How NASA’s Webb Helped Rule Out Asteroid’s Chance of 2032 Lunar Impact

Editor’s Note: This post highlights data from Webb science in progress, which has not yet been through the peer-review process. These results were reported as part of NASA’s role in the International Asteroid Warning Network.

NASA’s James Webb Space Telescope recently made new observations of the asteroid 2024 YR4, which we already knew poses no significant threat to Earth in 2032 and beyond. Webb’s new observations – among the faintest ever observations of an asteroid, in a challenging application of the telescope’s unique capabilities – helped determine that the asteroid also will safely pass the Moon in 2032.

We spoke with Andy Rivkin of the Johns Hopkins University Applied Physics Laboratory in Laurel, Maryland, and Julien de Wit of the Massachusetts Institute of Technology in Cambridge, the two co-principal investigators of the Webb Director’s Discretionary Time program used to refine our knowledge of the asteroid’s orbit.

Plane-of-sky position and associated uncertainties for asteroid 2024 YR4 on 2026 February 26. Stack exposures of JWST’s 2026 February 26 observations showing the high-significance detection of asteroid 2024 YR4 (green) offset by ~22 pixels (about 0.5 arcseconds) from the position that would have supported a non-zero 2032 lunar impact probability (red).

NASA, ESA, CSA, A. Rivkin (JHUAPL), and J. de Wit (MIT)

What is most important for people to know about these Webb observations?

We requested director’s discretionary time on Webb because there was a possibility for 2024 YR4 to impact the Moon in 2032. Without Webb, we would have needed to wait until 2028 with a large amount of uncertainty about what might happen, but with these observations that uncertainty is removed. Webb first constrained the asteroid’s size in 2025 and has now extended its observational arc to refine the orbit of 2024 YR4, demonstrating in practice how its sensitivity can support planetary-defense assessments for extremely faint objects long before they become observable again from Earth.

Why is Webb the only observatory that can measure the asteroid’s position prior to 2028?

2024 YR4 is exceedingly faint right now, reflecting about as much light as an almond at the distance of the Moon. It glows at a magnitude of about 30, which is 4 billion times fainter than the faintest star visible to the unaided eye. Webb is the only observatory that could hope to make these measurements, as it is the only one with the required sensitivity and stability combined with precise moving-target tracking needed to follow and study objects like this. This allowed Webb to make several hour-long exposures of 2024 YR4 without the asteroid moving even a pixel in any of them. No other observatory can make these measurements until 2028 during the asteroid’s next passage through the inner solar system.

How does the Webb data enable us to better predict 2024 YR4’s trajectory?

Two things help us do a better job of predicting the paths of asteroids: getting very accurate positions and increasing the amount of time over which they’ve been observed. These measurements of 2024 YR4 are very precise, and even more importantly extend the date of the most recent observations from May 2025 to late February 2026. This almost doubles the length of time the asteroid 2024 YR4 has been observed and allows orbital dynamicists to be very confident in predicting where it will be in 2032.

What have you learned?

With these observations, NASA has further refined the orbit of 2024 YR4 well enough to know it will miss the Moon in 2032, meaning a lunar impact will be one fewer thing for satellite operators — as well as astronauts — to worry about in the future. Also critically important, however, was the experience we gained using Webb to make these measurements. The extreme faintness of 2024 YR4 at the time of the measurements provided a challenge because it is difficult or impossible to get good images containing both something as faint as the asteroid and something as bright as some of the stars used to precisely measure its location on the sky. The excellent quality of Webb’s NIRCam (Near-Infrared Camera) design and optics allowed us to develop techniques that worked wonders, however, and that gives us confidence that we can make such measurements again if necessary in the future, and we will not need to learn how to do it from scratch.

How do the Webb observations fit within the larger picture of the study of this asteroid (and other near-Earth asteroids)?

Webb observations of 2024 YR4 were critical for our understanding of that asteroid. Specifically, they helped to constrain the object’s size and its orbit. In a larger sense, these observations demonstrate the utility of Webb for planetary defense — its unique capabilities for measuring the position and physical properties of an object beyond the capabilities of any other facility. Webb provides a unique capability to support such assessments well before objects return to the inner solar system. If and when NASA’s planetary defense assets discover another potentially hazardous object of interest, we will know that we could make these measurements in practice, not just in theory, and we have gained important experience in designing and analyzing those measurements.

Looking at an even larger picture, Webb is not the only NASA Astrophysics mission with planetary defense applications. For example, NASA’s next flagship science mission, the Nancy Grace Roman Space Telescope, will capture asteroids as it surveys the universe and could also help better constrain their orbits. And NASA’s Habitable Worlds Observatory mission concept will have unprecedented sensitivity unlike any space telescope before it, a powerful potential tool to help with earlier orbit refinement. NASA is also developing the Near-Earth Object Surveyor, bringing NASA’s space telescope heritage directly to bear on the asteroid hazard and demonstrating the strong collaboration across NASA Science in meeting NASA’s planetary defense objectives.

About the Authors

Andy Rivkin, a planetary astronomer at the Johns Hopkins University Applied Physics Laboratory, and Julien de Wit, a professor at the Massachusetts Institute of Technology, are co-principal investigators of the Webb Director’s Discretionary Time program (DD 9441) used to study asteroid 2024 YR4.   

Source: How NASA’s Webb Helped Rule Out Asteroid’s Chance of 2032 Lunar Impact - NASA Science

Experimental Alzheimer's drug reverses memory loss in mice by reprogramming gene activity - medicalxpress

Graphical abstract. Credit: Molecular Therapy (2025). DOI: 10.1016/j.ymthe.2025.12.038

A team from the University of Barcelona has designed and validated in animal models an innovative compound with a pioneering mechanism of action for the treatment of Alzheimer's disease. Unlike current drugs, which mainly remove beta-amyloid plaques that accumulate in the brain, this new experimental drug reprograms the neuronal epigenome by correcting alterations in gene expression that contribute to the progression of the disease.

The results of this study, published in Molecular Therapy, open the door to an epigenetic-based therapeutic strategy to fight Alzheimer's disease.

"The compound FLAV-27 represents an innovative and promising approach to Alzheimer's disease, with the potential to modify the disease process, as it acts not only on its symptoms or a single pathological biomarker, but directly on its underlying molecular mechanisms," says Aina Bellver, a researcher at the UB Institute of Neurosciences (UBneuro) and first author of the paper.

The study was led by Professor Christian Griñán and Professor Mercè Pallàs, from the Faculty of Pharmacy and Food Sciences, with the participation of researchers from UBneuro and the CIBER Area for Neurodegenerative Diseases (CIBERNED), as well as the UB Institute of Biomedicine (IBUB), the Institute of Nutrition and Food Safety (INSA-UB), the August Pi i Sunyer Biomedical Research Institute (IDIBAPS) and other national and international institutions.

Beyond beta-amyloid protein: a new epigenetic target

The drugs currently approved to treat Alzheimer's, such as lecanemab and donanemab, are monoclonal antibodies that work by removing beta-amyloid protein plaques from the brain.

"Although they represent a breakthrough, their efficacy is limited, as they only slow cognitive decline by 27% to 35%, have several side effects and only address the part of the pathology caused by beta-amyloid accumulation," the researchers explain.

In contrast, FLAV-27 works in a completely different way: it is the first inhibitor in its class to affect the G9a enzyme, which is essential in the epigenetic regulation of the brain, because it helps to silence genes that are fundamental for neuronal development, synaptic plasticity and memory consolidation.

To inhibit G9a, the new drug prevents access by the natural molecule S-adenosylmethionine (SAM), which the enzyme needs to modify DNA. It thus slows down the epigenetic dysregulation, characteristic of Alzheimer's disease, and allows neurons to regain normal function.

Functional cognitive recovery in animal models

The study shows that inhibiting G9a with FLAV-27 not only reduces classic pathological markers, such as beta-amyloid protein and phosphorylated tau, which accumulate in the brains of people with Alzheimer's disease, but also restores cognitive function, social behavior and the structure of neuronal synapses in various models: from in vitro assays, through the worm C. elegans—in which it improves mobility, life expectancy and mitochondrial respiration—to murine models of late-onset and early-onset Alzheimer's disease.

"In these models, there is evidence of improved short- and long-term memory, spatial memory and sociability, which demonstrates not only an effect on molecular markers, but also functional cognitive recovery," the researchers emphasize.

According to the authors, these results confirm that epigenetic dysregulation—changes in the chemical mechanisms that determine which genes are activated or not without altering the DNA sequence—is not just a side effect of Alzheimer's disease, but an active and controllable mechanism that links the main pathological features of the disease, such as beta-amyloid and tau proteins, neuroinflammation and synaptic dysfunction, through a common epigenetic axis.

This opens the door to a new category of therapies: epigenetic disease-modifying treatments, which could complement or even replace current strategies, which are based exclusively on the elimination of beta-amyloid.

The new experimental compound works through an epigenetic mechanism that acts not only on the symptoms of the disease, but directly on the molecular mechanisms that contribute to its progression.

Blood biomarkers to monitor treatment

A key finding that adds to the translational value of this treatment is the identification of a biomarker that can be measured in both the brain and blood plasma of patients.

The team has found that the epigenetic marker H3K9me2, the SMOC1 protein and the p-tau181 molecule are significantly elevated and that their blood levels correlate directly with symptoms such as tau protein accumulation, neuroinflammation and the degree of cognitive impairment.

When FLAV-27 is administered in animal models, these indicators return to normal levels, in parallel with cognitive recovery.

The availability of these peripheral bioindicators is one of the key aspects that distinguishes FLAV-27 from other drugs in development.

"It has important implications for future clinical trials, as it will allow the selection of suitable patients with a simple blood test, monitoring of treatment and demonstration that the drug actually modifies its therapeutic target," the authors stress.

Towards human trials

Despite these promising results, FLAV-27 still needs to pass further stages before clinical trials can begin in humans.

Currently in the advanced preclinical phase, the next steps include regulatory toxicology studies in at least two animal species, obtaining the pharmaceutical form, and preparing the regulatory dossier to apply for clinical trial authorization from the relevant agencies, a process that will take years.

This new phase will be led by Flavii Therapeutics, a spin-off from the UB founded in 2025 and holder of the exclusive license for FLAV-27.

The company will take on the preclinical and clinical development of the drug, as well as the management of intellectual property and fundraising, with the aim of converting the knowledge generated at the UB into new therapies for central nervous system diseases such as Alzheimer's. 

Provided by University of Barcelona 

by University of Barcelona

edited by Sadie Harley, reviewed by Robert Egan 

Source: Experimental Alzheimer's drug reverses memory loss in mice by reprogramming gene activity