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.

Slowing Down The Symptoms

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.

How Was The Research Conducted?

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.

More American women are starting GLP-1 medications such as Ozempic and Zepbound after giving birth, according to a new study

The findings, published in JAMA, found that the sharpest increases were seen among women with diabetes, obesity or overweight.

Researchers from the University of Southern California Schaeffer Center for Health Policy & Economics analyzed private insurance claims covering just over 1 million births over seven years.

They found that the share of new mothers starting a GLP-1 prescription within six months of childbirth rose from 0.08% in the first half of 2018 to 1.9% by the first quarter of 2025 — a 24-fold increase.

Which Women Are Driving The Rise?

Women with type 2 diabetes had the highest rate of GLP-1 prescriptions. Among them, use increased from 2.3% to 16.9% over the study period — roughly 1 in 6 women.

Prescribing also increased among women who had gestational diabetes, rising from 0.4% in mid-2021 to 2.7% in the first quarter of 2025. Gestational diabetes affects about 5% to 9% of pregnancies and substantially increases the risk of developing type 2 diabetes later.

The fastest relative increase was seen among women diagnosed with obesity or overweight before pregnancy. GLP-1 use in this group rose from 0.4% in the second half of 2021 to 3.9% by the first quarter of 2025.

Since the second half of 2024, women with diagnosed obesity or overweight have accounted for 40% of new postpartum GLP-1 prescriptions.

Another 21% of women had no documented qualifying diagnosis before giving birth. However, most of these women received a diagnosis — usually obesity or overweight — before starting a GLP-1 medication.

Most Women Started GLP-1s 3 Months After Birth

Patients are advised to stop using GLP-1 medications during pregnancy. Most postpartum women in the study who started a GLP-1 did so at least three months after giving birth.

“Postpartum is a critical window for addressing metabolic risk after pregnancy, and we're seeing GLP-1 use explode in this population. Because evidence on GLP-1 exposure during breastfeeding remains limited, rising postpartum initiation warrants further study,” said lead author and Schaeffer scholar Sih-Ting Cai.

Similar Rise Seen In Denmark

A 2025 JAMA study found a similar rise in Denmark. Fewer than five GLP-1 prescriptions per 10,000 women were recorded after childbirth in 2018, rising to 173 per 10,000 by 2024 — nearly 2% of new mothers.

Can GLP-1s Raise Health Risks After Childbirth?

GLP-1s are increasingly used for postpartum weight loss, but their safety after childbirth remains poorly studied. According to researchers, little is known about how these drugs affect normal postpartum hormonal changes or maternal recovery.

They also noted that evidence on GLP-1 exposure during breastfeeding remains limited, highlighting the need for further research as postpartum use increases.

“We simply do not know how weight-loss medication interacts with those processes or whether it could affect normal physiological recovery,” Dr. Jonathan Zipursky, a clinical pharmacologist and toxicologist at the University of Toronto, told The New York Times in 2025.

Evidence on GLP-1s during breastfeeding is also limited. A 2024 CMAJ paper suggested low breast-milk exposure, but researchers stressed that infant safety data remain insufficient. Zipursky recommended avoiding GLP-1s while breastfeeding as a precaution.

A new experimental obesity drug could offer an alternative to GLP-1 medicines for people who struggle with their gastrointestinal side effects.

Petrelintide, a once-weekly injectable drug that works on the hormone amylin, helped people with obesity lose more than 10% of their body weight in a Phase 2 trial.

Published in The Lancet Diabetes & Endocrinology, the drug showed a relatively low rate of gastrointestinal side effects.

The study, however, did not directly compare petrelintide with drugs like semaglutide or tirzepatide.

So, while the results suggest it may be better tolerated, researchers cannot yet say that it causes fewer side effects than GLP-1 drugs.

Petrelintide Works Differently From Ozempic And Mounjaro

Petrelintide is a long-acting amylin analogue. Amylin is a hormone produced by the pancreas alongside insulin and helps control appetite and food intake.

A yet-to-be approved drug, unlike Ozempic and Wegovy, which target the GLP-1 hormone, petrelintide focuses on amylin.

It is being developed by Danish drugmaker Zealand Pharma with Roche.

Also read: CSIR-CCMB Scientists Find Flu & COVID Viruses May Affect A Protein Linked To Parkinson’s Disease

Petrelintide’s Effect On Weight Loss

The Phase 2 ZUPREME-1 trial included 485 people who received at least one dose of petrelintide or placebo, with everyone also receiving lifestyle advice.

After 42 weeks, average weight loss ranged from 8.7% to 10.7%, depending on the petrelintide dose.

The group receiving placebo lost about 1.7% of their body weight. The 5 mg dose produced the largest average reduction, at 10.7%.

At 28 weeks, weight loss across the petrelintide groups ranged from about 7.9% to 9.8%, compared with 1.7% with placebo.

Also read: Type 1 Diabetes: Student Nearly Dies After Diet Advice To Stop Insulin; Why Insulin Is Essential

Petrelintide Shows Promise In Terms Of Tolerability

This is perhaps one of the biggest attractions of petrelintide. Nausea was the most common side effect, affecting 20% of people compared to 6% in the placebo group.

However, vomiting was uncommon, occurring in 3% of the petrelintide group compared with 6% of the placebo group. Diarrhoea occurred in 7% and constipation in 7% of those receiving petrelintide. Researchers also reported that most gastrointestinal side effects were mild.

This is a well-tolerated medication," lead investigator Dr. Timothy Garvey of the University of Alabama at Birmingham told HCPLive . Approved GLP-1 drugs have produced larger average weight loss in their own trials, but Garvey said "This current level of 10-15% is sufficient to treat a large number of patients who have obesity.

Three serious adverse events were considered related to petrelintide, including two cases of gallstones and one case of obstructive pancreatitis, according to an independent expert assessment of the study.

Petrelintide Vs Ozempic

One may be inclined to compare petrelintide's side-effects with that of GLP-1 drugs like Ozempic, Wegovy, Zepbound and Mounjaro, but the trial was designed to compare petrelintide with placebo, not with semaglutide or tirzepatide.

Dr Marie Spreckley of the University of Cambridge cautioned that the comparison with GLP-1 medicines is too strong because “the trial did not test petrelintide against any of those medicines, so we cannot say from these results that it causes fewer side effects.”

That means more investigation will be needed to compare petrelintide’s tolerability and existing obesity treatments.

However, the results have prompted further development of petrelintide, with Phase 3 trials planned. Researchers are particularly interested in whether the drug can provide sustained weight loss while allowing people to remain on treatment without gastrointestinal symptoms.

Repeated viral infections may play a key role in shaping Parkinson’s disease risk. A new study by researchers at CSIR-Centre for Cellular and Molecular Biology (CCMB), Hyderabad, has found that RNA viruses like influenza and even SARS-CoV-2 can interact with a protein called alpha-synuclein, accelerating the formation of abnormal protein clumps associated with Parkinson’s.

Published in Cell Reports, the study, which was led by Dr Swasti Raychaudhuri’s laboratory at CCMB, also identified a cellular protein that appears to act as a defense against this process.

What Is Alpha-Synuclein?

Alpha-synuclein is a protein that is naturally found in nerve cells. In Parkinson’s disease, the protein can accumulate into abnormal clumps called amyloid aggregates.

These aggregates are a characteristic feature of Parkinson’s and can interfere with the normal functioning of neurons.

The new study looked at what happens to alpha-synuclein when a cell is infected by an RNA virus.

Also read: Flu 2026: Symptoms To Watch For As New Season Begins

How Could Flu And COVID Affect Alpha-Synuclein?

Flu and COVID viruses contain RNA, which is their genetic material. The researchers found that parts of this viral RNA can fold into unusual shapes called RNA G-quadruplexes (rG4s).

These RNA structures can interact with a protein called alpha-synuclein. Alpha-synuclein normally exists in brain cells, but in Parkinson’s disease it can clump together and form abnormal deposits.

The researchers found that viral RNA structures may encourage alpha-synuclein to clump together more easily.

Also read: WHO Sets 2027 Flu Vaccine Strains; US States Can Now Order Free COVID Shots For Kids

Body Has Its Own Defense Mechanism

The researchers also identified a protein called DDX39A, which counters both viral multiplication and alpha-synuclein aggregation.

Normally found inside the cell nucleus, DDX39A moves into the cytoplasm during an RNA viral infection. There, it can interact with both viral RNA structures and alpha-synuclein.

DDX39A acts as an RNA “unwinding” protein. It breaks apart the rG4 structures in viral RNA, making it harder for the virus to replicate. At the same time, this process appears to slow the formation of alpha-synuclein amyloids.

Study first author Aanchal said, “The virus fails to replicate with its RNA structures dismantled, and thus, the viral load in the cells decreases. At the same time, the unwinding of viral RNA’s secondary structure effectively slows down α-Synuclein amyloid formation.”

Viral Infections Do Not Cause Parkinson’s: Researchers

The researchers caution against making that conclusion. Not every viral infection will increase amyloid formation, and not everyone who gets influenza or COVID-19 will develop Parkinson’s.

The study suggests that the outcome depends on a complex balance between the virus, viral RNA, alpha-synuclein, and the cell’s defence mechanisms.

There have been previous studies reporting an association between certain viral infections and an increased risk of neurodegenerative diseases. But the biological mechanism behind such associations has remained unclear.

The CCMB researchers are now investigating what happens to these molecular interactions over longer periods.

The concern is that repeated exposure to viral infections could alter the balance between protective cellular mechanisms and protein aggregation. However, this remains an area of investigation and cannot currently be used to predict an individual's Parkinson’s risk.