The city's lord mayor said modeling showed that up to 20,000 homes in his city of more than 3 million people could experience some level of flooding.

Only 1 percent of Vietnam's coral reefs are still healthy, and in those cases it's because of their remoteness, according to the World Resources Institute.

Nature Climate Change, Published online: 06 March 2025; doi:10.1038/s41558-025-02255-8

How discussions around key climate change topics evolve over time and which organizations drive such change are important questions. We found that business non-governmental organizations affiliated with fossil fuels focus on hosting renewable energy events but remain absent from anti-fossil-fuel discussions, led instead by a tightly connected network of environmental non-governmental organizations.

We recently learned that users of the Albion Online gaming forum have received direct messages purporting to be from us. That message, which leverages the fear of an account ban, is a phishing attempt.

If you’re an Albion Online forum user and receive a message that claims to be from “the EFF team,” don’t click the link, and be sure to use the in-forum reporting tool to report the message and the user who sent it to the moderators.

A screenshot of the message shared by a user of the forums.

The message itself has some of the usual hallmarks of a phishing attempt, including tactics like creating a sense of fear that your account may be suspended, leveraging the name of a reputable group, and further raising your heart rate with claims that the message needs a quick response. The goal appears to be to get users to download a PDF file designed to deliver malware. That PDF even uses our branding and typefaces (mostly) correctly.

A full walk through of this malware and what it does was discovered by the Hunt team. The PDF is a trojan, or malware disguised as a non malicious file or program, that has an embedded script that calls out to an attacker server. The attacker server then sends a “stage 2” payload that installs itself onto the user’s device. The attack structure used was discovered to be the Pyramid C2 framework. In this case, it is a Windows operating system intended malware. There’s a variety of actions it takes, like writing and modifying files to the victim’s physical drive. But the most worrisome discovery is that it appears to connect the user’s device to a malicious botnet and has potential access to the “VaultSvc” service. This service securely stores user credentials, such as usernames and passwords

File-based IoCs:
act-7wbq8j3peso0qc1.pages[.]dev/819768.pdf
Hash: 4674dec0a36530544d79aa9815f2ce6545781466ac21ae3563e77755307e0020

This incident is a good reminder that often, the best ways to avoid malware and phishing attempts are the same: avoid clicking strange links in unsolicited emails, keep your computer’s software updated, and always scrutinize messages claiming to come from computer support or fraud detection. If a message seems suspect, try to verify its authenticity through other channels—in this case, poking around on the forum and asking other users before clicking on anything. If you ever absolutely must open a file, do so in an online document reader, like Google Drive, or try sending the link through a tool like VirusTotal, but try to avoid opening suspicious files whenever possible.

For more information to help protect yourself, check out our guides for protecting yourself from malware and avoiding phishing attacks.

We've opposed the Take It Down Act because it could be easily manipulated to take down lawful content that powerful people simply don't like. Last night, President Trump demonstrated he has a similar view on the bill. He wants to sign the bill into law, then use it to remove content about — him. And he won't be the only powerful person to do so. 

Here’s what Trump said to a joint session of Congress:    

The Senate just passed the Take It Down Act…. Once it passes the House, I look forward to signing that bill into law. And I’m going to use that bill for myself too if you don’t mind, because nobody gets treated worse than I do online, nobody. 

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Video courtesy C-SPAN.

The Take It Down Act is an overbroad, poorly drafted bill that would create a powerful system to pressure removal of internet posts, with essentially no safeguards. While the bill is meant to address a serious problem—the distribution of non-consensual intimate imagery (NCII)—the notice-and-takedown system it creates is an open invitation for powerful people to pressure websites into removing content they dislike. There are no penalties for applying very broad, or even farcical definitions of what constitutes NCII, and then demanding that it be removed.  

take action

TELL CONGRESS: "Take It Down" Has No real Safeguards  

This Bill Will Punish Critics, and The President Wants It Passed Right Now 

Congress should believe Trump when he says he would use the Take It Down Act simply because he's "treated badly," despite the fact that this is not the intention of the bill. There is nothing in the law, as written, to stop anyone—especially those with significant resources—from misusing the notice-and-takedown system to remove speech that criticizes them or that they disagree with.  

Trump has frequently targeted platforms carrying content and speakers of entirely legal speech that is critical of him, both as an elected official and as a private citizen.  He has filed frivolous lawsuits against media defendants which threaten to silence critics and draw scarce resources away from important reporting work.   

Now that Trump issued a call to action for the bill in his remarks, there is a possibility that House Republicans will fast track the bill into a spending package as soon as next week. Non-consensual intimate imagery is a serious problem that deserves serious consideration, not a hastily drafted, overbroad bill that sweeps in legal, protected speech. 

How The Take It Down Act Could Silence People 

A few weeks ago, a "deepfake" video of President Trump and Elon Musk was displayed across various monitors in the Housing and Urban Development office. The video was subsequently shared on various platforms. While most people wouldn't consider this video, which displayed faked footage of Trump kissing Elon Musk's feet, "nonconsensual intimate imagery," the takedown provision of the bill applies to an “identifiable individual” engaged in “sexually explicit conduct.” This definition leaves much room for interpretation, and nudity or graphic displays are not necessarily required.  

Moreover, there are no penalties whatsoever to dissuade a requester from simply insisting that content is NCII. Apps and websites only have 48 hours to remove content once they receive a request, which means they won’t be able to verify claims. Especially if the requester is an elected official with the power to start an investigation or prosecution, what website would stand up to such a request?  

The House Must Not Pass This Dangerous Bill 

Congress should focus on enforcing and improving the many existing civil and criminal laws that address NCII, rather than opting for a broad takedown regime that is bound to be abused. Take It Down would likely lead to the use of often-inaccurate automated filters that are infamous for flagging legal content, from fair-use commentary to news reporting. It will threaten encrypted services, which may respond by abandoning encryption entirely in order to be able to monitor content—turning private conversations into surveilled spaces.   

Protecting victims of NCII is a legitimate goal. But good intentions alone are not enough to make good policy. Tell your Member of Congress to oppose censorship and to oppose H.R.633. 

take action

Tell the house to stop "Take it down" 

Treating severe or chronic injury to soft tissues such as skin and muscle is a challenge in health care. Current treatment methods can be costly and ineffective, and the frequency of chronic wounds in general from conditions such as diabetes and vascular disease, as well as an increasingly aging population, is only expected to rise.

One promising treatment method involves implanting biocompatible materials seeded with living cells (i.e., microtissue) into the wound. The materials provide a scaffolding for stem cells, or other precursor cells, to grow into the wounded tissue and aid in repair. However, current techniques to construct these scaffolding materials suffer a recurring setback. Human tissue moves and flexes in a unique way that traditional soft materials struggle to replicate, and if the scaffolds stretch, they can also stretch the embedded cells, often causing those cells to die. The dead cells hinder the healing process and can also trigger an inadvertent immune response in the body.

"The human body has this hierarchical structure that actually un-crimps or unfolds, rather than stretches," says Steve Gillmer, a researcher in MIT Lincoln Laboratory's Mechanical Engineering Group. "That's why if you stretch your own skin or muscles, your cells aren't dying. What's actually happening is your tissues are uncrimping a little bit before they stretch."

Gillmer is part of a multidisciplinary research team that is searching for a solution to this stretching setback. He is working with Professor Ming Guo from MIT's Department of Mechanical Engineering and the laboratory's Defense Fabric Discovery Center (DFDC) to knit new kinds of fabrics that can uncrimp and move just as human tissue does.

The idea for the collaboration came while Gillmer and Guo were teaching a course at MIT. Guo had been researching how to grow stem cells on new forms of materials that could mimic the uncrimping of natural tissue. He chose electrospun nanofibers, which worked well, but were difficult to fabricate at long lengths, preventing him from integrating the fibers into larger knit structures for larger-scale tissue repair.

"Steve mentioned that Lincoln Laboratory had access to industrial knitting machines," Guo says. These machines allowed him to switch focus to designing larger knits, rather than individual yarns. "We immediately started to test new ideas through internal support from the laboratory."

Gillmer and Guo worked with the DFDC to discover which knit patterns could move similarly to different types of soft tissue. They started with three basic knit constructions called interlock, rib, and jersey.

"For jersey, think of your T-shirt. When you stretch your shirt, the yarn loops are doing the stretching," says Emily Holtzman, a textile specialist at the DFDC. "The longer the loop length, the more stretch your fabric can accommodate. For ribbed, think of the cuff on your sweater. This fabric construction has a global stretch that allows the fabric to unfold like an accordion."

Interlock is similar to ribbed but is knitted in a denser pattern and contains twice as much yarn per inch of fabric. By having more yarn, there is more surface area on which to embed the cells. "Knit fabrics can also be designed to have specific porosities, or hydraulic permeability, created by the loops of the fabric and yarn sizes," says Erin Doran, another textile specialist on the team. "These pores can help with the healing process as well."

So far, the team has conducted a number of tests embedding mouse embryonic fibroblast cells and mesenchymal stem cells within the different knit patterns and seeing how they behave when the patterns are stretched. Each pattern had variations that affected how much the fabric could uncrimp, in addition to how stiff it became after it started stretching. All showed a high rate of cell survival, and in 2024 the team received an R&D 100 award for their knit designs.

Gillmer explains that although the project began with treating skin and muscle injuries in mind, their fabrics have the potential to mimic many different types of human soft tissue, such as cartilage or fat. The team recently filed a provisional patent that outlines how to create these patterns and identifies the appropriate materials that should be used to make the yarn. This information can be used as a toolbox to tune different knitted structures to match the mechanical properties of the injured tissue to which they are applied.

"This project has definitely been a learning experience for me," Gillmer says. "Each branch of this team has a unique expertise, and I think the project would be impossible without them all working together. Our collaboration as a whole enables us to expand the scope of the work to solve these larger, more complex problems."

A new MIT-led study confirms that the Antarctic ozone layer is healing, as a direct result of global efforts to reduce ozone-depleting substances.

Scientists including the MIT team have observed signs of ozone recovery in the past. But the new study is the first to show, with high statistical confidence, that this recovery is due primarily to the reduction of ozone-depleting substances, versus other influences such as natural weather variability or increased greenhouse gas emissions to the stratosphere.

“There’s been a lot of qualitative evidence showing that the Antarctic ozone hole is getting better. This is really the first study that has quantified confidence in the recovery of the ozone hole,” says study author Susan Solomon, the Lee and Geraldine Martin Professor of Environmental Studies and Chemistry. “The conclusion is, with 95 percent confidence, it is recovering. Which is awesome. And it shows we can actually solve environmental problems.”

The new study appears today in the journal Nature. Graduate student Peidong Wang from the Solomon group in the Department of Earth, Atmospheric and Planetary Sciences (EAPS) is the lead author. His co-authors include Solomon and EAPS Research Scientist Kane Stone, along with collaborators from multiple other institutions.

Roots of ozone recovery

Within the Earth’s stratosphere, ozone is a naturally occurring gas that acts as a sort of sunscreen, protecting the planet from the sun’s harmful ultraviolet radiation. In 1985, scientists discovered a “hole” in the ozone layer over Antarctica that opened up during the austral spring, between September and December. This seasonal ozone depletion was suddenly allowing UV rays to filter down to the surface, leading to skin cancer and other adverse health effects.

In 1986, Solomon, who was then working at the National Oceanic and Atmospheric Administration (NOAA), led expeditions to the Antarctic, where she and her colleagues gathered evidence that quickly confirmed the ozone hole’s cause: chlorofluorocarbons, or CFCs — chemicals that were then used in refrigeration, air conditioning, insulation, and aerosol propellants. When CFCs drift up into the stratosphere, they can break down ozone under certain seasonal conditions.

The following year, those relevations led to the drafting of the Montreal Protocol — an international treaty that aimed to phase out the production of CFCs and other ozone-depleting substances, in hopes of healing the ozone hole.

In 2016, Solomon led a study reporting key signs of ozone recovery. The ozone hole seemed to be shrinking with each year, especially in September, the time of year when it opens up. Still, these observations were qualitative. The study showed large uncertainties regarding how much of this recovery was due to concerted efforts to reduce ozone-depleting substances, or if the shrinking ozone hole was a result of other “forcings,” such as year-to-year weather variability from El Niño, La Niña, and the polar vortex.

“While detecting a statistically significant increase in ozone is relatively straightforward, attributing these changes to specific forcings is more challenging,” says Wang.

Anthropogenic healing

In their new study, the MIT team took a quantitative approach to identify the cause of Antarctic ozone recovery. The researchers borrowed a method from the climate change community, known as “fingerprinting,” which was pioneered by Klaus Hasselmann, who was awarded the Nobel Prize in Physics in 2021 for the technique. In the context of climate, fingerprinting refers to a method that isolates the influence of specific climate factors, apart from natural, meteorological noise. Hasselmann applied fingerprinting to identify, confirm, and quantify the anthropogenic fingerprint of climate change.

Solomon and Wang looked to apply the fingerprinting method to identify another anthropogenic signal: the effect of human reductions in ozone-depleting substances on the recovery of the ozone hole.

“The atmosphere has really chaotic variability within it,” Solomon says. “What we’re trying to detect is the emerging signal of ozone recovery against that kind of variability, which also occurs in the stratosphere.”

The researchers started with simulations of the Earth’s atmosphere and generated multiple “parallel worlds,” or simulations of the same global atmosphere, under different starting conditions. For instance, they ran simulations under conditions that assumed no increase in greenhouse gases or ozone-depleting substances. Under these conditions, any changes in ozone should be the result of natural weather variability. They also ran simulations with only increasing greenhouse gases, as well as only decreasing ozone-depleting substances.

They compared these simulations to observe how ozone in the Antarctic stratosphere changed, both with season, and across different altitudes, in response to different starting conditions. From these simulations, they mapped out the times and altitudes where ozone recovered from month to month, over several decades, and identified a key “fingerprint,” or pattern, of ozone recovery that was specifically due to conditions of declining ozone-depleting substances.

The team then looked for this fingerprint in actual satellite observations of the Antarctic ozone hole from 2005 to the present day. They found that, over time, the fingerprint that they identified in simulations became clearer and clearer in observations. In 2018, the fingerprint was at its strongest, and the team could say with 95 percent confidence that ozone recovery was due mainly to reductions in ozone-depleting substances.

“After 15 years of observational records, we see this signal to noise with 95 percent confidence, suggesting there’s only a very small chance that the observed pattern similarity can be explained by variability noise,” Wang says. “This gives us confidence in the fingerprint. It also gives us confidence that we can solve environmental problems. What we can learn from ozone studies is how different countries can swiftly follow these treaties to decrease emissions.”

If the trend continues, and the fingerprint of ozone recovery grows stronger, Solomon anticipates that soon there will be a year, here and there, when the ozone layer stays entirely intact. And eventually, the ozone hole should stay shut for good.

“By something like 2035, we might see a year when there’s no ozone hole depletion at all in the Antarctic. And that will be very exciting for me,” she says. “And some of you will see the ozone hole go away completely in your lifetimes. And people did that.”

This research was supported, in part, by the National Science Foundation and NASA.

Of the five, one is a Windows vulnerability, another is a Cisco vulnerability. We don’t have any details about who is exploiting them, or how.

News article. Slashdot thread.

Energy Secretary Chris Wright’s keynote speech on energy poverty will come on the heels of the gutting of Power Africa’s USAID programs.

The demise of the Chevron doctrine could weaken the Trump administration's effort to undo the scientific underpinning for climate rules.

The president also pushed an Alaska natural gas pipeline and export project.

A coalition of nonprofits urged the EPA chief Tuesday to lift a freeze on money it got in August from a fund to cut greenhouse gas emissions.

Chief Financial Officer Mary Comans was let go after approving payments for migrant housing.

A hearing Tuesday sidestepped President Donald Trump's suggestions to abolish the federal disaster agency and suggested improvements.

The executive body will put forward an amendment that calculates the target over three years, making it easier to reach.

Warm temperatures in the Anchorage area also caused headaches for race organizers Saturday during the ceremonial start of the Alaska race.

Many Wayuu families are forced to migrate in search of essential resources, putting even more pressure on already overcrowded urban areas.

It comes as OPEC+ met Monday and agreed to proceed with an increase in oil production starting in April, which is likely to push down oil prices further.

It’s not a stretch to suggest that when we disagree with other people, we often regard them as being irrational. Kevin Dorst PhD ’19 has developed a body of research with surprising things to say about that.

Dorst, an associate professor of philosophy at MIT, studies rationality: how we apply it, or think we do, and how that bears out in society. The goal is to help us think clearly and perhaps with fresh eyes about something we may take for granted.

Throughout his work, Dorst specializes in exploring the nuances of rationality. To take just one instance, consider how ambiguity can interact with rationality. Suppose there are two studies about the effect of a new housing subdivision on local traffic patterns: One shows there will be a substantial increase in traffic, and one shows a minor effect. Even if both studies are sound in their methods and data, neither may have a totally airtight case. People who regard themselves as rationally assessing the numbers will likely disagree about which is most valid, and — though this may not be entirely rational — may use their prior beliefs to poke holes in the study that does not represent their prior beliefs. 

Among other things, this process also calls into question the widespread “Bayesian” conception that people’s views shift and come into alignment as they’re presented with new evidence. It may be that instead, people apply rationality while their views diverge, not converge.

This is also the kind of phenomenon Dorst explores in the paper “Rational Polarization,” published in The Philosophical Review in 2023; currently Dorst is working on a book about how people can take rational approaches but still wind up with different conclusions about the world. Dorst combines careful argumentation, mathematically structured descriptions of thinking, and even experimental evidence about cognition and people’s views, an increasing trend in philosophy.

“There’s something freeing about how methodologically open philosophy is,” says Dorst, a good-humored and genial conversationalist. “A question can be philosophical if it’s important and we don’t yet have settled methods for answering it, because in philosophy it’s always okay to ask what methods we should be using. It’s one of the exciting things about philosophy.”

For his research and teaching, Dorst was awarded tenure at MIT last year.

Show me your work

Dorst grew up in Missouri, not exactly expecting to become a philosopher, but he started following in the academic trail of his older brother, who had become interested in philosophy.

“We didn’t know what philosophy was growing up, but once my brother started getting interested, there was a little bootstrapping, egging each other on, and having someone to talk to,” Dorst says.

As an undergraduate at Washington University in St. Louis, Dorst majored in philosophy and political science. By graduation, he had become sold on studying philosophy full-time, and was accepted into MIT’s program as a doctoral student.

At the Institute, he started specializing in the problems he now studies full-time, about how we know things and how much we are thinking rationally, while working with Roger White as his primary adviser, along with faculty members Robert Stalnaker and Kieran Setiya of MIT and Branden Fitelson of Northeastern University.

After earning his PhD, Dorst spent a year as a fellow at Oxford University’s Magdalen College, then joined faculty of the University of Pittsburgh. He returned to MIT, this time on the faculty, in 2022. Now settled in the MIT philosophy faculty, Dorst tries to continue the department’s tradition of engaged teaching with his students.

“They wrestle like everyone does with the conceptual and philosophical questions, but the speed with which you can get through technical things in a course is astounding,” Dorst says of MIT undergraduates.

New methods, time-honored issues

At present Dorst, who has published widely in philosophy journals, is grinding through the process of writing a book manuscript about the complexity of rationality. Chapter subjects include hindsight bias, confirmation bias, overconfidence, and polarization.

In the process, Dorst is also developing and conducting more experiments than ever before, to look at the way people process information and regard themselves as being rational.

“There’s this whole movement of experimental philosophy, using experimental data, being sensitive to cognitive science and being interested in connecting questions we have to it,” Dorst says.

In his case, he adds, “The big picture is trying to connect the theoretical work on rationality with the more empirical work about what leads to polarization,” he says. The salience of the work, meanwhile, applies to a wide range of subjects:  “People have been polarized forever over everything.”

As he explains all of this, Dorst looks up at the whiteboard in his office, where an extensive set of equations represents the output of some experiments and his ongoing effort to comprehend the results, as part of the book project. When he finishes, he hopes to have work broadly useful in philosophy, cognitive science, and other fields.

“We might use some different models in philosophy,” he says, “but let’s all try to figure out how people process information and regard arguments.”

Building on more than two decades of research, a study by MIT neuroscientists at The Picower Institute for Learning and Memory reports a new way to treat pathology and symptoms of fragile X syndrome, the most common genetically-caused autism spectrum disorder. The team showed that augmenting a novel type of neurotransmitter signaling reduced hallmarks of fragile X in mouse models of the disorder.

The new approach, described in Cell Reports, works by targeting a specific molecular subunit of “NMDA” receptors that they discovered plays a key role in how neurons synthesize proteins to regulate their connections, or “synapses,” with other neurons in brain circuits. The scientists showed that in fragile X model mice, increasing the receptor’s activity caused neurons in the hippocampus region of the brain to increase molecular signaling that suppressed excessive bulk protein synthesis, leading to other key improvements.

Setting the table

“One of the things I find most satisfying about this study is that the pieces of the puzzle fit so nicely into what had come before,” says study senior author Mark Bear, Picower Professor in MIT’s Department of Brain and Cognitive Sciences. Former postdoc Stephanie Barnes, now a lecturer at the University of Glasgow, is the study’s lead author.

Bear’s lab studies how neurons continually edit their circuit connections, a process called “synaptic plasticity” that scientists believe to underlie the brain’s ability to adapt to experience and to form and process memories. These studies led to two discoveries that set the table for the newly published advance. In 2011, Bear’s lab showed that fragile X and another autism disorder, tuberous sclerosis (Tsc), represented two ends of a continuum of a kind of protein synthesis in the same neurons. In fragile X there was too much. In Tsc there was too little. When lab members crossbred fragile X and Tsc mice, in fact, their offspring emerged healthy, as the mutations of each disorder essentially canceled each other out.

More recently, Bear’s lab showed a different dichotomy. It has long been understood from their influential work in the 1990s that the flow of calcium ions through NMDA receptors can trigger a form of synaptic plasticity called “long-term depression” (LTD). But in 2020, they found that another mode of signaling by the receptor — one that did not require ion flow — altered protein synthesis in the neuron and caused a physical shrinking of the dendritic “spine” structures housing synapses.

For Bear and Barnes, these studies raised the prospect that if they could pinpoint how NMDA receptors affect protein synthesis they might identify a new mechanism that could be manipulated therapeutically to address fragile X (and perhaps tuberous sclerosis) pathology and symptoms. That would be an important advance to complement ongoing work Bear’s lab has done to correct fragile X protein synthesis levels via another receptor called mGluR5.

Receptor dissection

In the new study, Bear and Barnes’ team decided to use the non-ionic effect on spine shrinkage as a readout to dissect how NMDARs signal protein synthesis for synaptic plasticity in hippocampus neurons. They hypothesized that the dichotomy of ionic effects on synaptic function and non-ionic effects on spine structure might derive from the presence of two distinct components of NMDA receptors: “subunits” called GluN2A and GluN2B. To test that, they used genetic manipulations to knock out each of the subunits. When they did so, they found that knocking out “2A” or “2B” could eliminate LTD, but that only knocking out 2B affected spine size. Further experiments clarified that 2A and 2B are required for LTD, but that spine shrinkage solely depends on the 2B subunit.

The next task was to resolve how the 2B subunit signals spine shrinkage. A promising possibility was a part of the subunit called the “carboxyterminal domain,” or CTD. So, in a new experiment Bear and Barnes took advantage of a mouse that had been genetically engineered by researchers at the University of Edinburgh so that the 2A and 2B CTDs could be swapped with one another. A telling result was that when the 2B subunit lacked its proper CTD, the effect on spine structure disappeared. The result affirmed that the 2B subunit signals spine shrinkage via its CTD.

Another consequence of replacing the CTD of the 2B subunit was an increase in bulk protein synthesis that resembled findings in fragile X. Conversely, augmenting the non-ionic signaling through the 2B subunit suppressed bulk protein synthesis, reminiscent of Tsc.

Treating fragile X

Putting the pieces together, the findings indicated that augmenting signaling through the 2B subunit might, like introducing the mutation causing Tsc, rescue aspects of fragile X.

Indeed, when the scientists swapped in the 2B subunit CTD of NMDA receptor in fragile X model mice they found correction of not only the excessive bulk protein synthesis, but also altered synaptic plasticity, and increased electrical excitability that are hallmarks of the disease. To see if a treatment that targets NMDA receptors might be effective in fragile X, they tried an experimental drug called Glyx-13. This drug binds to the 2B subunit of NMDA receptors to augment signaling. The researchers found that this treatment can also normalize protein synthesis and reduced sound-induced seizures in the fragile X mice.

The team now hypothesizes, based on another prior study in the lab, that the beneficial effect to fragile X mice of the 2B subunit’s CTD signaling is that it shifts the balance of protein synthesis away from an all-too-efficient translation of short messenger RNAs (which leads to excessive bulk protein synthesis) toward a lower-efficiency translation of longer messenger RNAs.

Bear says he does not know what the prospects are for Glyx-13 as a clinical drug, but he noted that there are some drugs in clinical development that specifically target the 2B subunit of NMDA receptors.

In addition to Bear and Barnes, the study’s other authors are Aurore Thomazeau, Peter Finnie, Max Heinreich, Arnold Heynen, Noboru Komiyama, Seth Grant, Frank Menniti, and Emily Osterweil.

The FRAXA Foundation, The Picower Institute for Learning and Memory, The Freedom Together Foundation, and the National Institutes of Health funded the study.