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.

Cancer cases linked to the September 11, 2001, World Trade Center terror attacks have surged 75%, according to new research, highlighting the ongoing health crisis even 25 years later.

The research was conducted by Northwell Health’s Long Island Jewish (LIJ) Medical Center, which provides free medical monitoring to people affected by the aftermath of the attacks at New York’s World Trade Center, where nearly 3,000 people were killed.

About two-thirds of all enrollees are certified for at least one WTC-related health condition, while 30% of those enrolled through Northwell have battled cancer. That number is expected to rise dramatically over the next decade.

“For over 25 years, we have cared for people who were exposed to the aftermath of September 11th,” said Jacqueline Moline, director of the Northwell WTC Health Program.

“Over 57,000 cases of cancer have been documented, and cancer rates — including rare cancers — are rising. There has been a two-fold increase in lung cancer in just five years. Our fear is that cancer diagnoses will only rise as we move into the next 25 years.”

Which Cancers Are Growing?

Northwell’s WTC Health Program saw 9/11-certified cancer cases increase from 177 in 2023 to 235 in 2025 — a 75% jump over three years.

Another 132 new cases were reported through the first half of 2026, continuing the trend. That brings the total to 811 new cases over 42 months.

Prostate and skin cancers were the most common, followed by breast and urinary tract cancers.

By comparison, the program recorded 1,634 cancer cases during the first decade from 2013 to 2022, and 2,445 all-time cases through June among 1,489 people.

Crisis Grows From Lung Diseases To Cancer

Researchers at the center noted that September 11 was not a one-day event. The toxic dust cloud at Ground Zero and the gruelling recovery work created a persistent environmental catastrophe that continues to affect lives.

A variety of lung diseases were seen earlier among those affected. Now, after a decades-long incubation, a range of cancers is emerging as a growing concern.

"Hundreds of thousands of people were at risk then and remain at risk for disease now. While we initially saw respiratory disease, we now are faced with increasing numbers of our patients developing cancer," Moline said.

Further, a trove of newly released files by New York City Mayor Zohran Mamdani indicates that toxic air persisted for months after the 9/11 attacks on the World Trade Center and that officials played down the health risks.

“People got sick because the leaders they trusted lied and told them they were safe to breathe in toxic air,” Mamdani said at a news conference with survivors.

“As the years pass and the human toll grows, we reckon with the cost of September 11th whenever another New Yorker is stolen from us too soon. Now, close to 25 years later, more people have died from 9/11-related illnesses than were killed on the day itself.

Google DeepMind has launched AlphaGenome Atlas, an AI-powered database that maps the predicted effects of all 9 billion possible single-letter changes in the human genome.

The novel tool could help scientists identify genetic changes linked to rare diseases, understand how mutations affect gene function and uncover new clues about human health and disease.

AlphaGenome Atlas: Explore DNA We Don’t Understand

Scientists have a strong understanding of the roughly 2% of the genome that codes for proteins. But interpreting mutations in the remaining 98% of non-coding regulatory DNA has been much more difficult.

Changes in these regions can disrupt how genes are regulated and affect cellular functions. By pre-computing the predicted effects of billions of genetic variations, AlphaGenome Atlas aims to give researchers a map for navigating this largely unexplored part of the genome.

The resource could help researchers investigate unsolved rare diseases, uncover biological mechanisms behind common illnesses and support drug discovery.

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One Score to Help Researchers Prioritize Variants

The Atlas introduces the AlphaGenome Variant Impact (AVI) score, a single score that combines predictions for genetic effects across coding and non-coding regions.

This allows researchers to prioritize potentially important variants without having to sift through thousands of individual data points.

Each AVI score is also linked to the biological features contributing to the prediction, including aspects of gene regulation predicted by AlphaGenome and protein-impact information from AlphaMissense.

A Genetic Database

AlphaGenome Atlas contains predictions for the effects of 9 billion single-nucleotide variants in the human genome.

The dataset is about 1 petabyte in size, making it more than 30 times larger than the previous AlphaFold Database.

The Atlas brings together several resources, including:

• Molecular effect predictions: Thousands of predictions for each variant across multiple aspects of gene regulation, covering hundreds of human and mouse cell types and tissues.
• AVI score: A single score indicating the predicted impact of each genetic variant.
• AVI feature attributions: Information showing the biological features driving each AVI score.
• DNA sequence motifs: A collection of more than 2,500 recurrent DNA sequences and their locations in the genome.

Helping Solve Rare Genetic Diseases

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One of the biggest challenges in rare disease research is identifying the few potentially causal variants among thousands of genetic changes.

Researchers at the Broad Institute, working with the GREGoR Consortium, used the AVI score to prioritise variants in unsolved rare disease cases and identified a variant affecting the DNM1 gene which is strongly linked to epileptic encephalopathy.

Finding Genetic Links To Complex Traits

AlphaGenome Atlas is also being used to study rare, non-coding variants linked to complex traits, where the large number of harmless genetic changes can create substantial statistical noise.

Researchers at the University of Exeter applied the Atlas to identify 22% more non-coding genetic associations.

Among the top 1% of variants predicted to have the greatest impact, the analysis identified 19 genetic regions linked to body mass index (BMI), helping direct further targeted research.

AlphaGenome Atlas Is Free For Research

Google DeepMind said AlphaGenome Atlas is being made free to the scientific community for academic research, with the aim of opening new pathways for genetic and biomedical discovery.

The company described it as a comprehensive catalogue of how genetic mutations are predicted to affect molecular biology, covering every possible single-letter genetic change across the human genome.

The US Food and Drug Administration (FDA) recently approved the first drug for Alexander disease, a rare and progressive neurological disorder. Alexander disease is marked by symptoms like seizures, slow development, muscle weakness, difficulty in walking and problems with speech and swallowing.

The FDA approved Zanvastro (zilganersen) for children and adults afflicted with Alexander disease. Being the first approved treatment for the condition, the drug is designed to directly target the abnormal protein buildup, one of the major factors that drives the disease.

Talking about the landmark drug, Emily Freilich, MD, Director of the Division of Neurology I at the FDA’s Center for Drug Evaluation and Research said, “For patients with Alexander disease and their families, there have been no approved treatment options, only supportive care while the disease progresses. Today’s approval is a landmark moment for this community, offering the first therapy that addresses the underlying cause of this rare and serious disease.”

What Is Alexander Disease?

According to the FDA, Alexander disease is extremely rare as it affects fewer than one in a million people. Alexander disease is a rare, genetic neurodegenerative disorder that is caused due to mutations in the GFAP gene. GFAP gene promotes the production of glial fibrillary acidic protein, a type of protein found in the central nervous system.

GFAP is found primarily in astrocytes, a type of specialised cells in the brain and spinal cord that support and protect nerve cells.

In Alexander disease, abnormal GFAP accumulates inside these cells. This leads to formation of cumulative protein called Rosenthal fibres. This disrupts the normal function of astrocytes and ultimately damages the nervous system.

In simple terms, the issue is not that the brain suddenly loses a particular protein. It is that a genetically altered version of GFAP is produced and progressively accumulates where it should not. This is why Alexander disease is considered an astrogliopathy, a disorder which is primarily driven by astrocyte dysfunction.

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Symptoms Of Alexander Disease

The disease can present very differently depending on the timing of its onset. In infants and young children, it can cause delay in development, loss of previously acquired essential skills, seizures, unusually large head, muscle weakness, feeding difficulties and problems with movement. Some severe early-onset cases may progress rapidly.

Juvenile and adult forms can be slower and may involve speech and swallowing difficulties, abnormal way of walking, muscle stiffness, poor coordination, weakness, breathing or sleep problems and autonomic dysfunction.

As symptoms of Alexander disease may overlap with many other neurological disorders, its diagnosis remains challenging. Doctors typically diagnose it by combining key findings in brain MRI with genetic testing for a disease-causing GFAP variant.

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What Makes The New Drug Different?

Until now, the treatment for Alexander Disease has largely focused on managing individual symptoms, like seizures, feeding problems and difficulties with movement, speech or swallowing.

Taking a different approach, Zanvastro, a type of RNA-targeted medicine is designed to reduce production of the abnormal GFAP protein.

Its goal is to lower the amount of disease-driving protein before it can continue accumulating and damaging astrocytes. The drug is administered once every three months as an injection into the spinal canal.

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Zanvastro's FDA Approval

The FDA's approval arrived after a controlled study involving 49 patients aged two and older, along with an open-label substudy involving four children younger than two.

Among patients aged five and older who already had walking difficulties, those receiving Zanvastro had significantly better walking speed after 61 weeks than others.

For children aged two to four, researchers used broader measures of motor development because walking speed alone is not a reliable measure at that age. Those children showed improvement in motor skills, while the control group declined.

The most common side effects included vomiting, back pain, cough, headache and post-lumbar-puncture syndrome. The FDA also warned that aseptic meningitis has been reported.

Alexander disease has long been a condition in which doctors treated complications but had no approved therapy that aimed at the biological process causing the disease.

Zanvastro does not reverse genetic mutations themselves. Instead, it targets one of the consequences of those mutations by reducing production of abnormal GFAP.

As Ionis Pharmaceuticals CEO Brett P. Monia said following the approval, the treatment allows the field to move “beyond managing individual manifestations of the disease to addressing its underlying biology.”