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 popular class of weight-loss drugs may prevent life-threatening cardiac complications by opening microscopic blood vessels that often remain blocked after a heart attack, according to a study published this week in Nature Communications.
The research, led by the University of Bristol and University College London, identified a biological brain-gut-heart signaling pathway.
This discovery appears to explain how GLP-1 drugs — which mimic glucagon-like peptide-1, a hormone that helps regulate blood sugar and appetite — protect heart tissue from a condition known as “no-reflow.”
“In nearly half of all heart attack patients, tiny blood vessels within the heart muscle remain narrowed, even after the main artery is cleared during emergency medical treatment,” Dr. Svetlana Mastitskaya, the study’s lead author and a senior lecturer at Bristol Medical School, said in a press release.
“This results in a complication known as ‘no-reflow,’ where blood is unable to reach certain parts of the heart tissue.”
In nearly half of all heart attack patients, tiny capillaries (blood vessels) remain narrowed even after the main blocked artery is cleared. (iStock)
This lack of blood flow increases the risk of heart failure and death within a year. GLP-1 medications could prevent this, according to the researchers.
How it works
When the GLP-1 hormone is released in the gut or administered as a drug, it sends a signal to the brain, which then sends a signal to the heart that switches on special potassium channels in tiny cells called pericytes.
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When these channels open, the pericytes relax, which allows the small blood vessels (capillaries) to widen and improve blood flow to the heart muscle, the researchers noted.
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The new study used animal models and cellular imaging to track how GLP-1 interacts with heart tissue. When the researchers removed the potassium channels, the drugs no longer protected the heart — confirming they play a key role.
The findings suggest that existing GLP-1 medications, already used for type 2 diabetes and obesity, could be repurposed as emergency treatments. (iStock)
The findings suggest that existing GLP-1 medications, already used for type 2 diabetes and obesity, could be repurposed as emergency treatments during or immediately after a heart attack to reduce tissue damage.
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The researchers noted several limitations, including that the study relied on animal models.
Clinical trials are necessary to determine whether the brain-gut-heart pathway operates with the same timing and efficacy in humans.
While the study highlights the drug’s immediate benefits during a heart attack, it des not establish whether long-term use of these drugs provides a pre-existing level of protection. (iStock)
Additionally, while the study highlights the drug’s immediate benefits during a heart attack, it does not establish whether long-term use of the medication provides a pre-existing level of protection.
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The research was primarily funded by the British Heart Foundation.
Related Article
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Collagen supplements have exploded in popularity, touted as everything from an anti-aging miracle to a muscle recovery booster.
But a sweeping new review conducted by U.K. researchers suggests that while collagen may help improve skin elasticity and ease arthritis pain, it does little for athletic performance or wrinkle reduction.
Researchers from Anglia Ruskin University analyzed 16 systematic reviews and 113 randomized controlled trials involving nearly 8,000 participants worldwide, which they say is the most extensive evaluation of collagen’s health effects to date.
The review found consistent evidence that collagen supplementation improves skin elasticity and hydration over time and provides significant relief from osteoarthritis-related joint pain and stiffness, according to findings published in Aesthetic Surgery Journal Open Forum.
A large U.K. review found that collagen supplements may improve skin elasticity and hydration over time. (iStock)
The researchers, however, did not find meaningful improvements in post-exercise muscle recovery, soreness or tendon mechanical properties (strength, springiness and stretch resistance).
“Collagen is not a cure-all, but it does have credible benefits when used consistently over time, particularly for skin and osteoarthritis,” co-author Lee Smith, professor of public health at Anglia Ruskin University, said in a statement.
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“Our findings show clear benefits in key areas of healthy aging, while also dispelling some of the myths surrounding its use,” Smith added.
Collagen, the most abundant protein in the body, supports skin, bones, tendons, cartilage and connective tissue, according to experts. Natural collagen production begins to drop in early adulthood and declines more sharply with age.
The study found that collagen supplements may help reduce joint pain and stiffness in people with osteoarthritis. (iStock)
The review found that long-term collagen supplementation was linked to improved skin firmness and hydration, but did not help skin roughness — a proxy for visible wrinkles.
Benefits appear to accumulate gradually, suggesting that collagen should not be viewed as an “anti-wrinkle ‘quick fix,’ but as a foundational dermal support for individuals seeking holistic skin maintenance,” the researchers said.
“If we define anti-aging as a product or technique designed to prevent the appearance of getting older, then I believe our findings do support this claim for some parameters,” Smith told the BBC. “For example, an improvement in skin tone and moisture is associated with a more youthful-looking appearance.”
Collagen supplementation was linked to reduced pain and stiffness in people with osteoarthritis, with stronger benefits seen over longer periods of use, and showed modest improvements in muscle mass and tendon structure that may support healthy aging.
Collagen did not significantly improve skin roughness, a marker of visible wrinkles. (iStock)
However, it did not show meaningful results when used as a fast-acting sports performance supplement, and evidence for benefits related to cholesterol, blood sugar, blood pressure and oral health was mixed or inconclusive.
Dr. Daniel Ghiyam, a California-based physician and longevity specialist, said the findings align with what he sees in clinical practice.
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“Collagen is a targeted support tool, not a foundation of health or performance,” Ghiyam, who was not involved in the study, told Fox News Digital. “When marketed that way, it makes sense. When marketed as a cure-all, it doesn’t hold up to the data.”
The authors noted that while many previous collagen studies have received financial support from the supplement industry, the current review did not receive industry funding.
Experts say collagen supplements may offer modest benefits for skin hydration and joint comfort, but they are not a cure-all. (iStock)
The team called for more high-quality clinical trials examining long-term outcomes, optimal dosages and differences between collagen sources, such as marine, bovine and plant-based alternatives.
Among its limitations, the review could not determine whether certain forms of collagen work better than others or what the optimal regimen should be.
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While the review included randomized controlled trials, the quality of the studies varied, with newer research generally showing stronger results.
Experts say more data and studies are needed to build on the findings. They also noted that diet plays a crucial role in skin health.
Collagen supplements, often sold as powders or pills, may improve skin elasticity and ease joint pain, experts say. (iStock)
Dr. Erum Ilyas, a Pennsylvania-based dermatologist and chair of dermatology at Drexel University College of Medicine, noted that the review analyzed previously published meta-analyses rather than generating new primary data.
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“At this time, I have not seen sufficiently strong independent evidence to routinely recommend collagen supplements to my patients,” Ilyas, who was not involved in the review, told Fox News Digital.
“Although some studies show modest improvements in markers such as hydration and elasticity, there remains limited independent, biopsy-confirmed evidence demonstrating sustained increases in dermal collagen content,” she added.
Fox News Digital has reached out to the researchers for comment.
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