Credits: Canva
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.
Credit: AI
A newly identified brain protein may help slow the progression of Alzheimer's disease, according to new research that sheds light on how the disease spreads through the brain.
Scientists have found that a protein called SORLA acts as a natural defense against the toxic tau protein, limiting the brain damage that causes memory loss and cognitive decline.
The findings, published in Nature Neuroscience, suggest that boosting SORLA activity could become a therapeutic strategy.
The study found that SORLA regulates how tau proteins move between neurons. While amyloid plaques have long dominated Alzheimer's research, mounting evidence suggests that the spread of tau in the brain is more closely linked to the symptoms of Alzheimer's.
When SORLA levels were low, toxic tau spread more easily from one brain cell to another. In contrast, increasing SORLA significantly reduced tau accumulation, protected brain tissue from shrinking, and preserved memory in mouse models of Alzheimer's disease.
"Our findings identify SORLA as a potent endogenous suppressor of tau propagation," the researchers wrote, adding that enhancing SORLA function "could represent a promising therapeutic strategy for limiting the progression of Alzheimer's disease."
Also read: Alzheimer's Drug Leqembi Helps Over 75% Of Patients Remain Stable Or Improve: Real-World Study
Current Alzheimer's drugs like Leqembi primarily target amyloid-beta plaques. Although these treatments can slow disease progression in some patients, they do not directly stop the spread of tau, which drives the loss of brain cells which worsens dementia.
The discovery of SORLA offers a different approach by targeting one of the disease's most dangerous aspects: tau propagation.
The SORLA findings were demonstrated primarily in laboratory models, meaning much more research is needed before therapies can be tested in people.
However, researchers say identifying the brain's own protective mechanisms provides an important roadmap for developing treatments that not only remove harmful proteins but also prevent them from spreading.
If future studies confirm these findings in humans, therapies that boost SORLA could potentially be combined with existing anti-amyloid medicines to slow Alzheimer's progression more effectively.
The SORLA discovery comes amid growing momentum in tau-based Alzheimer's research.
Just this month, researchers reported encouraging results from diranersen, an experimental therapy designed to reduce production of the tau protein itself.
In a mid-stage clinical trial involving around 400 people with early Alzheimer's disease, the drug lowered tau levels and showed signs of slowing cognitive decline in some participants, although larger studies are needed to confirm its effectiveness.
Also read: Excessive TV Watching In Midlife May Shrink Brain Areas Essential For Memory, Study Finds
SORLA (Sorting Protein-Related Receptor with LDLR Class A Repeats) is a receptor protein naturally present in brain cells.
Scientists have known for years that low SORLA levels are associated with an increased risk of Alzheimer's disease because the protein helps process amyloid precursor protein.
Tau is a normal protein that helps stabilize the internal structure of nerve cells. In Alzheimer's disease, however, tau becomes abnormally folded and forms neurofibrillary tangles.
These tangles spread through interconnected brain regions, disrupting communication between neurons, and eventually causing them to die.
Researchers believe the progression of tau pathology closely mirrors the progression of memory loss and cognitive impairment seen in Alzheimer's patients.
Credit: AI generated image
Women with polyendocrine metabolic ovarian syndrome (PMOS)—formerly known as polycystic ovarian syndrome (PCOS)—face a significantly higher risk of heart attacks, strokes, and other cardiovascular diseases, according to a large study published in The Lancet Obstetrics, Gynaecology & Women's Health.
PMOS affects an estimated 10–13% of women of reproductive age. Researchers analyzed data from more than 2 million women and found that those with PMOS had a substantially higher risk of serious cardiovascular events, even after accounting for established risk factors such as obesity, diabetes, high blood pressure, smoking, and high cholesterol.
The findings, by researchers from the University of Pennsylvania and the University of Rochester, suggest that PMOS should be recognized not only as a reproductive health condition but also as a major cardiometabolic disorder, underscoring the need for routine cardiovascular monitoring in affected women.
Also read: PCOS Is Now PMOS: What The Name Change Means For Millions Of Women
Women with PMOS were significantly more likely to develop atherosclerotic cardiovascular disease (ASCVD), including heart attacks and strokes.
After adjusting for traditional cardiovascular risk factors, researchers found that women with PMOS were:
"Our work shows that it is imperative for clinicians to closely track and evaluate cardiovascular health in patients with PMOS," said Dr. Anuja Dokras, senior author of the study and Founders Professor of Women's Health at the University of Pennsylvania.
She advised women with PMOS to lower their cardiovascular risk by:
PMOS is the new name for PCOS, adopted following an international consensus announced in May 2026 by the World Health Organization, the Endocrine Society, and other leading organizations.
The new name reflects the understanding that the condition affects multiple body systems—not just the ovaries. PMOS is a complex hormonal and metabolic disorder linked to an increased risk of:
The condition can affect:
Experts said the term PCOS was misleading because many patients believed it referred to ovarian cysts, whereas the condition is characterized by increased ovarian follicles rather than true cysts.
"My patients often assumed they had cysts on their ovaries, but instead, people with PMOS have increased follicles that can resemble cysts," said Dr. Dokras. "The effects of PMOS extend far beyond gynecologic health. The new name better reflects the multiple hormonal and metabolic systems involved and encourages more comprehensive care."
The new name aims to explain the condition more accurately and comprehensively.
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Former England forward and manager Kevin Keegan has died after battling stage 4 stomach cancer. He was 75.
Keegan died surrounded by his wife, Jean, and their daughters.
"It is with immense sadness that we announce that Kevin Keegan has passed away at the age of 75," a statement from Keegan's family read.
"The former England player and manager had been battling cancer and was surrounded by his wife and daughters in his final moments.
"Kevin, a double Ballon d'Or winner, was a much-loved husband, father and grandfather. The family would like to thank Kevin's incredible medical team for all their support. This is a hugely difficult time and they are requesting space and privacy."
Earlier this year, his family announced that the former England captain had been diagnosed with stage 4 cancer and was preparing to begin treatment. In June, Keegan revealed that the disease had spread to other parts of his body.
Known affectionately as "King Kev," Keegan spoke openly about his diagnosis during a public appearance in Newcastle, reflecting on his health with his trademark honesty and humor. Fans listened in silence as he shared his journey through the illness.
His death has prompted tributes from football fans around the world.
Also read: Cancer Kills Over 26,000 Daily; Cases to Hit 35 Million by 2050, Says WHO Report
Born in Armthorpe, Doncaster, on February 14, 1951, Keegan began his senior career with Scunthorpe United before joining Liverpool in 1972. He later played for Hamburger SV, Southampton and Newcastle United, ending his playing career with Blacktown City in Australia.
During a club career spanning 592 appearances, Keegan scored 204 goals. He also earned 63 caps for England, scoring 21 goals.
As a manager, Keegan had two spells at Newcastle United and also managed Fulham, England and Manchester City. He guided England to UEFA Euro 2000 through a play-off victory over Scotland before resigning later that year after a disappointing start to the tournament.
Read More: Don't Ignore These Cancer Symptoms: Oncologist Shares The Early Warning Signs
Stomach cancer, also known as gastric cancer, develops in the lining of the stomach. It is more common in older adults than in younger people. According to the American Cancer Society, about six in 10 people diagnosed with stomach cancer each year are aged 65 or older. The lifetime risk is also higher in men (about 1 in 101) than in women (about 1 in 155).
Scientists from the International Agency for Research on Cancer (IARC), part of the World Health Organization (WHO), estimate that infection with the common stomach bacterium Helicobacter pylori (H. pylori) causes 76% of stomach cancer cases globally. The infection often produces no obvious symptoms beyond common digestive complaints, allowing it to go undetected for years.
Doctors advise seeking medical attention if symptoms such as persistent indigestion, nausea, unexplained weight loss, loss of appetite, or upper abdominal discomfort last for more than three weeks.
Around 18 people in the UK and 83 people in the US are diagnosed with stomach cancer every day. Because the disease is often detected at an advanced stage, treatment can be challenging. In the UK, only about 17% of patients survive beyond 10 years after diagnosis.
H. pylori infection can be detected through simple tests and treated with antibiotics. Early diagnosis and treatment can significantly reduce the risk of stomach cancer. Health experts stress that recognizing persistent digestive symptoms and seeking timely medical care can save lives.
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