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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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Atherosclerosis, in which plaque builds up inside the arteries, is a major cause of cardiovascular disease and can lead to heart attacks, strokes and sudden death. A new study published in The New England Journal of Medicine found that plaque buildup can begin decades before symptoms appear.
An international team of researchers found atherosclerosis in many apparently healthy young adults, including those in their 20s.
Dr Borja Ibáñez, Scientific Director of the Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), said the findings point to a new approach to cardiovascular prevention: detecting atherosclerosis through imaging before symptoms appear, rather than relying only on risk factors such as blood pressure, cholesterol and smoking.
The study included 16,808 people aged 18 to 70 from Denmark and Spain. None had a known history of atherosclerotic cardiovascular disease.
Using advanced imaging, researchers examined the carotid, femoral and coronary arteries for plaque. Overall, 57.1% of participants had atherosclerotic plaques, despite having no symptoms or previous diagnosis of cardiovascular disease.
Atherosclerosis was detectable even among the youngest participants. Among those aged 18 to 29, plaque was found in:
The prevalence increased with age, reaching nearly 90% among people aged 60 to 70. By 60–70, only about 1.9% of men and 8.1% of women had no detectable plaque in any of the arteries examined.
The study found differences between men and women. Atherosclerosis began increasing at younger ages in men, with their atherosclerotic profile appearing five to 10 years earlier than in women.
In women, the sharpest increase occurred between 40 and 60, broadly coinciding with the menopausal transition.
Conventional cardiovascular risk scores, including SCORE2, identified only a small proportion of people who already had silent atherosclerosis.
Researchers found that people with coronary artery plaque often also had plaque in the carotid or femoral arteries. Because these arteries can be examined using relatively simple, non-invasive ultrasound, the finding could have implications for future screening.
Dr. Ibáñez said portable ultrasound devices could potentially become a tool for detecting atherosclerosis from early adulthood.
“The future of cardiovascular prevention must be more precise and personalized,” he said, adding that early detection could allow earlier intervention and more targeted treatment.
Dr. Sudhir Kumar, neurologist at Apollo Hospitals, Hyderabad, said atherosclerosis can remain silent for decades before causing a heart attack, ischemic stroke or peripheral arterial disease.
However, having plaque does not mean a heart attack or stroke is imminent. Greater plaque burden and more widespread disease are associated with higher cardiovascular risk.
He also stressed that atherosclerosis is not simply an unavoidable consequence of ageing. Its progression can be slowed by addressing modifiable risk factors.
Credit: AI
15-year-old Tanvi Pariyani’s death at AIIMS Delhi has raised questions about the treatment of a rare and complex congenital heart condition she had been living with since childhood.
Tanvi, from Kota, had been visiting AIIMS since she was two. Her medical records listed ventricular septal defect (VSD) with pulmonary atresia, a combination that can make treatment considerably more complicated than just a 'hole in the heart'.
Tanvi’s family has alleged that corrective surgery was repeatedly postponed. AIIMS, however, said its treating team concluded in 2017 that corrective surgery was not feasible because of the complexity of her cardiac anatomy and advised medical management.
The hospital has now constituted a committee to review her complete clinical records, investigations, treatment, expert opinions and the circumstances surrounding her death. An autopsy is also underway.
A VSD is a hole in the wall separating the heart’s two lower chambers. The right side of the heart pumps oxygen-poor blood towards the lungs through the pulmonary artery.
In pulmonary atresia, the normal route through which blood leaves the right side of the heart and reaches the lungs is blocked or has not developed properly.
This can severely block blood flow to the lungs and reduce the amount of oxygen entering the bloodstream.
When pulmonary atresia occurs along with VSD, doctors have to deal with multiple abnormalities rather than simply closing the hole.
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Some children may initially require procedures to ensure adequate blood reaches the lungs. Doctors may use medicines temporarily and later create an alternative pathway for blood flow through a shunt.
In some patients, the pulmonary arteries remain very small and the body develops additional blood vessels supplying the lungs.
These vessels, called major aortopulmonary collateral arteries (MAPCAs), may need to be brought together through a procedure called unifocalisation.
A conduit may then be used to connect the heart to the lungs, while the VSD may also need to be closed.
The anatomy can also change as a child grows. Small pulmonary arteries, abnormal blood vessels and rising pressure in the lungs can make later surgical repair more challenging.
According to AIIMS, Tanvi was admitted on August 24 after her condition deteriorated and was being evaluated for a possible heart-lung transplant.
On September 1, she developed severe cyanosis, and her oxygen saturation fell to around 48%. AIIMS said she subsequently suffered a hypoxic spell followed by cardiac arrest. Despite oxygen support and resuscitation, she could not be revived and was declared dead at 5:06 am.
“The Director, AIIMS, New Delhi has constituted a committee to examine the matter in detail, review the sequence of events and establish the facts,” the institute said.
The committee’s findings and autopsy report will be important in establishing what happened and whether any intervention could have altered the outcome.
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A new US CDC study has warned of a threefold rise in identifications of Trichophyton indotineae, a skin fungus that causes ringworm and is resistant to standard treatment.
Between 2022 and 2025, T. indotineae was identified in 29 countries, with resistance to terbinafine, a commonly used antifungal medication. The first US case was reported in 2023.
Most cases are treated with terbinafine, either as a cream or a pill.
“Our results reveal a marked global increase in T. indotineae isolation,” the authors wrote in their paper, published in the CDC’s monthly journal, Emerging Infectious Diseases.
During the study period, 566 users from 54 countries submitted 1,657,334 spectra that led to the identification of fungal agents.
However, the research cannot tell us how many people globally are contracting T. indotineae; it only shows that laboratories are detecting it more often.
Also read: 98 Years After Penicillin, Are We Running Out Of Effective Antibiotics?
Ringworm has nothing to do with worms. The misleading name refers to an infection caused by dermatophytes, fungi that thrive in warmth and moisture.
It can affect people of all ages and is highly contagious. Careful attention and immediate treatment are required to control the infection effectively.
Ringworm, also called tinea corporis, is a skin infection caused by fungal spores invading the dead outer layers of the skin. It typically presents as circular, red, scaly patches accompanied by itching or discomfort.
Symptoms of ringworm depend on where the infection develops:
Ringworm is highly infectious and can be transmitted through:
Preventing ringworm is largely about maintaining good hygiene and avoiding contact with infected people or animals.
Left untreated, ringworm can spread across the body or penetrate further, potentially leading to complications such as secondary bacterial infections.
See a doctor if:
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