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An experimental treatment happens to be the solution to delay Alzheimer's symptoms in some people. These people are the ones who are genetically destined to get the disease in their 40s or 50s. These new findings form ongoing research has now been caught up in Trump administration funding delas. The early results of the study has been published on Wednesday and the participants too are worried that politics could cut their access to a possible lifeline.
One of the participants had said, "It is still a study but it has given me an extension to my life that I never banked on having." The participant is named Jake Henrichs, form New York City, who is 50 years old. He is one of them to be treated in that study for more than a decade now and has remained symptom-free despite inheriting an Alzheimer's-causing gene that had killed his father and brother around the same age.
Two drugs which can modestly slow down early-stage Alzheimer's are sold in the United States. These drugs clear the brain of one of its hallmarks, a sticky gunk-like part called the amyloid. However, there have not been any hints that removing amyloid far earlier, way many years before the first symptoms appear, may postpone the disease.
The research is led by Washington University in St Louis, which involved families that passed down rare gene mutation as participants. This meant it was almost guaranteed that they will develop symptoms at the same age their affected relatives did.
The new findings is based on a subset of 22 participants who received amyloid-removing drugs the longest, on average eight years. Long-term amyloid removal cut in half their risk of symptom onset. The study is published in the journal Lancet Neurology.
Washington University's Dr Randall Bateman, who directs the Dominantly Inherited Alzheimer's Network of studies involving families with these rare genes says, "What we want to determine over the next five years is how strong is the protection. Will they ever get the symptoms of Alzheimer’s disease if we keep treating them?”
The researchers before though did not know what exactly caused Alzheimer's which affects nearly 7 million Americans, most of them in their later life. However, it is clear that these silent changes occur in the brain at least two decades before the first symptom shows up. The big contributor. At some point amyloid buildup can trigger a protein named tau that then starts to kill neurons, which can lead to cognitive decline.
Researchers are now thus studying the Tau-fighting drugs and are looking into other factors, like inflammation, brain's immune cells and certain virus.
The National Institute of Health (NIH) has expanded its focus as researchers have found more reasons for Alzheimer's. In 2013, the NIH's National Institute on Aging funded 14 trials of possible Alzheimer's drugs over a third targeting amyloid. By last fall, there were 68 drugs and 18% of them target amyloid. However, there are scientists too who think that amyloid is not everything and their is way more in the brain tissue, immune cells, and more which can be studied.
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British-Nigerian businessman and social media influencer Igho “Tiny” Ubiribo, 43, died after undergoing a cosmetic penis enlargement procedure in Bangkok, Thailand.
According to findings from a UK coroner’s inquest, Ubiribo, who was also known as Denisi or Ego, reportedly underwent the procedure on March 5, 2026, while travelling with his wife. The treatment involved injections containing hyaluronic acid and lidocaine.
According to reports on the inquest, Ubiribo developed chest pain and repeatedly lost consciousness later that day while receiving a massage.
He was taken to Sukhumvit Hospital in Bangkok, where his condition deteriorated rapidly. Doctors reportedly attempted CPR for more than 100 minutes, but he died before a CT scan could be completed.
A post-mortem examination in the UK subsequently found that he had suffered a pulmonary embolism, a potentially life-threatening blockage of blood flow in the lungs.
The coroner’s findings reportedly linked the fatal embolism to the substances injected during the cosmetic procedure. Reports say material consistent with the filler was found in the lungs.
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A pulmonary embolism occurs when a blood vessel supplying the lungs becomes blocked, most commonly by a blood clot that has travelled from another part of the body.
It can cause sudden chest pain, shortness of breath, rapid heartbeat, dizziness, or fainting and can become fatal if the blockage is severe.
In Ubiribo's case, the coroner’s findings linked the embolism to material associated with the cosmetic injection rather than describing a conventional blood clot travelling from the legs, which is unusual.
Complications can include infection, swelling, tissue damage, deformity, nodules, and vascular complications. If an injected substance enters a blood vessel, there can be potentially serious consequences.
The risks can also depend on the substance used, injection technique, the setting in which the procedure is performed, and the medical expertise and competence of the person administering it.
Ubiribo’s case does not mean that every penile filler procedure causes pulmonary embolism, but it indicates that cosmetic procedures are not risk-free simply because they are elective.
The American Urological Association and Urology Care Foundation have previously stated that subcutaneous fat injection for increasing penile girth has not been shown to be safe or effective.
Ubiribo’s death has now renewed attention on the risks associated with cosmetic penile augmentation, particularly when procedures are undertaken abroad.
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An international clinical trial in the UK is examining whether Alzheimer’s disease can be delayed or prevented before symptoms like memory loss and confusion begin. The trial marks a significant shift from treating existing symptoms to intervening much earlier to delay or prevent the disease.
The Phase III PrevenTRON trial, led in the UK by Surrey and Borders Partnership NHS Foundation Trust, will study the experimental drug trontinemab in around 1,600 adults aged 55 to 80 who have no symptoms of Alzheimer’s but are at high risk of developing the disease in the future.
To be eligible to participate, the participant must have no memory problems. Researchers will use blood testing to look for p-tau217, a biomarker associated with Alzheimer’s-related changes in the brain and increased future risk of cognitive decline.
The trial is recruiting internationally. At least 15 UK hospitals are expected to participate. Surrey and Borders Partnership is the first site in the UK and Europe to open the study.
Participants will be randomly assigned to receive either trontinemab or a placebo. Researchers will then follow them for around four to six years to determine whether treating the disease before symptoms appear can delay or prevent dementia.
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Trontinemab, developed by pharmaceutical company Roche, targets amyloid plaques, abnormal deposits of the protein that build up in the brains of people with Alzheimer’s disease.
The drug, with an antibody-based approach, intends to cross the blood-brain barrier more efficiently and remove amyloid from the brain.
Early studies have shown encouraging results. According to reports on the new trial, trontinemab cleared amyloid plaques in about 90% of people with early Alzheimer’s within 28 weeks.
However, these results came from people who already had early onset of the disease, not people being treated before symptoms, so they cannot prove that the drug will prevent Alzheimer’s.
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Changes in the brain due to Alzheimer’s can begin in the brain years before memory problems develop. By the time symptoms become obvious, substantial biological changes may already have occurred.
Professor Ramin Nilforooshan, consultant psychiatrist and chief investigator for PrevenTRON, said the trial is asking a fundamentally different question from many previous Alzheimer’s studies. With this trial, researchers intend to intervene before symptoms begin.
“PrevenTRON addresses a different question, whether we can act earlier, before symptoms begin,” he said.
Trontinemab remains an experimental drug, and researchers do not yet know whether removing amyloid in people who have no symptoms will actually prevent or delay dementia.
The study will also help establish whether identifying people at increased risk using blood biomarkers and treating them years before symptoms is practical and safe. If successful, this could eventually change how Alzheimer’s disease is managed, as healthcare professionals can move from risk detection and prevention rather than waiting for symptoms.
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Bladder cancer detection could get easier, faster and much less invasive as a new urine test can help identify it. According to new UK research, patients may not have to wait for an invasive bladder examination just to get their cancer diagnosis.
The test, called GALEAS Bladder, detected almost 92.2% of bladder cancers in a study involving 964 patients across seven NHS urology departments. The findings were published in European Urology Oncology recently .
In the study, patients had been referred for urgent investigation because of haematuria, or blood in the urine, one of the key warning signs of bladder cancer. Their urine samples were tested alongside the standard diagnostic method, which included cystoscopy.
Among the 964 patients who had a final diagnosis, 77 were found to have bladder cancer. The urine test detected 71 of those 77 cancers, making the success rate almost 92%.
It detected all 17 muscle-invasive bladder cancers identified in the study. It also picked up 35 of 36 high-grade cancers, equivalent to 97.2%.
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Cystoscopy remains an important part of bladder cancer diagnosis. The procedure involves passing a camera through the urethra into the bladder, so doctors can directly examine the organ.
While effective, cystoscopy is invasive and requires hospital resources. The researchers believe a urine-based test could help doctors decide which patients need an urgent cystoscopy and which patients may be able to safely defer the procedure.
According to this study, a negative GALEAS result was linked with a 99.3% likelihood of not having bladder cancer. Researchers estimated that using the test to triage patients could reduce urgent cystoscopies by about 730 per 1,000 patients, without reducing overall clinical benefit.
Professor Richard Bryan, Director of the University of Birmingham’s Bladder Cancer Research Centre and a study co-author, said the findings show that molecular urine testing can help clinicians determine which patients need urgent cystoscopy.
The test performed particularly well in patients whose blood in the urine was not visible to the naked eye. In this group, which represented about 30% of participants, the test identified all bladder cancers diagnosed in the study.
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The researchers describe GALEAS as a tool to support decision-making before cystoscopy, rather than a complete replacement for diagnostic procedures. A positive result can help prioritise patients for cystoscopy, while a negative result may allow immediate cystoscopy to be deferred in appropriate cases.
The study does not mean that a person with symptoms can simply take a urine test and rule out cancer on their own. A suspected bladder cancer diagnosis still requires appropriate clinical assessment.
In the study, just 8% of participants were diagnosed with bladder cancer. The findings offer a useful way to make bladder cancer investigations more targeted, particularly where large numbers of people are referred for blood in the urine, but only a small proportion ultimately get diagnosed cancer.
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