementia, with an average of 685 individuals being diagnosed each day.
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There are many things Canadians can do to improve their health and reduce the impact of dementia, says the organization. Much like Hemsworth stated in his interview, these include being more physically and socially active, following a healthy diet and challenging one’s brain by engaging in games, reading, and learning new languages, hobbies and skills, among other things.
Chris Hemsworth helps return Tasmanian devils to Australian mainland after 3,000-year absence
For a while, Barbara Hebner would grab whatever things she could find, bundle them into her bathrobe, and then tie everything to her walker and head for the door. She wanted to go home.
Her first breakout attempt happened in 2018. Hebner somehow slipped past her vigilant daughter, Kimberly Hayes Bock, and got as far as the back gate, when a neighbor raised the alarm. The near-escape frightened Hayes Bock – and, as the fear wore off, made her feel guilty. She installed double-sided locks on the doors and a padlock on the gate.
The runaway phase lasted a few months. Once, during an episode, her mother slammed a walker into Hayes Bock, hitting her hard.
Now, 5 years later, Hebner still tries doors, but less often, and with less determination. Around 6 months ago, her thinking skills worsened. She can no longer put sentences together that make sense, says Hayes Bock, of Joplin, MO.
Day after day, year after year, the struggles caregivers face, both big and small, take their toll. Caregiving for a parent is a kind of role reversal: a dark mirror of the nurture and support that once went the other direction.
Hayes Bock’s situation is not a rare one; she’s one of 16 million unpaid caregivers in the U.S. But here, there is no strength in numbers. The job itself is so solitary that many struggle alone.
With a young child, even on difficult days, it’s easy to imagine the happy milestones: the first steps, or the first day of school. Caregivers don’t see a bright future for their loved one – only decline. Alzheimer’s disease and other types of dementia chip away at your dignity and independence, while caregivers figure out how to manage jobs, family obligations, and ever-present guilt and sleeplessness.
There are moments of grace, like a smile of recognition, or a squeeze of the hand. There are also flashes of humor. Hayes Bock recalls the time she was looking for her mom’s 40-ounce purple bottle, and found it on the nightstand wearing a lampshade. The lamp was in the trash. “We struggle because they have changed,” she says. “The moments of grace come when we realize that a lot of the suffering is ours, as caregivers.”
Hebner moved in with Hayes Bock in 2016, not long after she was diagnosed with mild cognitive impairment. They tried memantine and Aricept, drugs for moderate to severe Alzheimer’s that can help with confusion and memory loss. Neither drug helped, and the side effects were intolerable.
Today, at age 80, Hebner needs 24/7 care. She no longer recognizes her daughter, who calls her “Barbara” instead of “Mom” sometimes, because Hebner no longer responds to “Mom” or “Mother.” She needs help bathing, but she can still dress herself, even if she ends up with mismatched clothes and her shoes on the wrong feet. Her habit of ripping the crotch out of her depends and then flushing it once earned a $450 charge from the plumber.
Hayes Bock recently posted in a caregiver support group on Facebook that she didn’t know what was worse: finding feces on the floor, or being properly prepared to clean it up, because such messes happen so often. Hayes Bock has learned to laugh it off. “It’s the ugly, hard situations that bring out the patience you never knew you had. Those moments when keeping their dignity becomes top priority,” she says. “As caregivers, we are looked at like rock stars. If I can just get us through this with that dignity intact, whether she knows it or not, it will be a win. No rock star here, just a daughter trying to do right by my mom.”
Over the years, Hayes Bock has relied on paid caregivers to fill in when she couldn’t be around. Fortunately, Hebner’s escape attempts never included wandering at night, so when the house powered down in the evening, Hayes Bock would make sure her mom was in bed, and then lock up for the night. Last January, she was able to rearrange her work schedule to accommodate caregiving. Today she works the night shift, Thursday through Sunday, in her job as a machine operator at a nearby food plant. While she’s working at the plant, her husband takes over caregiving. Hayes Bock gets home from work around 7 a.m. and sleeps until around 11. She’ll check on her mom and feed her if she’s awake. “In these later stages, they sleep a lot. Then I go back to sleep until 3:30 or so and do it all over,” she says.
Although Hebner is far from catatonic, she sits in a chair all day having conversations with people who aren’t there. Now, she only takes her walker on laps around the house when she’s hungry, sometimes putting cookies in her pocket. Hayes Bock worries about her mom’s nutrition and adds Ensure to her cereal to boost the vitamin count. She recently asked the doctor what comes next, and they talked about difficulty swallowing. She dreads the day her mom stops eating completely.
“If I get two meals in her, and pants on her, it’s a good day,” Hayes Bock says. “We decided it was laugh or scream. You have to laugh or you’ll lose your mind.”
Caregivers all over the world could tell the same stories. “With dementia, grief and loss begins before death and doesn’t stop afterwards,” says Karen Moss, PhD, an assistant professor at Ohio State University’s colleges of Nursing and Medicine, and a nurse-scientist who studies dementia in family caregivers. Moss’s work focuses on the anxiety and stress of caregiving, pain, and the end of life of older adults who have dementia. Moss specifically focuses on Black adults with dementia and their family caregivers.
Dementia and Alzheimer’s are extremely difficult conditions for the person going through the disease, especially early on as they struggle to figure out what’s wrong, says Moss. And family caregivers struggle too.
For starters, caregivers have to cope with changes brought on by normal physical aging – like decreased mobility and worsening vision – as well as the anguish of watching the person they love slowly disappear. As they fade, caregivers are left with heavy decisions to make – alone. If, say, a loved one falls, caregivers need to know whether to call the doctor or head to the ER.
In these scenarios, financial concerns loom large. Was that fall bad enough to head to the ER, which is so much more expensive than urgent care? What if it was the third one in a month?
As the disease gets worse and people with dementia need more and more help with everyday tasks like balancing the checkbook and paying bills, caregivers need to shift how they manage jobs and family obligations, all the while struggling to create a life that’s calm and happy, says Jason Karlawish, MD, a geriatrician and professor of medicine at the University of Pennsylvania Perelman School of Medicine in Philadelphia.
There is no cure for Alzheimer’s disease. Three drug trials are awaiting the FDA’s review, but of the more than 100 that have come before, none have had much success. But advocates would settle for less than a cure.
Even the ability to slow down the disease’s symptoms would be life-changing for many. “I think that’s a vision we have to have in this disease,” Karlawish says. “This idea that we are going to drug our way out of Alzheimer’s and turn it into polio, where all you need to do is get the vaccine and you’re done, is not a sensible position for science policy or for public policy.”
Even if a drug manages to affect the disease’s course, the treatment likely won’t be simple – and may need to begin years before symptoms even appear, says Eric McDade, DO, a neurologist at Washington University School of Medicine in St. Louis and principal investigator on a global clinical trial in a group of patients with dominantly inherited Alzheimer’s disease. “I hesitate to get too excited just knowing how difficult these trials are and how surprised we’ve been in the past,” he says
Moss finds that both current and former caregivers are eager volunteers for clinical trials – especially her projects covering caregiver stress. They also volunteer what information they can on how the disease is affecting their loved ones. “With Alzheimer’s disease and other related dementias or any disease for which there is no cure, people want to feel that there’s a saving grace; many of us want to know there’s something that can help turn around the disease for their loved one.”
And they come prepared with questions of their own.
“Caregivers are super savvy individuals,” she says. “When we approach them for research, they want to know what we are going to do with this information. They ask, ‘How am I going to get the results?’ They want to know, and they deserve to know.”
Susan Hersey Guilmain learned about her husband’s dementia when she signed them both up for a clinical trial at nearby Butler Hospital. The trial was supposed to test whether a Mediterranean diet could stave off cognitive decline. Neither qualified for the trial. Hersey Guilmain’s diet was already too close to what was being tested, and medical tests showed that her husband Roger already had significant cognitive impairment.
At first, he didn’t believe the tests. But the team at the hospital reassured him that they could help. “They put a positive vibe on it, so he was OK with going to his doctor and getting further testing and treatment options,” says Hersey Guilmain.
The Butler team eliminated over-the-counter sleep medications, including Tylenol PM and the three Benadryl tablets he was taking every night. They changed his diet and upped his exercise. Roger started to show improvement. He’s also taking Aricept and the herb Bacopa monnieri. A few months ago, he joined an early clinical trial testing whether Emtriva, an HIV drug that reduces inflammation, is safe for people with mild to moderate Alzheimer’s.
He was diagnosed a little over a year ago, and he’s still at the stage that Hersey Guilmain, a retired occupational therapist in Smithfield, RI, calls “the funny stuff.” He gets confused; he thought their Dunkin’ Donuts moved, and that someone had changed the buttons around on the microwave. “He actually said, ‘Who did this?’” says Hersey Guilmain.
She adds moments of calm to their days by making certain they take walks in the sunshine, around the neighborhood or a nearby lake. They also enjoy a cocktail hour every day at 5, sipping either wine or cider. The TV is off and they spend half an hour or so connecting with one another.
“Right now, it’s not as intense as it can or will be,” she says. “It’s stuff I can laugh at.” Sometimes, Hersey Guilmain gets frustrated when her husband is uncooperative about brushing his teeth, or when he tells a story that didn’t happen. She reminds herself that this is a disease, and she chooses to make jokes, rather than getting into an argument.
“It’s not an argument I can win,” she says.
After caring for an aunt and her mother, both of whom died with late-stage dementia, Hersey Guilmain knows what’s ahead. Even with the spectacular progress Karlawish says the Alzheimer’s field has made in less than 20 years, there’s still very little help for caregivers.
Hersey Guilmain says she fights every day to stay positive. “I am not going to think ahead to ‘what if,’ because I can’t,” she says. “I am just doing today, and today is good.”
This year’s event will feature renowned scientists and an opening meditation with special guest Deepak Chopra, M.D.
Press Release –
updated: Nov 11, 2020
RICHMOND, Va., November 11, 2020 (Newswire.com)
– The Rick Sharp Alzheimer’s Foundation, named in memory of the late CEO of Circuit City and founder of CarMax, has announced its 3rd annual “Alzheimer’s Day 2020.” While previous events have been held at the University of Richmond and the Science Museum of Virginia, this year’s event will be held virtually. Complimentary registration in advance is required – www.ricksharpalz.org. Previous speakers have included famed researcher Dr. Rudy Tanzi and New York Times best-selling author of “Still Alice” Lisa Genova.
Panelists will include Dr. John Lazo of the University of Virginia, Dr. Constantine Lykestsos of Johns Hopkins, and Dr. Robert Innis from the National Institute of Mental Health. The evening will include special guest Deepak Chopra. The panel will be moderated by Dr. Catherine Franssen. The panel discussion will include the status of current research, the impact of COVID-19, and brain health.
Sherry Sharp, founder of the Rick Sharp Alzheimer’s Foundation, said, “Since our inaugural event, we’ve met thousands of people and raised hundreds of thousands of dollars to achieve our goal of curing Alzheimer’s Disease. Together, with your support, we have donated over $2 million and every penny raised goes directly to research.”
Sherry also serves on the Board of Directors of Cure Alzheimer’s Fund (www.curealz.org).
For more information about the event and sponsorship opportunities, contact Director of Donor Engagement Carli Nelson at 833.CURE ALZ, Option 1, and/or visit www.ricksharpalz.org.
About Dr. John Lazo:Dr. Lazo is a professor of Pharmacology and Chemistry at the University of Virginia School of Medicine.
About Dr. Constantine Lyketsos:Dr. Lyketsos is the Chair of Psychiatry at Johns Hopkins Bayview Medical Center.
About Dr. Robert Innis:Dr. Innis is Chief of the Molecular Imaging Brand at the National Institute of Mental Health.
About Deepak Chopra, M.D.:Chopra is an expert in the field of mind-body healing and a world-renowned speaker and author on the subject of alternative medicine.
About Dr. Catherine L. Franssen:Dr. Franssen is currently the Scientist in Residence at the Science Museum of Virginia. She is an Associate Professor in the Department of Psychology at Longwood University.
About the Rick Sharp Alzheimer’s Foundation: Rick Sharp was a business leader, husband, father, and friend to many. For over a decade, he served as the CEO of electronics retailer Circuit City. He went on to found car superstore CarMax, was a founding investor and Chairman of the Board of footwear brand Crocs, and electronics company Flextronics. Shortly after his death at age 67 from Alzheimer’s in 2014, Sherry founded the Rick Sharp Alzheimer’s Foundation. The non-profit focuses on supporting world-class research and increasing ALZ awareness. 100% of all money raised goes to finding a cure.
World’s first “Citizen Science” award will be presented to students by the Human Computation Institute at a middle school assembly tomorrow
Press Release –
updated: Dec 20, 2017
BOISE, Idaho, December 20, 2017 (Newswire.com)
– Middle school students are being awarded the world’s first “Citizen Science” trophy by the Human Computation Institute (HCI) at Lake Hazel Middle School (Boise, ID) on Thursday, 21st December. 250 students formed the winning “Middle School STEM” team in HCI’s science game – Stall Catchers, which speeds up Alzheimer’s research. The custom-built award will be presented by HCI’s director, Dr. Pietro Michelucci, during an all-hands assembly.
This award highlights a shift in attitudes toward “science” in education and public engagement contexts, and puts STEM activities on par with sports and other extracurricular activities in schools. As demonstrated by the middle school students, who triumphed over other teams in the “#CrushALZ” contest earlier this year, citizen science can effectively engage students in scientific activities, which are not only competitive but advance real science.
We hope this award fosters a trend of better integration between science and community. By making this connection early, we are not just grooming scientists for the future, but preparing future citizens to engage with science regardless of their vocation.
Pietro Michelucci, Dr.
According to the students’ technologies teacher, Ms. Erin Davis, games such as Stall Catchers teach students important concepts in biomedical science, show how research is done, and empower them to exercise civic responsibility through digital citizenship.
“I am always looking for ways to motivate my students to explore areas of STEM.” – says Ms. Davis, who created the team. “STEM careers are growing, and in dire need of talented individuals. My students are highly competitive, so this seemed like a great opportunity to get involved, and further the technology conversations with a real-life example.”
According to Ms. Davis, the students were “obsessed” with the Stall Catchers competition, and that prompted them to establish their own “Citizen Science Club” at the school, which takes science out of the “science fair” setting and makes it a participatory activity.
Dr. Michelucci and his team hope this Citizen Science trophy will seed a culture of rewarding volunteer science at schools everywhere.
“We hope this award fosters a trend of better integration between science and community. By making this connection early, we are not just grooming scientists for the future, but preparing future citizens to engage with science regardless of their vocation,” says Dr. Michelucci.
Together with other competitors, Lake Hazel students helped achieve up to eight months of lab work in four short weeks of competitive gameplay, advancing Alzheimer’s disease research at Cornell University.
Ithaca, NY, April 6, 2017 (Newswire.com)
– EyesOnALZ (http://eyesonalz.com) – a project to crowdsource Alzheimer’s research is launching an online competition to #CrushALZ on April 6th, in partnership with The Crowd & The Cloud – a public television documentary series about citizen science.
The documentary, created by a producer of Carl Sagan’s original COSMOS series, shines first light on a growing movement of citizens participating en masse in the advancement of scientific research. The creators of this 4-part mini-series are dedicated to “turning viewers into doers” by encouraging hands-on participation in science.
Normally it would take a year for Cornell to analyze these data, but with the momentum of the documentary, we hope to enlist the help of millions of viewers to answer a key research question that will help us leap forward toward a treatment.
Pietro Michelucci, Director, Human Computation Institute
Stall Catchers (http://stallcatchers.com), developed as part of the EyesOnALZ project, is the first citizen science game to tackle Alzheimer’s disease. EyesOnALZ and Stall Catchers are featured in Episode 1 of the The Crowd and The Cloud, which will premier on National Public Television across the US on April 6th, and is available to watch online at http://crowdandcloud.org.
EyesOnALZ founder Pietro Michelucci will kick-off the “#CrushALZ Team Competition” on Stall Catchers during the social media event immediately following the series premiere. This live after-show event will take place at 10PM ET April 6, on The Crowd and The Cloud Facebook page (https://www.facebook.com/crowdandcloudTV/).
Dr. Michelucci will join the live video stream with other subjects of the series, including EyesOnALZ biomedical collaborator Chris Schaffer from Cornell University. The month-long team competition aims to accelerate Cornell’s groundbreaking Alzheimer’s research program, which, according to Dr. Schaffer, “would be impractical without Stall Catchers”.
Any interested organization will be able to create a team on Stall Catchers and compete with other organizations who want to help eliminate Alzheimer’s. The team registration will open up at 6AM ET, April 6 at StallCatchers.com. Instructions on how to set up teams and invite members will be posted on the EyesOnALZ blog (http://blog.eyesonalz.com) that morning.
The most active teams in the competition will receive daily exposure via EyesOnALZ media channels and those of partner organizations. A number of PBS stations, also set to participate in the competition, will invite their local viewers to join forces and #CrushALZ.
According to Dr. Michelucci, a new Alzheimer’s dataset has been loaded into Stall Catchers just for the competition: “Normally it would take a year for Cornell to analyze these data, but with the momentum of the documentary, we hope to enlist the help of millions of viewers to answer a key research question that will help us leap forward toward a treatment.”
Players’ collective progress toward answering the research question will be reported throughout the competition. Dr. Michelucci plans to reveal the potential impact of this research question during the after-show event. “If all goes well, in one month we will have our answer and move on to the next question.”
