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Alzheimer’s-related dementia could be prevented by experimental drug, researchers say

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Alzheimer’s-related dementia could be prevented by experimental drug, researchers say

An experimental drug has shown promise in preventing Alzheimer’s for people at higher risk of developing the disease.

That’s according to a new study from Washington University School of Medicine in St. Louis, where researchers ran a clinical trial of people with rare genetic mutations that almost “guarantee” future Alzheimer’s development, according to a press release.

The study included 73 people in their 30s, 40s and 50s who have the mutation, which causes an overproduction of amyloid in the brain.

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Amyloid, a protein that builds up in the brain and can interfere with cognitive function, is one of the hallmarks of Alzheimer’s. 

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An experimental drug has shown promise in preventing Alzheimer’s for people at higher risk of developing the disease. (iStock)

All participants had no (or very mild) cognitive decline, had a family history of Alzheimer’s, and were within 15 years before to 10 years after their expected age of developing symptoms, the release stated.

For 22 of the participants who received a drug called gantenerumab for eight years, their risk of developing symptoms was cut in half — from 100% to 50% — the researchers reported.

“What we do know is that it’s possible to at least delay the onset of the symptoms of Alzheimer’s disease and give people more years of healthy life.”

“There was no effect seen in those only treated for two to three years of treatment,” senior author Randall J. Bateman, MD, the Charles F. and Joanne Knight Distinguished Professor of Neurology at WashU Medicine, told Fox News Digital.

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The findings were published in the journal The Lancet Neurology on March 19.

For 22 of the participants who received a drug called gantenerumab for eight years, their risk of developing symptoms was cut in half — from 100% to 50% — the researchers reported. (iStock)

Gantenerumab, a monoclonal antibody designed to target and remove amyloid plaques in the brain, was in development by Roche in Switzerland and its U.S. affiliate, Genentech.

Development was stopped in 2023, however, after Roche/Genentech’s own clinical trials found that the drug did not meet their “primary endpoint” for slowing cognitive decline in people with early symptomatic Alzheimer’s disease, according to the release.

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“Everyone in this study was destined to develop Alzheimer’s disease and some of them haven’t yet,” said Bateman in the release.  

“We don’t yet know how long they will remain symptom-free – maybe a few years or maybe decades. In order to give them the best opportunity to stay cognitively normal, we have continued treatment with another anti-amyloid antibody in hopes they will never develop symptoms at all,” he went on.

The hope is that if late-onset Alzheimer’s trials have similar results, prevention methods could ultimately be available to the general population, according to the researchers. (iStock)

“What we do know is that it’s possible to at least delay the onset of the symptoms of Alzheimer’s disease and give people more years of healthy life.”

The hope is that if late-onset Alzheimer’s trials have similar results, prevention methods could ultimately be available to the general population, according to Bateman.

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“I am highly optimistic now, as this could be the first clinical evidence of what will become preventions for people at risk of Alzheimer’s disease,” he said. “One day soon, we may be delaying the onset of Alzheimer’s disease for millions.”

Howard Fillit, MD, co-founder and chief science officer at the Alzheimer’s Drug Discovery Foundation in New York, noted that the study shows for the first time that early treatment to clear the plaques before symptoms arise can delay the onset of Alzheimer’s — “similar to how we treat and prevent other chronic diseases.”

Although gantenerumab is no longer being developed, researchers are evaluating other anti-amyloid drugs — such as remternetug, which is made by Eli Lilly — to determine whether they may prevent Alzheimer’s disease. (iStock)

“We’ve entered into a new era of Alzheimer’s research where we can not only modify the course of the disease, but where prevention is possible with therapeutic intervention,” Fillit, who was not involved in the study, told Fox News Digital.

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Potential limitations and risks

There were several main limitations to the research, Bateman told Fox News Digital.

The number of people was limited due to the rarity of Alzheimer’s disease caused by mutations, the use of external controls, and the fact that the study started with lower doses, he said.

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“Many of the participants are still cognitively normal and near or past their expected age of onset even after more than eight years of treatment, so the effects could be larger or smaller with continued treatment and follow-up,” Bateman noted.

The researchers noted that anti-amyloid medications like gantenerumab have been shown to cause amyloid-related imaging abnormalities (ARIA).

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Amyloid, a protein that builds up in the brain and can interfere with cognitive function, is one of the hallmarks of Alzheimer’s.  (iStock)

These appear on brain scans as “tiny spots of blood in the brain or localized swelling of the brain,” the release stated. 

The majority of these side effects do not cause symptoms and resolve without treatment, but in rare cases ARIA can cause serious medical issues or can even be fatal.

This most recent study showed that 30% of participants experienced ARIA, likely due to the higher doses of the drug. 

Although two participants had to stop using gantenerumab due to severe ARIA, there were no “life-threatening adverse events and no deaths,” the researchers noted. 

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“Overall, the safety profile of gantenerumab in the extension was similar to that in the original trial and in other clinical trials of gantenerumab,” they stated.

More research needed, experts agree

Dr. Chris Vercammen, a board-certified internal medicine physician who specializes in geriatrics and palliative care, said that while these initial findings are “encouraging,” more research is needed on the effects of these medications.

“Large, randomized trials, including diverse populations and individuals with late-onset Alzheimer’s, are needed to validate these early results and determine the full potential of these treatments,” Vercammen, who is also medical director at Remo Health in California, told Fox News Digital. (He was not involved in the new study.)

   

“It’s important to note that this study’s design focused on high-risk individuals in the pre-clinical stage, and therefore does not provide sufficient data on the impact of these medications on later-stage Alzheimer’s.”

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Fillit added that this new research opens the door for further exploration of treating preclinical Alzheimer’s.

Anti-amyloid medications like gantenerumab have been shown to cause amyloid-related imaging abnormalities (ARIA), which appear on brain scans as “tiny spots of blood in the brain or localized swelling of the brain.” (iStock)

“We look forward to seeing the longitudinal data as well as further studies around this approach,” he told Fox News Digital.

“These efforts bring us one step closer to our ultimate goal of preventing the disease before it begins.”

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Although gantenerumab is no longer being developed, researchers are evaluating other anti-amyloid drugs — such as remternetug, which is made by Eli Lilly — to determine whether they may prevent Alzheimer’s disease.

“These efforts bring us one step closer to our ultimate goal of preventing the disease before it begins.”

“These rare families with mutations may wish to participate in ongoing trials,” Bateman told Fox News Digital.  

“The older general population might be interested to know that there are ongoing trials in people with amyloid plaques to test this approach to determine if Alzheimer’s symptoms could be prevented.”

For more Health articles, visit www.foxnews.com/health

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The study was funded primarily by the Alzheimer’s Association, GHR Foundation and the National Institutes of Health (NIH).

Fox News Digital reached out to Roche/Genentech for comment.

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Aging process could accelerate due to ‘forever chemicals’ exposure, study finds

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Aging process could accelerate due to ‘forever chemicals’ exposure, study finds

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A new study suggests that middle-aged men may be more vulnerable to faster biological aging, potentially linked to exposure to “forever chemicals.”

The research, published in the journal Frontiers in Aging, examined how perfluoroalkyl and polyfluoroalkyl substances, more commonly known as PFAS, could impact aging at the cellular level.

PFAS are synthetic chemicals commonly used in nonstick cookware, food packaging, water-resistant fabrics and other consumer products, the study noted. 

Their chemical structure makes them highly resistant to breaking down, allowing them to accumulate in water, soil and the human body.

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Chinese researchers analyzed blood samples from 326 adults enrolled in the U.S. National Health and Nutrition Examination Survey between 1999 and 2000.

A new study suggests that middle-aged men could face accelerated biological aging at the cellular level due to exposure to PFAS. (iStock)

The researchers measured levels of 11 PFAS compounds in participants’ blood and used DNA-based “epigenetic clocks” — tools that analyze chemical changes to DNA to estimate biological age — to determine how quickly their bodies were aging at the cellular level, the study stated.

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Two compounds, perfluorononanoic acid (PFNA) and perfluorooctanesulfonamide (PFOSA), were detected in 95% of participants.

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Higher concentrations of those chemicals were associated with faster biological aging in men of certain age groups, but not in women.

“People should not panic.”

The compounds most strongly linked to accelerated aging were not the PFAS chemicals that typically receive the most public attention, the researchers noted.

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“The associations were strongest in adults aged 50 to 64, particularly in men,” Dr. Xiangwei Li, professor at Shanghai Jiao Tong University School of Medicine and the study’s corresponding author, told Fox News Digital. 

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“While this does not establish that PFAS cause aging, it suggests that these widely present ‘forever chemicals’ may be linked to molecular changes related to long-term health and aging.”

The study found that two of the compounds were detected in 95% of participants, and higher levels were linked to faster biological aging in men ages 50–64. (iStock)

Midlife may represent a more sensitive biological period, when the body becomes more vulnerable to age-related stressors, according to the researchers.

Lifestyle factors, such as smoking, may influence biological aging markers, potentially increasing vulnerability to environmental pollutants.

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While Li said “people should not panic,” she does recommend looking for reasonable ways to reduce exposure. 

That might mean checking local drinking water reports, using certified water filters designed to reduce PFAS, and limiting the use of stain- or grease-resistant products when alternatives are available.

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Meaningful reductions in PFAS exposure will likely depend on broader regulatory action and environmental cleanup efforts, Li added.

The researchers noted that midlife could be a particularly sensitive stage, when the body is more susceptible to stressors associated with aging. (iStock)

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Study limitations

The researchers outlined several important limitations of the research, including that the findings show an association, but do not prove that PFAS directly causes accelerated aging.

“The study is cross-sectional, meaning exposure and aging markers were measured at the same time, so we cannot determine causality,” Li told Fox News Digital.

The study was also relatively small, limited to 326 adults age 50 or older, which means the findings may not apply to younger people or broader populations.

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Researchers measured PFAS levels using data collected between 1999 and 2000, and today’s exposure patterns may differ.

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Li added that while PFAS is known to persist in the environment and the body, these results should be validated through larger, more recent studies that follow participants over time.

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Melissa Joan Hart, 49, Opens up About Weight Loss in Perimenopause

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Alzheimer’s prevention breakthrough found in decades-old seizure drug

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Alzheimer’s prevention breakthrough found in decades-old seizure drug

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A drug that has long been used to treat seizures has shown promise as a potential means of Alzheimer’s prevention, a new study suggests.

The anti-seizure medication, levetiracetam, was first approved by the FDA in November 1999 under the brand name Keppra as a therapy for partial-onset seizures in adults. The approval has since expanded to include children and other types of seizures.

Northwestern University researchers recently found that levetiracetam prevented the formation of toxic amyloid beta peptides, which are small protein fragments in the brain that are commonly seen in Alzheimer’s patients.

The medication was found to prevent the formation of amyloid-beta 42 in both animal models and cultured human neurons, according to the study findings, which were published in Science Translational Medicine.

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The effect was also seen in post-mortem human brain tissue obtained from individuals with Down syndrome, who are at high risk for Alzheimer’s disease.

The medication was found to prevent the formation of amyloid-beta 42 in both animal models and cultured human neurons. (iStock)

“While many of the Alzheimer’s drugs currently on the market, such as lecanemab and donanemab, are approved to clear existing amyloid plaques, we’ve identified this mechanism that prevents the production of the amyloid‑beta 42 peptides and amyloid plaques,” said corresponding author Jeffrey Savas, associate professor of behavioral neurology at Northwestern University Feinberg School of Medicine, in a press release. 

“Our new results uncovered new biology while also opening doors for new drug targets.”

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The brain is better able to avoid the pathway that produces toxic amyloid‑beta 42 proteins in younger years, but the aging process gradually weakens that ability, Savas noted. 

“This is not a statement of disease; this is just a part of aging. But in brains developing Alzheimer’s, too many neurons go astray, and that’s when you get amyloid-beta 42 production,” he said. 

The effect was also seen in post-mortem human brain tissue obtained from individuals with Down syndrome, who are at high risk for Alzheimer’s disease. (iStock)

That then leads to tau (“tangles”) — abnormal clumps of protein inside brain neurons — which can kill brain cells, trigger neuroinflammation and lead to dementia.

In order for levetiracetam to function as an Alzheimer’s blocker, high-risk patients would have to start taking it “very, very early,” Savas said — up to 20 years before elevated amyloid-beta 42 levels would be detected.

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“You couldn’t take this when you already have dementia, because the brain has already undergone a number of irreversible changes and a lot of cell death,” the researcher noted.

The researchers also did a deep dive into previous human clinical data to determine whether Alzheimer’s patients who were taking the anti-seizure drug had slower cognitive decline. They reported that the patients in that category had a “significant delay” in the span from cognitive decline to death compared to those not taking the drug.

“This analysis supports the positive effect of levetiracetam to slow the progression of Alzheimer’s pathology,” the researcher said. (iStock)

“Although the magnitude of change was small (on the scale of a few years), this analysis supports the positive effect of levetiracetam to slow the progression of Alzheimer’s pathology,” Savas said.

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Looking ahead, the research team aims to find people who have genetic forms of Alzheimer’s to participate in testing, Savas said.

Limitations and caveats

The study had several limitations, including that it relied on animal models and cultured cells, with no human trials conducted.

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Because the study was observational in nature, it can’t prove that the medication caused the prevention of the toxic brain proteins, the researchers acknowledged.

Savas noted that levetiracetam “is not perfect,” cautioning that it breaks down in the body very quickly.

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The team is currently working to create a “better version” that would last longer in the body and “better target the mechanism that prevents the production of the plaques.”

“You couldn’t take this when you already have dementia, because the brain has already undergone a number of irreversible changes and a lot of cell death.”

The medication’s common documented side effects include drowsiness, weakness, dizziness, irritability, headache, loss of appetite and nasal congestion.

It has also been linked to potential mood and behavior changes, including anxiety, depression, agitation and aggression, according to the prescribing information. In rare cases, it could lead to severe allergic reactions, skin reactions, blood disorders and suicidal ideation.

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Funding for the study was provided by the National Institutes of Health and the Cure Alzheimer’s Fund.

Fox News Digital reached out to the drug manufacturer and the researchers for comment.

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