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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Scientists at UCLA have developed an “off-the-shelf” cell-based immunotherapy that was able to track down and kill pancreatic cancer cells even after they had spread to other organs.
In a mouse study, the treatment slowed cancer growth, extended survival and remained effective even within the harsh environment of solid tumors.
“Even when the cancer tries to evade one attack pathway by changing its molecular signature, our therapy is hitting it from multiple other angles at the same time. The tumor simply can’t adapt fast enough,” lead author Dr. Yanruide Li, a post-doctoral scholar at UCLA, said in a press release.
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To build the therapy, researchers took human stem cells and turned them into a special type of immune cell called an invariant natural killer T cell (or NKT cell).
Next, they genetically modified those cells by adding a CAR receptor (chimeric antigen receptor), which enables the cells to recognize and attack pancreatic cancer cells.
UCLA scientists created an off-the-shelf CAR-NKT cell therapy that killed pancreatic tumors in multiple pre-clinical models. (iStock)
NKT cells are naturally compatible with any immune system, which means they can enter the body without causing dangerous reactions, according to the researchers. They can also be mass-produced using any donated blood stem cells.
“One donor could provide sufficient cells for thousands of treatments,” potentially offering a more affordable and accessible approach, according to the press release.
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The team tested the therapy in several lab models. These included models where the cancer was placed directly into the pancreas and others designed to mimic how the disease spreads to other organs, like the liver and lungs.
The CAR-NKT cells were able to push their way into the tumor itself, rather than getting stuck on the outside like many immune treatments do, the researchers found.
Researchers emphasized that one dose could cost around $5,000, far lower than personalized CAR-T treatments. (iStock)
Once they got inside the body, these engineered immune cells could spot cancer cells in several different ways and kill them using multiple built-in attack methods.
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Most importantly, they stayed active. Many immune cells that enter a solid tumor quickly become overwhelmed and shut down, but these engineered cells kept working instead of burning out, allowing them to continue fighting the cancer for a longer period.
The findings were published in the journal PNAS (Proceedings of the National Academy of Sciences).
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“Developing a therapy that targets both the primary tumor and its metastases in pre-clinical studies — one that can be ready to use off-the-shelf — represents a fundamental shift in how we might treat this disease,” said senior author Dr. Lili Yang, a professor of microbiology, immunology and molecular genetics at UCLA, in the same press release.
The researchers noted that one dose could cost around $5,000, far lower than personalized CAR-T treatments.
The therapy can be mass-produced from donor stem cells, potentially lowering cost and expanding access. (iStock)
Pancreatic cancer is notoriously aggressive and difficult to treat, according to the researchers. Most patients aren’t diagnosed until the disease has already spread, and the tumor’s biology creates multiple physical and chemical barriers that weaken the impact of traditional treatments.
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Since the therapy targets a protein that is common in breast, ovarian and lung cancers, the same cell product could potentially treat multiple cancer types.
In separate studies, the team has already demonstrated the therapy’s effectiveness against triple-negative breast cancer and ovarian cancer.
Most patients aren’t diagnosed until the disease has already spread, and the tumor’s biology creates multiple physical and chemical barriers that weaken the impact of traditional treatments. (iStock)
Based on the early findings, the UCLA researchers are preparing to submit applications to the Food and Drug Administration to begin human trials.
“We’ve developed a therapy that’s potent, safe, scalable and affordable,” Yang said in the release. “The next critical step is proving it can deliver the same results in patients we’ve seen in our preclinical work.”
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All testing so far has been done in mice, as the researchers noted that solid tumors in humans are far more complex. Human tumors can evolve and lose the targets that treatments are designed to recognize, raising the risk of the cancer escaping detection and continuing to grow.
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Long-term safety and side effects in humans are unknown ahead of clinical trials.
The researchers also noted that making big batches of identical, safe cells poses logistical and regulatory challenges.
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Dick Van Dyke turns 100 this year, and he says he feels “really good.”
In a recent conversation with People, he credits his attitude for both his age and the fact that he has “no pain, no discomfort.”
“I’ve always thought that anger is one thing that eats up a person’s insides – and hate,” Van Dyke said, explaining how people often ask what he did right.
He added that he’s “rather lazy” and never felt driven by the kind of resentment that can harden over time.
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Dick Van Dyke credits his longevity largely to avoiding anger and hate rather than following any strict lifestyle regimen. (Gilbert Flores/Variety via Getty Images)
“Sometimes I have more energy than others – but I never wake up in a bad mood,” he told People.
The actor explained that while there were always things and people he didn’t like or approve of, he “never really was able to work up a feeling of hate,” and certainly not “a white-heat kind of hate.”
He contrasted himself with his father, who was “constantly upset by the state of things in his life,” noting to People that his father died at 73.
Van Dyke believes avoiding that emotional pattern is one of the chief things that kept him going.
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Modern research appears to back up this idea that emotional states play a meaningful role in long-term health.
Studies on aging adults show that anger can heighten inflammation in the body, raising levels of markers like IL-6 and increasing risk of illness.
He says he has “no pain, no discomfort” at nearly 100, attributing it in part to emotional steadiness. (Monica Schipper/Getty Images)
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These effects can accelerate the wear-and-tear process associated with aging.
The broader scientific picture suggests that patterns of hostility or persistent irritation function like a physiological tax, straining the systems that keep the body resilient.
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Van Dyke explained in the interview his belief that “people are born with an outlook.”
“I just think I was born with a brighter outlook,” while others, he says, are born having to fight against downward spirals.
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Studies suggest reducing hostility and negative emotions can support resilience, slow aging, and potentially extend lifespan. (Amanda Edwards/Getty Images)
“And after 100 years, I think I’m right.”
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“When you expire, you expire,” he told People. “I don’t have any fear of death for some reason. I can’t explain that but I don’t. I’ve had such a wonderfully full and exciting life… I can’t complain.”
Van Dyke’s 100th birthday falls on Dec. 13.
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