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.
Credits: iStock
Statin pain and what is it, scientists finally explain. A study by University of British Columbia finally explained what statin muscle pain is and what triggers it. Statins have long been a cornerstone of cardiovascular care. By lowering “bad” LDL cholesterol, these drugs have significantly reduced the risk of heart attacks and strokes for millions worldwide. Yet, for a notable number of users, statins come with an uncomfortable trade-off: muscle pain, weakness, and, in rare cases, severe muscle breakdown that can even lead to kidney failure.
For years, doctors have known that these side effects occur, but not why. Now, a new study offers a detailed answer.
Researchers from the University of British Columbia (UBC), in collaboration with the University of Wisconsin–Madison, have identified the molecular trigger behind statin-related muscle problems. Their findings, published in Nature Communications, could pave the way for safer cholesterol-lowering drugs in the future.
Muscle-related side effects are among the most common reasons people stop taking statins. Symptoms range from mild soreness and fatigue to rhabdomyolysis, a rare but dangerous condition where muscle tissue breaks down and releases proteins that can damage the kidneys.
Until now, the biological mechanism behind this damage remained unclear. The new research zooms in on what happens inside muscle cells when statins are present.
To understand the problem, researchers focused on a protein called the ryanodine receptor (RyR1), which plays a critical role in muscle contraction. RyR1 acts as a gatekeeper, controlling the release of calcium inside muscle cells. Calcium is essential for muscle movement, but only in carefully regulated amounts.
Using cryo-electron microscopy, an advanced imaging technique that allows scientists to view proteins in near-atomic detail—the team observed how statins interact with this receptor.
What they found was striking: when statins bind to RyR1, they force the channel to remain open. This leads to a constant leak of calcium into the muscle cell. Over time, this calcium overload becomes toxic, damaging muscle tissue and explaining the pain, weakness, and, in severe cases, muscle breakdown seen in some patients.
The study examined atorvastatin, one of the most widely prescribed statins globally. However, researchers suggest the same mechanism may apply across the statin class.
They discovered that statins bind to RyR1 in an unusual three-part formation. One statin molecule attaches while the channel is closed, priming it to open. Two additional molecules then bind, forcing the channel fully open and keeping it that way. This sustained opening is what causes the harmful calcium leak.
This detailed binding pattern offers the clearest explanation yet for statin-induced muscle side effects.
While severe muscle injury affects only a small fraction of the more than 200 million statin users worldwide, milder symptoms are far more common and often lead patients to discontinue treatment. This is a serious concern, as stopping statins increases cardiovascular risk.
The new findings provide a potential solution. By modifying the parts of statin molecules that interact with RyR1—while preserving their cholesterol-lowering effects—scientists may be able to develop safer statins with fewer muscle-related side effects.
Beyond statins, the research highlights how advanced imaging technologies are transforming medicine. By visualizing drug–protein interactions at near-atomic resolution, scientists can move from observing side effects to understanding their exact cause.
For patients, this could mean a future where statins remain just as effective—but far easier on the muscles, improving long-term adherence and overall quality of life.
Credits: PR Thai Government (X)
Nipah virus outbreak in India triggered airport screenings of travelers. Many reports claim that passengers are being checked in similar ways as they were during the COVID-19 virus spread.
In Thailand, health officials have announced: "passenger screening points for arrival from affected areas" on its official X account, along with the information on airports to start "enhanced cleaning of shared areas to ensure the safety of both passengers and staff".
On January 27, Thailand's Tourism Ministry announced that they had "not detected any cases of Nipah virus, affirming that strict screening and preventive measures are in place at all international airports to safeguard public health and reassure tourists."
The screening includes:
Anyone suspected of having Nipah will be immediately isolated and referred to public health system "in accordance with International Health Regulations".
Read: Australia Is Monitoring Nipah Virus Outbreak In India
In Thailand, the screenings are happening in these following airports:

Two cases of Nipah virus were detected in India's eastern state of West Bengal, in Kolkata. While other airports have also geared up for travel checks, Thailand is taking it to a next level with COVID-19 like checks. The reason is due to a huge number of international travel form Kolkata to Bangkok and Phuket. Many reports claim that Thailand is a premier international destination for travelers from Kolkata, due to its proximity, affordability, and being a visa-free detination. There are roughly 55 weekly direct flights from Netaji Subhash Chandra Bose International Airport to Bangkok and Phuket.
As per the World Health Organization (WHO), Nipah virus infection is a zoonotic illness that is transmitted to people from animals, and can also be transmitted through contaminated food or directly from person to person.
In infected people, it causes a range of illnesses from asymptomatic (subclinical) infection to acute respiratory illness and fatal encephalitis. The virus can also cause severe disease in animals such as pigs, resulting in significant economic losses for farmers.
Read: Nipah Virus Outbreak In India: How Did It All Begin?
Although Nipah virus has caused only a few known outbreaks in Asia, it infects a wide range of animals and causes severe disease and death in people.
Nipah virus is infectious and can spread from animals like bats and pigs to humans through bodily fluids or contaminated food. It can also pass between people through close contact, especially in caregiving settings. While it can spread via respiratory droplets in enclosed spaces, it is not considered highly airborne and usually requires close, prolonged contact for transmission. Common routes include direct exposure to infected animals or their fluids, consuming contaminated fruits or date palm sap, and contact with bodily fluids such as saliva, urine, or blood from an infected person.
Credit: Canva
Bacteria from the Thar desert is being transported by wind to the Eastern Himalayas and causing respiratory and skin diseases in locals, according to a Science of the Total Environment study.
Researchers from Bose Institute found that powerful dust storms filled with disease-causing bacteria can travel hundreds of kilometers, crossing densely populated and polluted Indo-Gangetic Plain before finally settling over Himalayan hilltops, where they are affecting local populations and ecosystems.
The scientists noted: "In addition to respiratory and skin diseases due to the transported pathogens, vertical uplift injects locally sourced pathogens into high-altitude atmosphere, where they mix with long-range travellers arriving from afar. Together, they reshape the bacterial community floating above the Himalayas, contributing to gastrointestinal infections as well."
These changes were driven by horizontal wind patterns that carry particles across vast distances, combined with rising air pollution from lower elevations.
Riddled with airborne bacteria, including pathogens that can affect overall physical health, this air can increase vulnerability in people living in colder regions, who are already at a high risk of developing conditions related to the weather such as hypoxia (a condition where tissues don't get enough oxygen, often causing confusion, rapid heart rate, shortness of breath and bluish skin)
“About 80 percent of the total Himalayan bacterial population is due to long-range transport via horizontal and vertical movement of atmosphere, causing about 60 percent perturbation in Himalayan bacterial diversity,” the researchers said.
Cold weather and excessive exposure to airborne bacteria also increases disease risks by weakening immune responses, causing blood vessels to constrict and promoting close indoor confinement, which accelerates the spread of bacteria and viruses.
Some common conditions include respiratory infections (pneumonia, bronchitis), cardiovascular strain (heart attacks, strokes) and bacterial infections like Strep throat.
READ MORE: AI Detects More Breast Cancer Cases in Landmark Swedish Study
Dr HB Veena Kumari of the Department of Neuromicrobiology, National Institute of Mental Health and Neurosciences, claims: "The Covid-19 pandemic has significantly contributed to rising antimicrobial resistance. The World Health Organisation projects that 10 million deaths will occur annually by 2025."
According to the National Foundation for Infectious Diseases, antibiotic resistance occurs when bacteria in the body learns to withstand and remain unaffected by the medicines (antibiotics) meant to kill them.
In such cases, doctors have to switch to different antibiotics, but these backup medicines might not work as well or might cause more side effects. Additionally, infections may also worsen over time as bacteria can become resistant to all available drugs.
Alarmingly is that these tough, drug-resistant bacteria can spread from one person to another, both in hospitals and at home.
According to Dr TS Balganesh, Gangagen Biotechnologies, nearly 36 percent of haemodialysis patients die from fatal infections, which is second only to cardiovascular diseases as a cause of death.
He tells Deccan Herald: "The risk for infective endocarditis in haemodialysis patients is approximately 18 times higher than in the general population and up to 58 percent of these episodes are caused by a bacteria named 'S aureus', with an in-hospital mortality of more than 50 percent."
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