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Donald Trump’s health has once again become a hot talking point, but this time it is not about his diet or late-night Twitter habits. Instead, two psychologists are raising red flags about something far more serious: dementia. According to them, the US president has been showing what they describe as a “dead ringer telltale sign” of frontotemporal dementia (FTD) and they warn that the symptoms appear to be getting “worse and worse”.
Clinical psychologists Dr. Harry Segal and Dr. John Gartner, hosts of the podcast Shrinking Trump, claim that Trump’s psychomotor functioning has visibly deteriorated. Speaking to The Guardian, Dr. Gartner said, “Some of the more evidence that we've been talking about recently has been his psychomotor performance, that we're seeing a deterioration in his motor performance, which also goes with dementia because with dementia there's a deterioration of all faculties, all functions.”
Adding to the intrigue, the Mirror reported that Trump has been spotted “frantically” trying to hide the back of his hand, fuelling speculation about his health. According to Dr. Gartner, Trump’s verbal slips, struggles with language, and now motor difficulties fit the pattern of a neurodegenerative disorder. He even suggested Trump may have more than one form of dementia, but he believes one stands out: frontotemporal dementia.
“One of the things that one of the neuropsychologists that we were working with last year pointed out that is almost a dead ringer telltale sign of frontotemporal dementia is something they call a wide-based gait, where you have a sort of one of your limbs, one of your legs, and you kind of swing it in a semicircle,” Dr. Gartner explained.
Frontotemporal dementia (FTD) is not a single disease but a group of disorders that attack the brain’s frontal and temporal lobes. These regions control personality, social behaviour, and language, the very things that often change first in people with the condition.
Unlike Alzheimer’s disease, which is better known, FTD often shows up earlier, typically between the ages of 40 and 65. However, it can appear later in life, making it tricky to diagnose. Many patients are first misdiagnosed with psychiatric conditions or even Alzheimer’s because the symptoms overlap.
The Mayo Clinic states that the symptoms of FTD vary depending on the most affected part of the brain. The progression is gradual but relentless.
Behavioural symptoms include:
Language-related symptoms include:
Movement-related symptoms (less common but significant) include:
The “wide-based gait” noted by Dr. Gartner falls into this movement-related cluster, aligning with the suspicion of FTD.
FTD literally shrinks the brain; the frontal and temporal lobes undergo atrophy while abnormal proteins accumulate. The precise cause is not always clear, but genetics plays a role in some cases. Mutations in certain genes overlap with conditions like ALS (amyotrophic lateral sclerosis), hinting at a deeper biological link that scientists are still trying to untangle.
Interestingly, over half of people diagnosed with FTD have no family history of dementia, meaning the condition can strike seemingly out of the blue.
The only established risk factor is family history. Unlike heart disease or type 2 diabetes, lifestyle choices have not been clearly tied to developing FTD. Still, because it often appears earlier than Alzheimer’s, it can be devastating for families, robbing individuals of their personality, judgement, and communication skills during what should be the prime of life.
While Trump’s team has not confirmed or denied any health concerns, the observations of Dr. Segal and Dr. Gartner point to a broader issue: recognising the early signs of dementia in public figures and ordinary people alike. If the psychologists are correct, the president may be experiencing symptoms that fit squarely within the profile of frontotemporal dementia.
Bruce Willis Health Update: Besides Trump's news, there is an update on Bruce Willis's health. At the preview of ABC's special Emma & Bruce Willis: The Unexpected Journey, Willis' wife Emma opened up about her husband's battle with frontotemporal dementia, saying his “brain is failing him” and his “language is going.” Despite the heartbreaking progression of the disease, she says their family has found new ways of communicating and cherishes the rare moments when his true personality shines through.
The 70-year-old “Die Hard” and “Sixth Sense” star was diagnosed with frontotemporal dementia more than three years ago. In 2023, his family revealed the condition.
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You wake up with a scratchy throat, runny nose, and persistent cough, but your at-home COVID-19 test reads negative. How is this possible? The short answer is yes—you can still be infected. Many other viruses like influenza are currently circulating at high levels across the US, making it increasingly difficult to distinguish COVID-19 from other infections based on symptoms alone.
The Centers for Disease Control and Prevention (CDC) emphasizes that a negative test does not guarantee absence of infection. Viral loads may be too low to detect initially, and testing timing, sample collection, and test sensitivity all play critical roles. For individuals showing symptoms, the CDC recommends considering additional tests, such as PCR tests, which are more sensitive than rapid antigen tests.
Yes, you can test negative for COVID-19 and still be infected. This usually happens if the viral load is too low to detect at the time of testing, if the sample was collected improperly, or if the test used (like a rapid antigen test) is less sensitive than PCR. Early infection, prior immunity, or variations in viral shedding can all lead to negative test results despite being contagious. Repeating the test after a day or two, or using a PCR test, increases detection accuracy.
Lateral flow tests (LFTs), widely used for rapid detection, are most accurate when viral concentrations are high. In the early stages of infection or in individuals with prior immunity from vaccines or past infections, viral loads may be low, resulting in negative tests despite active infection. Immune systems respond faster in previously exposed individuals, producing symptoms before the virus reaches detectable levels.
Virologist explain that SARS-CoV-2 exhibits diverse behavior in the human body. Some individuals experience peak viral loads thousands of times higher than others, while some clear the virus within days. This variation explains why symptoms alone do not correlate perfectly with infectiousness.
PCR tests conducted in clinical settings are more sensitive than at-home antigen tests and may detect infections earlier. Healthcare providers can also help differentiate COVID-19 from other viral illnesses, allowing for timely treatment and guidance. Early detection remains essential, especially for high-risk populations or individuals with underlying conditions.
A negative test result can stem from several factors:
It is also possible to be co-infected with multiple viruses simultaneously, further complicating interpretation. Experts recommend repeating tests a day or two after initial negative results if symptoms persist, rather than assuming one negative result is conclusive.
With variable viral shedding patterns, determining when someone is contagious is not straightforward. The CDC’s updated Respiratory Virus Guidance advises individuals to stay home until at least 24 hours after symptoms improve and fever resolves without medication. Continued precautions, such as masking, improved ventilation, and distancing for five additional days, are recommended to minimize transmission risk.
Serial testing—taking multiple tests over several days—can offer a more reliable picture of viral activity. A series of negative results after prior positives may indicate reduced infectiousness, though the timing and type of test are key considerations.
If symptoms appear but rapid tests are negative, consider PCR testing for confirmation.
Monitor symptoms closely, and seek medical evaluation to rule out other viral infections.
Follow CDC guidance for isolation and post-recovery precautions to protect others.
Be aware of local virus circulation trends, as multiple respiratory viruses may be active simultaneously.
COVID-19 testing, while essential, has limitations. Negative results, especially early in infection or amid widespread viral circulation, do not rule out the disease. Awareness of overlapping respiratory viruses, timing of tests, immune history, and viral load variability is critical for interpreting results accurately. As SARS-CoV-2 continues to circulate alongside influenza, RSV, and norovirus, individuals should exercise caution, use sensitive testing methods when appropriate, and adhere to updated isolation and prevention guidelines.
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Age is a universal truth—every second that passes, we move closer to our later years. But growing older and ageing aren’t exactly the same. Ageing refers not merely to the passage of time but to how our bodies and minds cope with it. Intriguingly, some people maintain vitality and health well into their 80s or 90s, while others experience frailty, cognitive decline, or chronic illnesses far earlier.
A recent study led by an international team at the University of Colorado Boulder sheds light on why this happens. Published in Nature Genetics, the research identifies six distinct biological pathways that accelerate ageing, revealing how genetics and lifestyle combine to influence our longevity and overall health.
Frailty, defined as multisystem physiological decline, is a hallmark of unhealthy ageing. In the United States, more than 40% of adults over 65 are considered frail, showing symptoms like slower walking speed, weaker grip, and a higher number of diagnosed illnesses. But frailty isn’t uniform. Two people with identical frailty scores could be struggling with entirely different issues—one might face mobility limitations, while the other battles cognitive decline.
Dr. Kenneth Rockwood, a frailty expert at Dalhousie University in Canada and co-author of the study, emphasizes that ageing is not a single process. “Aging is not just one thing. There are many ways to be frail. The question then becomes: What genes are involved?”
To tackle this question, researchers examined DNA and health data from hundreds of thousands of participants in the UK Biobank, mapping 408 genes linked to 30 frailty symptoms. This was a dramatic increase from the 37 genes previously associated with accelerated ageing, revealing a much broader genetic landscape than previously understood.
The study highlights six distinct pathways that contribute to unhealthy ageing, each with its own underlying biology:
Disability-Linked Ageing: Genes affecting mobility, coordination, and physical strength. Individuals in this group often experience reduced walking speed, poor balance, and difficulty performing daily tasks.
Cognitive Decline: Genes influencing brain function, memory, and learning. Those affected are more likely to develop dementia, Alzheimer’s disease, or other forms of cognitive impairment.
Metabolic Dysfunction: Genes involved in metabolism and energy regulation. This pathway can result in obesity, insulin resistance, or diabetes, accelerating age-related deterioration.
Multiple Disease Burden: A combination of genetic predispositions that increase susceptibility to several chronic conditions simultaneously, including cardiovascular disease, arthritis, and cancer.
Unhealthy Lifestyle: Environmental and behavioral factors such as poor diet, smoking, sedentary habits, and insufficient sleep, which interact with genetic susceptibility to exacerbate ageing.
Limited Social Support: Genes and psychosocial factors that influence mental health, stress response, and social engagement. Lack of social networks can compound physical and cognitive decline.
Senior author Andrew Grotzinger, assistant professor of psychology and neuroscience at CU Boulder, highlights that while the study focuses on genetic underpinnings, lifestyle factors cannot be ignored. “This paper not only identifies sub-facets of disordered aging but also demonstrates that there is very different biology underlying them,” he explains.
For example, someone with genetic vulnerabilities in metabolism may mitigate accelerated ageing by maintaining a balanced diet and regular exercise, while social isolation may amplify cognitive and physical decline in another individual. Understanding the intersection of genes and lifestyle is critical for designing personalized interventions.
This study represents the largest genetic exploration of frailty to date, providing a roadmap for future interventions aimed at slowing or reversing unhealthy ageing. By identifying the distinct subtypes, researchers hope to develop targeted therapies that address the root biological causes rather than just the symptoms of frailty.
Potential interventions could include cognitive training programs for those genetically predisposed to mental decline, metabolic regulation therapies, or community-based programs to improve social engagement and psychological resilience.
Moreover, the findings could inform public health strategies, helping clinicians identify at-risk populations earlier and provide tailored guidance on diet, exercise, and social habits.
While ageing is inevitable, unhealthy ageing is not. The insights from this study could revolutionize how we approach longevity, offering the possibility of personalized ageing plans based on genetic profiling and lifestyle interventions.
As Dr. Isabelle Foote, co-author and postdoctoral researcher at CU’s Institute for Behavioral Genetics, notes, “To be able to identify treatments to stop or reverse accelerated biological aging, you need to know what the underlying biology is. This is the largest study yet to use genetics to try to do that.”
By recognizing the six distinct triggers of accelerated ageing, scientists are laying the foundation for therapies that could help millions of people maintain health, mobility, and cognitive function well into their later years.
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The search for stronger, longer-lasting teeth has been a cornerstone of dentistry. From the widespread use of fluoride to modern resin fillings, the field has steadily advanced but has never managed to replicate the extraordinary natural material that coats our teeth: enamel. Once it erodes, it’s gone forever—or at least, that’s what we’ve always believed.
Now, researchers from King’s College London are challenging this assumption with an unusual but promising source: keratin, the protein that makes up human hair and animal wool. Their findings suggest that something as simple as a haircut could one day contribute to regenerating tooth enamel and transforming oral care.
Tooth enamel may look simple—a hard, shiny coating that gives teeth their strength and luster—but it is one of the most remarkable substances in the human body. Harder than bone, enamel is designed to withstand decades of grinding, chewing, and exposure to temperature extremes.
Unlike bone, however, enamel is non-living. It lacks the cells and blood supply necessary to heal itself. That’s why a small cavity or a patch of erosion, if left untreated, can become a permanent problem. Once enamel wears away, it exposes dentin, a softer layer that appears yellow and is far more vulnerable to decay.
The impact of enamel erosion is staggering. Dental decay weakens a tooth’s strength by up to 95 percent, leaving it prone to fractures, sensitivity, and eventually loss. According to the Global Burden of Disease 2019, untreated cavities affect an estimated two billion people worldwide, making dental decay the most common disease on the planet.
Modern dentistry has developed tools to slow or mask the damage caused by enamel loss, but not to restore it. Fluoride can strengthen remaining enamel and delay erosion, but it cannot rebuild what has already vanished. Resin-based fillings, while effective in patching cavities, are no match for the natural durability and resilience of enamel. Worse still, resins can contain toxic compounds and lack the long-term strength of natural tooth material.
The result is a cycle of temporary fixes. Cavities are filled, fillings fail, larger restorations follow, and eventually, teeth are lost. As populations age and diets grow increasingly sugar-heavy, the financial and health burden of this cycle is enormous. The challenge has been clear: how can dentistry move beyond patchwork solutions to true biological regeneration?
The answer may lie in keratin, the fibrous protein best known for forming hair, nails, and wool. In their study, researchers at King’s College London extracted keratin from sheep wool and introduced it into a solution designed to mimic human saliva. To their surprise, the keratin didn’t simply dissolve or degrade—it began pulling minerals from the artificial saliva and assembling them into structures that closely resembled natural tooth enamel.
The regenerated material didn’t just look like enamel under a microscope; it behaved like enamel, too. It demonstrated the same stiffness, resistance to wear, and pearly shine that makes natural teeth so resilient.
What’s more, the team discovered that mixing different types of keratin produced superior results. By layering proteins in a hierarchical structure—similar to Russian nesting dolls—they achieved enamel-like material with remarkable strength, durability, and resistance to various forms of degradation.
Attempts to regrow enamel are not new. Previous efforts have focused on peptides, stem cells, and synthetic biomaterials. Yet these approaches have often stumbled over practical barriers, from poor bioavailability to the inability to repair deep cavities.
Keratin may offer a way around these roadblocks. It is abundant, renewable, and can be sourced from waste materials like wool or hair, aligning with a circular economy model. Unlike synthetic resins, keratin-based materials are biocompatible and less likely to trigger toxicity or rejection.
As Dr. Sherif Elsharkawy, the study’s senior author, put it: “We are entering an exciting era where biotechnology allows us to not just treat symptoms but restore biological function using the body’s own materials.”
While the concept might sound futuristic, researchers believe keratin-based enamel boosters could be available within two to three years. Potential applications range from everyday products like toothpaste to more targeted dental gels applied by clinicians.
Imagine visiting your dentist not for a drill-and-fill appointment but for a keratin “varnish” that coats your teeth, hardening over time into new enamel. Or brushing daily with a toothpaste that rebuilds microscopic enamel loss before it develops into a cavity.
If successful, these products could revolutionize dental care by shifting the focus from repair to regeneration.
The implications stretch far beyond whiter smiles. Dental decay is a leading cause of pain, disability, and lost productivity worldwide, especially in low-resource settings where access to dental care is limited. A safe, affordable way to restore enamel could dramatically reduce the burden of oral disease across populations.
The study, published in Advanced Healthcare Materials, is still in early stages. Researchers must test keratin-based enamel in real-world conditions, ensuring it can withstand the stresses of chewing, exposure to bacteria, and years of daily use. Clinical trials will be critical before any commercial rollout.
Still, the concept is generating excitement as co-author Elsharkawy noted, “With further development and the right industry partnerships, we may soon be growing stronger, healthier smiles from something as simple as a haircut.”
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