When cells are healthy, we don’t expect them to suddenly change cell types. A skin cell on your hand won’t naturally morph into a brain cell, and vice versa. That’s thanks to epigenetic memory, which enables the expression of various genes to “lock in” throughout a cell’s lifetime. Failure of this memory can lead to diseases, such as cancer.

Traditionally, scientists have thought that epigenetic memory locks genes either “on” or “off” — either fully activated or fully repressed, like a permanent Lite-Brite pattern. But MIT engineers have found that the picture has many more shades.

In a new study appearing today in Cell Genomics, the team reports that a cell’s memory is set not by on/off switching but through a more graded, dimmer-like dial of gene expression.

The researchers carried out experiments in which they set the expression of a single gene at different levels in different cells. While conventional wisdom would assume the gene should eventually switch on or off, the researchers found that the gene’s original expression persisted: Cells whose gene expression was set along a spectrum between on and off remained in this in-between state.

The results suggest that epigenetic memory — the process by which cells retain gene expression and “remember” their identity — is not binary but instead analog, which allows for a spectrum of gene expression and associated cell identities.

“Our finding opens the possibility that cells commit to their final identity by locking genes at specific levels of gene expression instead of just on and off,” says study author Domitilla Del Vecchio, professor of mechanical and biological engineering at MIT. “The consequence is that there may be many more cell types in our body than we know and recognize today, that may have important functions and could underlie healthy or diseased states.”

The study’s MIT lead authors are Sebastian Palacios and Simone Bruno, with additional co-authors.

Beyond binary

Every cell shares the same genome, which can be thought of as the starting ingredient for life. As a cell takes shape, it differentiates into one type or another, through the expression of genes in its genome. Some genes are activated, while others are repressed. The combination steers a cell toward one identity versus another.

A process of DNA methylation, by which certain molecules attach to the genes’ DNA, helps lock their expression in place. DNA methylation assists a cell to “remember” its unique pattern of gene expression, which ultimately establishes the cell’s identity.

Del Vecchio’s group at MIT applies mathematics and genetic engineering to understand cellular molecular processes and to engineer cells with new capabilities. In previous work, her group was experimenting with DNA methylation and ways to lock the expression of certain genes in ovarian cells.

“The textbook understanding was that DNA methylation had a role to lock genes in either an on or off state,” Del Vecchio says. “We thought this was the dogma. But then we started seeing results that were not consistent with that.”

While many of the cells in their experiment exhibited an all-or-nothing expression of genes, a significant number of cells appeared to freeze genes in an in-between state — neither entirely on or off.

“We found there was a spectrum of cells that expressed any level between on and off,” Palacios says. “And we thought, how is this possible?”

Shades of blue

In their new study, the team aimed to see whether the in-between gene expression they observed was a fluke or a more established property of cells that until now has gone unnoticed.

“It could be that scientists disregarded cells that don’t have a clear commitment, because they assumed this was a transient state,” Del Vecchio says. “But actually these in-between cell types may be permanent states that could have important functions.”

To test their idea, the researchers ran experiments with hamster ovarian cells — a line of cells commonly used in the laboratory. In each cell, an engineered gene was initially set to a different level of expression. The gene was turned fully on in some cells, completely off in others, and set somewhere in between on and off for the remaining cells.

The team paired the engineered gene with a fluorescent marker that lights up with a brightness corresponding to the gene’s level of expression. The researchers introduced, for a short time, an enzyme that triggers the gene’s DNA methylation, a natural gene-locking mechanism. They then monitored the cells over five months to see whether the modification would lock the genes in place at their in-between expression levels, or whether the genes would migrate toward fully on or off states before locking in.

“Our fluorescent marker is blue, and we see cells glow across the entire spectrum, from really shiny blue, to dimmer and dimmer, to no blue at all,” Del Vecchio says. “Every intensity level is maintained over time, which means gene expression is graded, or analog, and not binary. We were very surprised, because we thought after such a long time, the gene would veer off, to be either fully on or off, but it did not.”

The findings open new avenues into engineering more complex artificial tissues and organs by tuning the expression of certain genes in a cell’s genome, like a dial on a radio, rather than a switch. The results also complicate the picture of how a cell’s epigenetic memory works to establish its identity. It opens up the possibility that cell modifications such as those exhibited in therapy-resistant tumors could be treated in a more precise fashion.

“Del Vecchio and colleagues have beautifully shown how analog memory arises through chemical modifications to the DNA itself,” says Michael Elowitz, professor of biology and biological engineering at the California institute of Technology, who was not involved in the study. “As a result, we can now imagine repurposing this natural analog memory mechanism, invented by evolution, in the field of synthetic biology, where it could help allow us to program permanent and precise multicellular behaviors.”

“One of the things that enables the complexity in humans is epigenetic memory,” Palacios says. “And we find that it is not what we thought. For me, that’s actually mind-blowing. And I think we’re going to find that this analog memory is relevant for many different processes across biology.”

This research was supported, in part, by the National Science Foundation, MODULUS, and a Vannevar Bush Faculty Fellowship through the U.S. Office of Naval Research.

A couple of months ago, a new paper demonstrated some new attacks against the Fiat-Shamir transformation. Quanta published a good article that explains the results.

This is a pretty exciting paper from a theoretical perspective, but I don’t see it leading to any practical real-world cryptanalysis. The fact that there are some weird circumstances that result in Fiat-Shamir insecurities isn’t new—many dozens of papers have been published about it since 1986. What this new result does is extend this known problem to slightly less weird (but still highly contrived) situations. But it’s a completely different matter to extend these sorts of attacks to “natural” situations...

After meeting with reinsurance companies abroad, the state’s insurance commissioner pushed for new laws to expand property insurance.

The country's explosive growth in wind and solar is moving it toward peak coal and gas, according to new research.

Fiscal 2026 legislation would roll back spending to the lowest level in decades.

The power needs of electric vehicles will compel "investment in new wind, solar, storage, and natural gas capacity," new research finds.

The regional transportation agency is tapping its capital funds to restore routes shortened or canceled amid a budget showdown.

Harvesting specialists say home gardeners can benefit from collecting rain and runoff to irrigate plants.

The financial secretary added that Hong Kong is on track to meet its goal to reduce carbon emissions by 50 percent by 2035.

Many parts of Europe that once saw air conditioning as a U.S. excess are beginning to embrace the idea.

The boost was driven by expectations of higher footfall — and sales — as shoppers sought refuge from Japan’s elevated temperatures.

Using tiny particles shaped like bottlebrushes, MIT chemists have found a way to deliver a large range of chemotherapy drugs directly to tumor cells.

To guide them to the right location, each particle contains an antibody that targets a specific tumor protein. This antibody is tethered to bottlebrush-shaped polymer chains carrying dozens or hundreds of drug molecules — a much larger payload than can be delivered by any existing antibody-drug conjugates.

In mouse models of breast and ovarian cancer, the researchers found that treatment with these conjugated particles could eliminate most tumors. In the future, the particles could be modified to target other types of cancer, by swapping in different antibodies.

“We are excited about the potential to open up a new landscape of payloads and payload combinations with this technology, that could ultimately provide more effective therapies for cancer patients,” says Jeremiah Johnson, the A. Thomas Geurtin Professor of Chemistry at MIT, a member of the Koch Institute for Integrative Cancer Research, and the senior author of the new study.

MIT postdoc Bin Liu is the lead author of the paper, which appears today in Nature Biotechnology.

A bigger drug payload

Antibody-drug conjugates (ADCs) are a promising type of cancer treatment that consist of a cancer-targeting antibody attached to a chemotherapy drug. At least 15 ADCs have been approved by the FDA to treat several different types of cancer.

This approach allows specific targeting of a cancer drug to a tumor, which helps to prevent some of the side effects that occur when chemotherapy drugs are given intravenously. However, one drawback to currently approved ADCs is that only a handful of drug molecules can be attached to each antibody. That means they can only be used with very potent drugs — usually DNA-damaging agents or drugs that interfere with cell division.

To try to use a broader range of drugs, which are often less potent, Johnson and his colleagues decided to adapt bottlebrush particles that they had previously invented. These particles consist of a polymer backbone that are attached to tens to hundreds of “prodrug” molecules — inactive drug molecules that are activated upon release within the body. This structure allows the particles to deliver a wide range of drug molecules, and the particles can be designed to carry multiple drugs in specific ratios.

Using a technique called click chemistry, the researchers showed that they could attach one, two, or three of their bottlebrush polymers to a single tumor-targeting antibody, creating an antibody-bottlebrush conjugate (ABC). This means that just one antibody can carry hundreds of prodrug molecules. The currently approved ADCs can carry a maximum of about eight drug molecules.

The huge number of payloads in the ABC particles allows the researchers to incorporate less potent cancer drugs such as doxorubicin or paclitaxel, which enhances the customizability of the particles and the variety of drug combinations that can be used.

“We can use antibody-bottlebrush conjugates to increase the drug loading, and in that case, we can use less potent drugs,” Liu says. “In the future, we can very easily copolymerize with multiple drugs together to achieve combination therapy.”

The prodrug molecules are attached to the polymer backbone by cleavable linkers. After the particles reach a tumor site, some of these linkers are broken right away, allowing the drugs to kill nearby cancer cells even if they don’t express the target antibody. Other particles are absorbed into cells with the target antibody before releasing their toxic payload.

Effective treatment

For this study, the researchers created ABC particles carrying a few different types of drugs: microtubule inhibitors called MMAE and paclitaxel, and two DNA-damaging agents, doxorubicin and SN-38. They also designed ABC particles carrying an experimental type of drug known as PROTAC (proteolysis-targeting chimera), which can selectively degrade disease-causing proteins inside cells.

Each bottlebrush was tethered to an antibody targeting either HER2, a protein often overexpressed in breast cancer, or MUC1, which is commonly found in ovarian, lung, and other types of cancer.

The researchers tested each of the ABCs in mouse models of breast or ovarian cancer and found that in most cases, the ABC particles were able to eradicate the tumors. This treatment was significantly more effective than giving the same bottlebrush prodrugs by injection, without being conjugated to a targeting antibody.

“We used a very low dose, almost 100 times lower compared to the traditional small-molecule drug, and the ABC still can achieve much better efficacy compared to the small-molecule drug given on its own,” Liu says.

These ABCs also performed better than two FDA-approved ADCs, T-DXd and TDM-1, which both use HER2 to target cells. T-DXd carries deruxtecan, which interferes with DNA replication, and TDM-1 carries emtansine, a microtubule inhibitor.

In future work, the MIT team plans to try delivering combinations of drugs that work by different mechanisms, which could enhance their overall effectiveness. Among these could be immunotherapy drugs such as STING activators.

The researchers are also working on swapping in different antibodies, such as antibodies targeting EGFR, which is widely expressed in many tumors. More than 100 antibodies have been approved to treat cancer and other diseases, and in theory any of those could be conjugated to cancer drugs to create a targeted therapy.

The research was funded in part by the National Institutes of Health, the Ludwig Center at MIT, and the Koch Institute Frontier Research Program. 

Nature Climate Change, Published online: 09 September 2025; doi:10.1038/s41558-025-02420-z

Africa’s future climate could be shaped by solar radiation management (SRM) decisions made elsewhere. To ensure these technologies, if ever pursued, reflect principles of justice and local priorities, Africa must move from passive recipient to active leader in SRM research, governance and public engagement.

Nature Climate Change, Published online: 09 September 2025; doi:10.1038/s41558-025-02419-6

The authors combine tracking and body mass data from five migratory waterfowl species to understand their capacity to accelerate migration in response to earlier spring. They show considerable scope for faster migration by reducing the fuelling time before departure and subsequently on stopovers

The Whitehead Institute for Biomedical Research fondly remembers its founding director, David Baltimore, a former MIT Institute Professor and Nobel laureate who died Sept. 6 at age 87.

With discovery after discovery, Baltimore brought to light key features of biology with direct implications for human health. His work at MIT earned him a share of the 1975 Nobel Prize in Physiology or Medicine (along with Howard Temin and Renato Dulbecco) for discovering reverse transcriptase and identifying retroviruses, which use RNA to synthesize viral DNA.

Following the award, Baltimore reoriented his laboratory’s focus to pursue a mix of immunology and virology. Among the lab’s most significant subsequent discoveries were the identification of a pair of proteins that play an essential role in enabling the immune system to create antibodies for so many different molecules, and investigations into how certain viruses can cause cell transformation and cancer. Work from Baltimore’s lab also helped lead to the development of the important cancer drug Gleevec — the first small molecule to target an oncoprotein inside of cells.

In 1982, Baltimore partnered with philanthropist Edwin C. “Jack” Whitehead to conceive and launch the Whitehead Institute and then served as its founding director until 1990. Within a decade of its founding, the Baltimore-led Whitehead Institute was named the world’s top research institution in molecular biology and genetics.

“More than 40 years later, Whitehead Institute is thriving, still guided by the strategic vision that David Baltimore and Jack Whitehead articulated,” says Phillip Sharp, MIT Institute Professor Emeritus, former Whitehead board member, and fellow Nobel laureate. “Of all David’s myriad and significant contributions to science, his role in building the first independent biomedical research institute associated with MIT and guiding it to extraordinary success may well prove to have had the broadest and longest-term impact.” 

Ruth Lehmann, director and president of the Whitehead Institute, and professor of biology at MIT, says: “I, like many others, owe my career to David Baltimore. He recruited me to Whitehead Institute and MIT in 1988 as a faculty member, taking a risk on an unproven, freshly-minted PhD graduate from Germany. As director, David was incredibly skilled at bringing together talented scientists at different stages of their careers and facilitating their collaboration so that the whole would be greater than the sum of its parts. This approach remains a core strength of Whitehead Institute.”

As part of the Whitehead Institute’s mission to cultivate the next generation of scientific leaders, Baltimore founded the Whitehead Fellows program, which provides extraordinarily talented recent PhD and MD graduates with the opportunity to launch their own labs, rather than to go into traditional postdoctoral positions. The program has been a huge success, with former fellows going on to excel as leaders in research, education, and industry.

David Page, MIT professor of biology, Whitehead Institute member, and former director who was the Whitehead's first fellow, recalls, “David was both an amazing scientist and a peerless leader of aspiring scientists. The launching of the Whitehead Fellows program reflected his recipe for institutional success: gather up the resources to allow young scientists to realize their dreams, recruit with an eye toward potential for outsized impact, and quietly mentor and support without taking credit for others’ successes — all while treating junior colleagues as equals. It is a beautiful strategy that David designed and executed magnificently.”

Sally Kornbluth, president of MIT and a member of the Whitehead Institute Board of Directors, says that “David was a scientific hero for so many. He was one of those remarkable individuals who could make stellar scientific breakthroughs and lead major institutions with extreme thoughtfulness and grace. He will be missed by the whole scientific community.”

“David was a wise giant. He was brilliant. He was an extraordinarily effective, ethical leader and institution builder who influenced and inspired generations of scientists and premier institutions,” says Susan Whitehead, member of the board of directors and daughter of Jack Whitehead.

Gerald R. Fink, the Margaret and Herman Sokol Professor Emeritus at MIT who was recruited by Baltimore from Cornell University as one of four founding members of the Whitehead Institute, and who succeeded him as director in 1990, observes: “David became my hero and friend. He upheld the highest scientific ideals and instilled trust and admiration in all around him.”

     David Baltimore - Infinite History (2010)
     Video: MIT | Watch with transcript

Baltimore was born in New York City in 1938. His scientific career began at Swarthmore College, where he earned a bachelor’s degree with high honors in chemistry in 1960. He then began doctoral studies in biophysics at MIT, but in 1961 shifted his focus to animal viruses and moved to what is now the Rockefeller University, where he did his thesis work in the lab of Richard Franklin.

After completing postdoctoral fellowships with James Darnell at MIT and Jerard Hurwitz at the Albert Einstein College of Medicine, Baltimore launched his own lab at the Salk Institute for Biological Studies from 1965 to 1968. Then, in 1968, he returned to MIT as a member of its biology faculty, where he remained until 1990. (Whitehead Institute’s members hold parallel appointments as faculty in the MIT Department of Biology.)

In 1990, Baltimore left the Whitehead Institute and MIT to become the president of Rockefeller University. He returned to MIT from 1994 to 1997, serving as an Institute Professor, after which he was named president of Caltech. Baltimore held that position until 2006, when he was elected to a three-year term as president of the American Association for the Advancement of Science.

For decades, Baltimore has been viewed not just as a brilliant scientist and talented academic leader, but also as a wise counsel to the scientific community. For example, he helped organize the 1975 Asilomar Conference on Recombinant DNA, which created stringent safety guidelines for the study and use of recombinant DNA technology. He played a leadership role in the development of policies on AIDS research and treatment, and on genomic editing. Serving as an advisor to both organizations and individual scientists, he helped to shape the strategic direction of dozens of institutions and to advance the careers of generations of researchers. As Founding Member Robert Weinberg summarizes it, “He had no tolerance for nonsense and weak science.”  

In 2023, the Whitehead Institute established the endowed David Baltimore Chair in Biomedical Research, honoring Baltimore’s six decades of scientific, academic, and policy leadership and his impact on advancing innovative basic biomedical research.

“David was a visionary leader in science and the institutions that sustain it. He devoted his career to advancing scientific knowledge and strengthening the communities that make discovery possible, and his leadership of Whitehead Institute exemplified this,” says Richard Young, MIT professor of biology and Whitehead Institute member. “David approached life with keen observation, boundless curiosity, and a gift for insight that made him both a brilliant scientist and a delightful companion. His commitment to mentoring and supporting young scientists left a lasting legacy, inspiring the next generation to pursue impactful contributions to biomedical research. Many of us found in him not only a mentor and role model, but also a steadfast friend whose presence enriched our lives and whose absence will be profoundly felt.”

Most people recognize Alzheimer’s disease from its devastating symptoms such as memory loss, while new drugs target pathological aspects of disease manifestations, such as plaques of amyloid proteins. Now, a sweeping new open-access study in the Sept. 4 edition of Cell by MIT researchers shows the importance of understanding the disease as a battle over how well brain cells control the expression of their genes. The study paints a high-resolution picture of a desperate struggle to maintain healthy gene expression and gene regulation, where the consequences of failure or success are nothing less than the loss or preservation of cell function and cognition.

The study presents a first-of-its-kind, multimodal atlas of combined gene expression and gene regulation spanning 3.5 million cells from six brain regions, obtained by profiling 384 post-mortem brain samples across 111 donors. The researchers profiled both the “transcriptome,” showing which genes are expressed into RNA, and the “epigenome,” the set of chromosomal modifications that establish which DNA regions are accessible and thus utilized between different cell types.

The resulting atlas revealed many insights showing that the progression of Alzheimer’s is characterized by two major epigenomic trends. The first is that vulnerable cells in key brain regions suffer a breakdown of the rigorous nuclear “compartments” they normally maintain to ensure some parts of the genome are open for expression but others remain locked away. The second major finding is that susceptible cells experience a loss of “epigenomic information,” meaning they lose their grip on the unique pattern of gene regulation and expression that gives them their specific identity and enables their healthy function.

Accompanying the evidence of compromised compartmentalization and the erosion of epigenomic information are many specific findings pinpointing molecular circuitry that breaks down by cell type, by region, and gene network. They found, for instance, that when epigenomic conditions deteriorate, that opens the door to expression of many genes associated with disease, whereas if cells manage to keep their epigenomic house in order, they can keep disease-associated genes in check. Moreover, the researchers clearly saw that when the epigenomic breakdowns were occurring people lost cognitive ability, but where epigenomic stability remained, so did cognition.

“To understand the circuitry, the logic responsible for gene expression changes in Alzheimer’s disease [AD], we needed to understand the regulation and upstream control of all the changes that are happening, and that’s where the epigenome comes in,” says senior author Manolis Kellis, a professor in the Computer Science and Artificial Intelligence Lab and head of MIT’s Computational Biology Group. “This is the first large-scale, single-cell, multi-region gene-regulatory atlas of AD, systematically dissecting the dynamics of epigenomic and transcriptomic programs across disease progression and resilience.”

By providing that detailed examination of the epigenomic mechanisms of Alzheimer’s progression, the study provides a blueprint for devising new Alzheimer’s treatments that can target factors underlying the broad erosion of epigenomic control or the specific manifestations that affect key cell types such as neurons and supporting glial cells.

“The key to developing new and more effective treatments for Alzheimer’s disease depends on deepening our understanding of the mechanisms that contribute to the breakdowns of cellular and network function in the brain,” says Picower Professor and co-corresponding author Li-Huei Tsai, director of The Picower Institute for Learning and Memory and a founding member of MIT’s Aging Brain Initiative, along with Kellis. “This new data advances our understanding of how epigenomic factors drive disease.”

Kellis Lab members Zunpeng Liu and Shanshan Zhang are the study’s co-lead authors.

Compromised compartments and eroded information

Among the post-mortem brain samples in the study, 57 came from donors to the Religious Orders Study or the Rush Memory and Aging Project (collectively known as “ROSMAP”) who did not have AD pathology or symptoms, while 33 came from donors with early-stage pathology and 21 came from donors at a late stage. The samples therefore provided rich information about the symptoms and pathology each donor was experiencing before death.

In the new study, Liu and Zhang combined analyses of single-cell RNA sequencing of the samples, which measures which genes are being expressed in each cell, and ATACseq, which measures whether chromosomal regions are accessible for gene expression. Considered together, these transcriptomic and epigenomic measures enabled the researchers to understand the molecular details of how gene expression is regulated across seven broad classes of brain cells (e.g., neurons or other glial cell types) and 67 subtypes of cell types (e.g., 17 kinds of excitatory neurons or six kinds of inhibitory ones).

The researchers annotated more than 1 million gene-regulatory control regions that different cells employ to establish their specific identities and functionality using epigenomic marking. Then, by comparing the cells from Alzheimer’s brains to the ones without, and accounting for stage of pathology and cognitive symptoms, they could produce rigorous associations between the erosion of these epigenomic markings, and ultimately loss of function.

For instance, they saw that among people who advanced to late-stage AD, normally repressive compartments opened up for more expression and compartments that were normally more open during health became more repressed. Worryingly, when the normally repressive compartments of brain cells opened up, they became more afflicted with disease.

“For Alzheimer’s patients, repressive compartments opened up, and gene expression levels increased, which was associated with decreased cognitive function,” explains Liu.

But when cells managed to keep their compartments in order such that they expressed the genes they were supposed to, people remained cognitively intact.

Meanwhile, based on the cells’ expression of their regulatory elements, the researchers created an epigenomic information score for each cell. Generally, information declined as pathology progressed, but that was particularly notable among cells in the two brain regions affected earliest in Alzheimer’s: the entorhinal cortex and the hippocampus. The analyses also highlighted specific cell types that were especially vulnerable including microglia that play immune and other roles, oligodendrocytes that produce myelin insulation for neurons, and particular kinds of excitatory neurons.

Risk genes and “chromatin guardians”

Detailed analyses in the paper highlighted how epigenomic regulation tracked with disease-related problems, Liu notes. The e4 variant of the APOE gene, for instance, is widely understood to be the single biggest genetic risk factor for Alzheimer’s. In APOE4 brains, microglia initially responded to the emerging disease pathology with an increase in their epigenomic information, suggesting that they were stepping up to their unique responsibility to fight off disease. But as the disease progressed, the cells exhibited a sharp drop off in information, a sign of deterioration and degeneration. This turnabout was strongest in people who had two copies of APOE4, rather than just one. The findings, Kellis said, suggest that APOE4 might destabilize the genome of microglia, causing them to burn out.

Another example is the fate of neurons expressing the gene RELN and its protein Reelin. Prior studies, including by Kellis and Tsai, have shown that RELN- expressing neurons in the entorhinal cortex and hippocampus are especially vulnerable in Alzheimer’s, but promote resilience if they survive. The new study sheds new light on their fate by demonstrating that they exhibit early and severe epigenomic information loss as disease advances, but that in people who remained cognitively resilient the neurons maintained epigenomic information.

In yet another example, the researchers tracked what they colloquially call “chromatin guardians” because their expression sustains and regulates cells’ epigenomic programs. For instance, cells with greater epigenomic erosion and advanced AD progression displayed increased chromatin accessibility in areas that were supposed to be locked down by Polycomb repression genes or other gene expression silencers. While resilient cells expressed genes promoting neural connectivity, epigenomically eroded cells expressed genes linked to inflammation and oxidative stress.

“The message is clear: Alzheimer’s is not only about plaques and tangles, but about the erosion of nuclear order itself,” Kellis says. “Cognitive decline emerges when chromatin guardians lose ground to the forces of erosion, switching from resilience to vulnerability at the most fundamental level of genome regulation.

“And when our brain cells lose their epigenomic memory marks and epigenomic information at the lowest level deep inside our neurons and microglia, it seems that Alheimer’s patients also lose their memory and cognition at the highest level.”

Other authors of the paper are Benjamin T. James, Kyriaki Galani, Riley J. Mangan, Stuart Benjamin Fass, Chuqian Liang, Manoj M. Wagle, Carles A. Boix, Yosuke Tanigawa, Sukwon Yun, Yena Sung, Xushen Xiong, Na Sun, Lei Hou, Martin Wohlwend, Mufan Qiu, Xikun Han, Lei Xiong, Efthalia Preka, Lei Huang, William F. Li, Li-Lun Ho, Amy Grayson, Julio Mantero, Alexey Kozlenkov, Hansruedi Mathys, Tianlong Chen, Stella Dracheva, and David A. Bennett.

Funding for the research came from the National Institutes of Health, the National Science Foundation, the Cure Alzheimer’s Fund, the Freedom Together Foundation, the Robert A. and Renee E. Belfer Family Foundation, Eduardo Eurnekian, and Joseph P. DiSabato.

When I announced my latest book last week, I forgot to mention that you can pre-order a signed copy here. I will ship the books the week of 10/20, when it is published.

At any given moment, trillions of particles called neutrinos are streaming through our bodies and every material in our surroundings, without noticeable effect. Smaller than electrons and lighter than photons, these ghostly entities are the most abundant particles with mass in the universe.

The exact mass of a neutrino is a big unknown. The particle is so small, and interacts so rarely with matter, that it is incredibly difficult to measure. Scientists attempt to do so by harnessing nuclear reactors and massive particle accelerators to generate unstable atoms, which then decay into various byproducts including neutrinos. In this way, physicists can manufacture beams of neutrinos that they can probe for properties including the particle’s mass.

Now MIT physicists propose a much more compact and efficient way to generate neutrinos that could be realized in a tabletop experiment.

In a paper appearing in Physical Review Letters, the physicists introduce the concept for a “neutrino laser” — a burst of neutrinos that could be produced by laser-cooling a gas of radioactive atoms down to temperatures colder than interstellar space. At such frigid temps, the team predicts the atoms should behave as one quantum entity, and radioactively decay in sync.

The decay of radioactive atoms naturally releases neutrinos, and the physicists say that in a coherent, quantum state this decay should accelerate, along with the production of neutrinos. This quantum effect should produce an amplified beam of neutrinos, broadly similar to how photons are amplified to produce conventional laser light.

“In our concept for a neutrino laser, the neutrinos would be emitted at a much faster rate than they normally would, sort of like a laser emits photons very fast,” says study co-author Ben Jones PhD ’15, an associate professor of physics at the University of Texas at Arlington.

As an example, the team calculated that such a neutrino laser could be realized by trapping 1 million atoms of rubidium-83. Normally, the radioactive atoms have a half-life of about 82 days, meaning that half the atoms decay, shedding an equivalent number of neutrinos, every 82 days. The physicists show that, by cooling rubidium-83 to a coherent, quantum state, the atoms should undergo radioactive decay in mere minutes.

“This is a novel way to accelerate radioactive decay and the production of neutrinos, which to my knowledge, has never been done,” says co-author Joseph Formaggio, professor of physics at MIT.

The team hopes to build a small tabletop demonstration to test their idea. If it works, they envision a neutrino laser could be used as a new form of communication, by which the particles could be sent directly through the Earth to underground stations and habitats. The neutrino laser could also be an efficient source of radioisotopes, which, along with neutrinos, are byproducts of radioactive decay. Such radioisotopes could be used to enhance medical imaging and cancer diagnostics.

Coherent condensate

For every atom in the universe, there are about a billion neutrinos. A large fraction of these invisible particles may have formed in the first moments following the Big Bang, and they persist in what physicists call the “cosmic neutrino background.” Neutrinos are also produced whenever atomic nuclei fuse together or break apart, such as in the fusion reactions in the sun’s core, and in the normal decay of radioactive materials.

Several years ago, Formaggio and Jones separately considered a novel possibility: What if a natural process of neutrino production could be enhanced through quantum coherence? Initial explorations revealed fundamental roadblocks in realizing this. Years later, while discussing the properties of ultracold tritium (an unstable isotope of hydrogen that undergoes radioactive decay) they asked: Could the production of neutrinos be enhanced if radioactive atoms such as tritium could be made so cold that they could be brought into a quantum state known as a Bose-Einstein condensate?

A Bose-Einstein condensate, or BEC, is a state of matter that forms when a gas of certain particles is cooled down to near absolute zero. At this point, the particles are brought down to their lowest energy level and stop moving as individuals. In this deep freeze, the particles can start to “feel” each others’ quantum effects, and can act as one coherent entity — a unique phase that can result in exotic physics.

BECs have been realized in a number of atomic species. (One of the first instances was with sodium atoms, by MIT’s Wolfgang Ketterle, who shared the 2001 Nobel Prize in Physics for the result.) However, no one has made a BEC from radioactive atoms. To do so would be exceptionally challenging, as most radioisotopes have short half-lives and would decay entirely before they could be sufficiently cooled to form a BEC.

Nevertheless, Formaggio wondered, if radioactive atoms could be made into a BEC, would this enhance the production of neutrinos in some way? In trying to work out the quantum mechanical calculations, he found initially that no such effect was likely.

“It turned out to be a red herring — we can’t accelerate the process of radioactive decay, and neutrino production, just by making a Bose-Einstein condensate,” Formaggio says.

In sync with optics

Several years later, Jones revisited the idea, with an added ingredient: superradiance — a phenomenon of quantum optics that occurs when a collection of light-emitting atoms is stimulated to behave in sync. In this coherent phase, it’s predicted that the atoms should emit a burst of photons that is “superradiant,” or more radiant than when the atoms are normally out of sync.

Jones proposed to Formaggio that perhaps a similar superradiant effect is possible in a radioactive Bose-Einstein condensate, which could then result in a similar burst of neutrinos. The physicists went to the drawing board to work out the equations of quantum mechanics governing how light-emitting atoms morph from a coherent starting state into a superradiant state. They used the same equations to work out what radioactive atoms in a coherent BEC state would do.

“The outcome is: You get a lot more photons more quickly, and when you apply the same rules to something that gives you neutrinos, it will give you a whole bunch more neutrinos more quickly,” Formaggio explains. “That’s when the pieces clicked together, that superradiance in a radioactive condensate could enable this accelerated, laser-like neutrino emission.”

To test their concept in theory, the team calculated how neutrinos would be produced from a cloud of 1 million super-cooled rubidium-83 atoms. They found that, in the coherent BEC state, the atoms radioactively decayed at an accelerating rate, releasing a laser-like beam of neutrinos within minutes.

Now that the physicists have shown in theory that a neutrino laser is possible, they plan to test the idea with a small tabletop setup.

“It should be enough to take this radioactive material, vaporize it, trap it with lasers, cool it down, and then turn it into a Bose-Einstein condensate,” Jones says. “Then it should start doing this superradiance spontaneously.”

The pair acknowledge that such an experiment will require a number of precautions and careful manipulation.

“If it turns out that we can show it in the lab, then people can think about: Can we use this as a neutrino detector? Or a new form of communication?” Formaggio says. “That’s when the fun really starts.”

In the search for habitable exoplanets, atmospheric conditions play a key role in determining if a planet can sustain liquid water. Suitable candidates often sit in the “Goldilocks zone,” a distance that is neither too close nor too far from their host star to allow liquid water. With the launch of the James Webb Space Telescope (JWST), astronomers are collecting improved observations of exoplanet atmospheres that will help determine which exoplanets are good candidates for further study.

In an open-access paper published today in The Astrophysical Journal Letters, astronomers used JWST to take a closer look at the atmosphere of the exoplanet TRAPPIST-1e, located in the TRAPPIST-1 system. While they haven’t found definitive proof of what it is made of — or if it even has an atmosphere — they were able to rule out several possibilities.

“The idea is: If we assume that the planet is not airless, can we constrain different atmospheric scenarios? Do those scenarios still allow for liquid water at the surface?” says Ana Glidden, a postdoc in the MIT Department of Earth, Atmospheric and Planetary Sciences (EAPS) and the MIT Kavli Institute for Astrophysics and Space Research, and the first author on the paper. The answers they found were yes.

The new data rule out a hydrogen-dominated atmosphere, and place tighter constraints on other atmospheric conditions that are commonly created through secondary-generation, such as volcanic eruptions and outgassing from the planet’s interior. The data were consistent enough to still allow for the possibility of a surface ocean.

“TRAPPIST-1e remains one of our most compelling habitable-zone planets, and these new results take us a step closer to knowing what kind of world it is,” says Sara Seager, Class of 1941 Professor of Planetary Science at MIT and co-author on the study. “The evidence pointing away from Venus- and Mars-like atmospheres sharpens our focus on the scenarios still in play.”

The study’s co-authors also include collaborators from the University of Arizona, Johns Hopkins University, University of Michigan, the Space Telescope Science Institute, and members of the JWST-TST DREAMS Team.

Improved observations

Exoplanet atmospheres are studied using a technique called transmission spectroscopy. When a planet passes in front of its host star, the starlight is filtered through the planet’s atmosphere. Astronomers can determine which molecules are present in the atmosphere by seeing how the light changes at different wavelengths.

“Each molecule has a spectral fingerprint. You can compare your observations with those fingerprints to suss out which molecules may be present,” says Glidden.

JWST has a larger wavelength coverage and higher spectral resolution than its predecessor, the Hubble Space Telescope, which makes it possible to observe molecules like carbon dioxide and methane that are more commonly found in our own solar system. However, the improved observations have also highlighted the problem of stellar contamination, where changes in the host star’s temperature due to things like sunspots and solar flares make it difficult to interpret data.

“Stellar activity strongly interferes with the planetary interpretation of the data because we can only observe a potential atmosphere through starlight,” says Glidden. “It is challenging to separate out which signals come from the star versus from the planet itself.”

Ruling out atmospheric conditions

The researchers used a novel approach to mitigate for stellar activity and, as a result, “any signal you can see varying visit-to-visit is most likely from the star, while anything that’s consistent between the visits is most likely the planet,” says Glidden.

The researchers were then able to compare the results to several different possible atmospheric scenarios. They found that carbon dioxide-rich atmospheres, like those of Mars and Venus, are unlikely, while a warm, nitrogen-rich atmosphere similar to Saturn’s moon Titan remains possible. The evidence, however, is too weak to determine if any atmosphere was present, let alone detecting a specific type of gas. Additional, ongoing observations that are already in the works will help to narrow down the possibilities.

“With our initial observations, we have showcased the gains made with JWST. Our follow-up program will help us to further refine our understanding of one of our best habitable-zone planets,” says Glidden.

Just a few months after Elon Musk’s retreat from his unofficial role leading the Department of Government Efficiency (DOGE), we have a clearer picture of his vision of government powered by artificial intelligence, and it has a lot more to do with consolidating power than benefitting the public. Even so, we must not lose sight of the fact that a different administration could wield the same technology to advance a more positive future for AI in government.

To most on the American left, the DOGE end game is a dystopic vision of a government run by machines that benefits an elite few at the expense of the people. It includes AI ...