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Alzheimer’s disease found to be transmitted through medical procedures decades ago, study finds

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Alzheimer’s disease found to be transmitted through medical procedures decades ago, study finds

Alzheimer’s disease has been considered something that happens from within, generally speaking — but for the first time, researchers have identified cases that were triggered by a specific medical treatment.

The most common type of dementia, Alzheimer’s is caused by a buildup of amyloid proteins in the brain, with risk factors including age, family history, unhealthy lifestyle behaviors and certain medical conditions.

But in a study published in Nature Medicine, researchers from the University College London (UCL) linked growth hormone treatments to the development of Alzheimer’s, according to a UCL press release.

NEW ALZHEIMER’S TREATMENT ACCELERATES REMOVAL OF PLAQUE FROM THE BRAIN IN CLINICAL TRIALS

The researchers studied patients who received a type of human growth hormone that was extracted from the pituitary glands of deceased people (c-hGH). 

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The c-hGH has been shown to lead to greater amounts of amyloid-beta protein in the brain, the researchers found.

The researchers (not pictured) studied patients who received a type of human growth hormone that was extracted from the pituitary glands of deceased people (c-hGH).  (iStock)

Of eight people studied who were treated with c-hGH as children, five developed symptoms of dementia and had already been diagnosed with Alzheimer’s or met the criteria of the disease.

All of them were between ages 38 and 55 when they began experiencing symptoms of cognitive decline, the paper indicated. Genetic testing confirmed that the early disease was not inherited.

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“We have found that it is possible for amyloid-beta pathology to be transmitted and contribute to the development of Alzheimer’s disease,” said first author Dr. Gargi Banerjee, a researcher at the UCL Institute of Prion Diseases, in the press release.

“This transmission occurred following treatment with a now-obsolete form of growth hormone, and involved repeated treatments with contaminated material, often over several years,” he went on.

“There is no suggestion whatsoever that Alzheimer’s disease can be transmitted between individuals during activities of daily life or routine medical care.”

The researchers emphasized that Alzheimer’s disease cannot be transmitted from person-to-person contact.

“There is no suggestion whatsoever that Alzheimer’s disease can be transmitted between individuals during activities of daily life or routine medical care,” said the lead author of the research, Professor John Collinge, director of the UCL Institute of Prion Diseases and a consultant neurologist at UCLH, in the release.

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“The patients we have described were given a specific and long-discontinued medical treatment that involved injecting patients with material now known to have been contaminated with disease-related proteins,” he added.

Amyloid deposition in brain tissue, seen in post-mortem analysis, as captured by University College London researchers. (University College London)

The type of growth hormone treatment named in the study was suspended in 1985 when it was found to cause Creutzfeldt-Jakob disease (CJD) in some people. 

CJD is a degenerative brain disorder that causes dementia and death.

The findings should be used to help prevent any “accidental transmission via other medical or surgical procedures” in the future, Coolidge stated.

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Fox News Digital reached out to the UCL team requesting additional comment.

The most common type of dementia, Alzheimer’s is caused by a buildup of amyloid proteins in the brain. (REUTERS/Brian Snyder/File Photo)

Dr. Rehan Aziz, a geriatric psychiatrist with Jersey Shore University Medical Center, was not involved in the study but recognized that the paper shows potential evidence for a “very rare but transmissible form” of Alzheimer’s disease.

“The study describes just five Alzheimer’s patients out of the more than 1,800 people who were known to have received growth hormone in this way,” Aziz noted. 

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“Remarkably, the patients all developed Alzheimer’s dementia at young ages, though several of them had complicated histories that may have contributed.”

The unusually young age at which these patients developed symptoms suggested they did not have the usual form of Alzheimer’s associated with old age, Aziz said.

“The research raises the question of whether beta-amyloid protein can propagate itself, leading to cascading memory loss and worsening Alzheimer’s pathology,” he added.

A man who suffers from Alzheimer’s prepares to receive a PET scan. (Michael Robinson Chávez/The Washington Post via Getty Images)

Christopher Weber, PhD, director of global science initiatives at the Alzheimer’s Association, was also not involved in the UNC research but reiterated that Alzheimer’s is not contagious.

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“You can’t catch Alzheimer’s by taking care of someone with Alzheimer’s,” he told Fox News Digital. “Alzheimer’s disease is not transmissible through the air, or by touching or being near someone with Alzheimer’s.”

“We shouldn’t put amyloid-beta into people’s brains, either accidentally or on purpose.”

In analyzing the study, Weber noted a few limitations.

“Based on the handful of cases they examined, the authors propose the idea of a ‘rare acquired’ Alzheimer’s, a third explanation for the beginnings of the disease along with sporadic Alzheimer’s and genetic Alzheimer’s,” he said. 

“However, the study population (eight in this paper) is very small, and these are the only known cases in the literature. Thus, this possible third type of Alzheimer’s is a novel idea, but needs replication and confirmation to add credibility.”

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“You can’t catch Alzheimer’s by taking care of someone with Alzheimer’s,” an expert told Fox News Digital. “Alzheimer’s disease is not transmissible through the air, or by touching or being near someone with Alzheimer’s.” (iStock)

The possibility of creating abnormal amyloid buildup isn’t new, Weber noted, as it’s been demonstrated via injections into animals’ brains.

“We also transfer human Alzheimer’s genes into animals to initiate abnormal, Alzheimer’s-like processes in their brains — but these things do not happen in daily life or in routine medical procedures,” he said. “They are extraordinary occurrences.”

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Although the type of transmission of amyloid beta identified in the UNC study is rare, Weber emphasized that “the scientific and clinical communities must understand the possible risks and ensure that all methods of pathogen transmission are eliminated.”

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One of these methods is the “complete and conscientious sterilization of surgical instruments,” Weber said, which is common practice today. 

“Bottom line: We shouldn’t put amyloid-beta into people’s brains, either accidentally or on purpose,” he said. “And appropriate measures should be in place to ensure that doesn’t happen.”

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

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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.”

HIDDEN BRAIN CONDITION MAY QUADRUPLE DEMENTIA RISK IN OLDER ADULTS, STUDY SUGGESTS

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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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