Health
He carries the Alzheimer’s gene but never got the disease — scientists want to know why
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A Washington man appeared to be destined to develop Alzheimer’s disease — but against all genetic odds, he has eluded the common dementia for decades.
Researchers at the Washington University School of Medicine in St. Louis recently published a study focusing on Doug Whitney, 76, who lives near Seattle.
He has a rare inherited genetic mutation in the presenilin 2 (PSEN2) gene, which virtually guarantees early-onset Alzheimer’s.
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All of Whitney’s family members who inherited the gene have experienced cognitive decline starting in their early 50s or sooner, according to a WashU press release.
Whitney, however, shows no signs of mental decline. WashU researchers wondered if the reason for his continued cognitive health could help protect others against the disease.
Doug Whitney, Alzheimer’s research participant, appeared to be destined to develop Alzheimer’s disease — but against all genetic odds, he has eluded the common dementia for decades. (UWash Medicine/Megan Farmer)
In a study published in the journal Nature Medicine, the researchers analyzed his genetic data and brain scans, identifying “changes in genes and proteins” that could explain how he has defied the odds to remain mentally sharp.
The researchers also discovered that Whitney’s brain had virtually no buildup of tau, the hallmark protein that signals the onset of cognitive decline.
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“These extensive studies indicate a remarkable resistance to tau pathology and neurodegeneration,” said senior study author Randall J. Bateman, M.D., the Charles F. and Joanne Knight Distinguished Professor of Neurology at WashU Medicine, in the press release.
Urged by his cousin, Whitney first came to WashU in 2011 to participate in a study focused on families with inherited forms of Alzheimer’s, as many of his relatives had developed early-onset disease. At the time, he believed he did not have the gene.
“He actually was able to escape the expected course of the disease.”
Whitney’s mother was one of 14 children, nine of whom had the Alzheimer’s gene. Ten of them died before they were 60. Whitney’s own brother developed the disease before dying at age 55.
“I was 61 at the time — well past the age where it should have onset,” he told Fox News Digital during an on-camera interview. “But they tested me, and lo and behold, I did have the gene. I was amazed.”
In a study published in the journal Nature Medicine, the researchers analyzed Whitney’s genetic data and brain scans. (UWash Medicine/Megan Farmer)
The researchers were just as “confounded,” Whitney recalled.
“They tested me three times to make sure that there wasn’t some slip-up. But it’s true. I had the gene. And now I’m 76 years old and still haven’t had any symptoms.”
Cognitive clues
Jorge Llibre-Guerra, M.D., an assistant professor of neurology and co-first author of the study, echoed that it was a “big surprise” to learn that Whitney was a carrier of the genetic mutation — officially known as an “exceptional resilience mutation carrier.”
“He actually was able to escape the expected course of the disease,” he said in the release.
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Now, in this most recent study, the WashU researchers aimed to explore potential reasons for Whitney’s absence of Alzheimer’s.
“If we are able to uncover the mechanism behind this resilience, we could try to replicate it with a targeted therapy designed to delay or prevent the onset of Alzheimer’s, leveraging the same protective factors that have kept Mr. Whitney from developing this disease to benefit others,” said Llibre-Guerra.
Doug and Ione Whitney often work on puzzles together to help maintain mental sharpness. (UWash Medicine/Megan Farmer)
Those who have the PSEN2 mutation tend to have an “over-production” of amyloid protein, which builds up in the brain during the first stage of Alzheimer’s, according to the researchers.
In the second stage, as symptoms of cognitive decline begin, there is typically a buildup of tau protein in the brain.
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In Whitney’s case, brain scans showed a “significant accumulation” of amyloid, but almost a complete absence of tau.
One theory for how Whitney may have escaped his genetic fate stems from his time in the Navy.
The researchers discovered that Whitney’s brain (not pictured) had virtually no buildup of tau, the hallmark protein that signals the onset of cognitive decline. (AP Photo/Evan Vucci, File)
When the researchers analyzed Whitney’s cerebrospinal fluid, they found a “a significantly higher-than-normal level” of “heat shock” proteins, protective molecules that cells produce when they’re under stress, including high heat exposure.
During his many years of working as a shipboard mechanic in the Navy, Whitney was exposed to high temperatures for extended periods of time.
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“In the engine room of ships, the temperatures … would range from 100 to 110 degrees, for four hours at a time,” he told Fox News Digital. “They concluded that possibly there was some gene or protein that could mutate and protect me genetically from the disease.”
“We don’t yet understand how or if heat shock proteins may be mediating the effect,” Llibre-Guerra noted in the release. “However, in this case, they may be involved in preventing aggregation and misfolding of tau proteins, but we do not know for sure.”
“They tested me three times to make sure that there wasn’t some slip-up. But it’s true. I had the gene. And now I’m 76 years old and still haven’t had any symptoms,” Whitney said. (REUTERS/Brian Snyder/File photo)
The research was supported in part by the Dominantly Inherited Alzheimer Network, the National Institute on Aging and the Alzheimer’s Association, among others.
‘It’s my calling’
To help him stay sharp, Whitney often does crossword puzzles and sudoko along with his wife.
“I think I’m pretty healthy at 76,” he said. “I’m pretty active, and I hardly have any medications to take.”
For those who are experiencing symptoms, Whitney recommends contacting the Alzheimer’s Association.
“Get into research as soon as possible — the earlier you get in, the better chance you have,” he said. “Don’t give up. Nobody’s alone out there anymore. There are lots of people waiting to help you.”
“Looking at the advances they’ve made over the last 14 years — it’s amazing,” Whitney said. “It’s imperative that we keep going.” (iStock)
Whitney said he is optimistic about the future of Alzheimer’s treatment.
“Looking at the advances they’ve made over the last 14 years — it’s amazing,” he said. “It’s imperative that we keep going.”
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Llibre-Guerra said he’s hopeful that the insights gleaned from Whitney’s case will spark broader studies — in both people and animals — aimed at uncovering the biological secrets behind his resistance to Alzheimer’s.
“As long as they need me, I’ll be here. I’m in it for the long haul.”
“We have made all of the data we have available, as well as the tissue samples,” he said. “If researchers want to request those to do additional analysis, that’s something we would welcome.”
Whitney said he is committed to helping advance Alzheimer’s research, which his wife refers to as his “third career.”
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“It’s become my calling,” he said. “When we go for testing, it’s a pretty rigorous day, but after 14 years, I’m used to it now, so that’s not a concern.”
“As long as they need me, I’ll be here. I’m in it for the long haul.”
Fox News Digital reached out to the researchers for comment.
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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.
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.
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.
“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.
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)
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.
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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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.
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.
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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