Turning low-energy light into higher-energy light seems to break the usual rules of physics, since energy is supposed to run downhill, not uphill. Yet a process called photon upconversion achieves exactly this, without breaking any laws of thermodynamics. Instead of absorbing one photon and releasing a single photon of lower energy, as most light-absorbing molecules do, an upconversion system absorbs two lower-energy photons and combines their energy to release one higher-energy photon. Because it takes two photons to make one, the total energy is still conserved; the trick is repackaging it into a more useful form. The phenomenon was first observed in the 1960s in simple organic mixtures cooled to very low temperatures, but it only became practical decades later, once chemists identified metal-containing dyes able to hold their excited states at room temperature. Since then, scientists have pursued upconversion as a way to make better use of sunlight, to power light-driven chemical reactions, to improve imaging inside living tissue, and to build new kinds of optoelectronic devices.

Triplet-triplet annihilation

The most developed route to upconversion relies on a process called triplet-triplet annihilation. A light-absorbing molecule known as a sensitizer first captures a low-energy photon and passes that energy to a second type of molecule, the annihilator. The annihilator settles into a triplet excited state, an unusually long-lived condition that allows it to persist until it meets a second annihilator molecule in the same state. When two such molecules collide, one drops back to its ground state while the other is pushed up into a higher-energy singlet state, from which it emits a photon of higher energy than either of the photons that started the process.

A long-standing problem with this scheme is that ordinary sensitizer molecules lose a portion of the absorbed energy internally, as the initially excited state converts into the lower-energy triplet state that gets passed along. This loss caps how large an energy jump the whole system can ultimately achieve. One promising way around the problem is to replace the conventional sensitizer with an organic radical, a molecule carrying a single unpaired electron. That unpaired electron gives radicals unusual electronic and magnetic behavior and can make the conversion from absorbed light into a usable excited state considerably more efficient, since it opens transitions that are otherwise very weak in conventional molecules.

A single hydrogen to control it all

New research examined ¹ a pair of molecules built on this idea, both based on a radical component linked directly to an anthracene unit, the same type of light-emitting building block used in classic annihilators. The two molecules are nearly identical, differing at a single carbon atom: in one, that carbon carries the unpaired electron of the radical; in the other, an ordinary hydrogen atom has been added, pairing up the electron and removing the radical character entirely. That single hydrogen atom turns out to control everything. The radical version behaves as an efficient sensitizer, while the hydrogen-added version behaves as an annihilator, even though the two molecules share almost the same overall structure.

To work out why, the investigation combined light-based spectroscopy, electron spin resonance (a technique that detects unpaired electrons), and quantum chemical calculations. After the radical absorbs red light, its excitation transfers within about ten picoseconds (ten trillionths of a second) to the attached anthracene unit, creating a long-lived excited state that still carries some radical character. This internal handoff stretches the effective excited-state lifetime to more than 250 nanoseconds, roughly ten times longer than the 27 nanoseconds measured for the radical unit on its own. A longer-lived excited state gives the sensitizer far more opportunity to encounter another molecule and hand off its energy before simply decaying back to the ground state. The calculations independently pointed to the same conclusion, showing that energy transfer to a nearby annihilator proceeds far more readily through this long-lived triplet-like state than directly from the radical’s first excited state.

A mix needed

The work also tested an idea proposed in earlier research, that a single radical-containing molecule of this kind might act as both sensitizer and annihilator on its own, a so-called single-component upconversion system. The new experiments argue against this. Solutions containing only the radical molecule, across a range of concentrations, showed no detectable upconverted light, consistent with the radical’s higher excited states relaxing away too quickly for the necessary emission to compete.

Efficient upconversion instead required mixing the radical sensitizer with its hydrogen-added counterpart, or with the well-established annihilator 9,10-diphenylanthracene. Because the two molecules share nearly the same molecular framework, this two-molecule mixture is described as a “pseudo-single-component” system. Shining red light at 658 nanometres onto the radical paired with its hydrogenated twin produced blue emission at 450 nanometres, an apparent energy gain of about 0.9 electronvolts, with 7 percent of absorbed photon pairs converted into upconverted light. Pairing the same radical sensitizer with 9,10-diphenylanthracene instead produced blue emission at 437 nanometres, a slightly larger energy gain of about 1.0 electronvolt, with 12 percent efficiency. Both figures mark a large improvement over earlier all-organic radical sensitizers, which had reached efficiencies of only a few tenths of a percent, and the upconverted emission remained stable over hours of continuous illumination.

A practical strategy for photon upconversion

Beyond these specific molecules, the study illustrates how a minimal change in molecular structure, adding or removing a single hydrogen atom, can completely redirect a molecule’s photochemical role, switching it from an energy donor to an energy acceptor. Combining optical measurements, spin resonance, and computation made it possible to trace exactly why this switch occurs at the level of electronic structure, rather than simply observing that it happens.

The findings offer a clearer picture of how organic radicals can be harnessed for photon upconversion and point toward a practical strategy for building more efficient materials from radicals and their closed-shell relatives together. Such materials could eventually help capture more of the solar spectrum, drive light-powered chemical synthesis, or improve the efficiency of light-emitting technologies, by putting to use photons that would otherwise be wasted.

Author: César Tomé López is a science writer and the editor of Mapping Ignorance

Disclaimer: Parts of this article may have been copied verbatim or almost verbatim from the referenced research paper/s.

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Researchers at the University of Michigan have created a device that enables them to control the flow of electrons through a semiconductor using only laser light—no electrical power source required.

This device was built ¹ to explore fundamental physics and realize a previously unobserved behavior, but it could also open doors for new applications in areas that bridge optics and electronics, including sensing, imaging and telecommunications. The phenomenon could help improve how signals are sent through and between devices, as well as create new opportunities to store more information in those signals.

 

“This electrical device that we manufactured at the Lurie Nanofabrication Facility has the potential to turn into something that measures different aspects of light,” said Yiming Gong, who helped lead the project as a doctoral student in the U-M Department of Physics. “But this originates from a very fundamental level of physics, which is the interference between different optical absorption processes.”

 

The researchers showed they could induce the orderly flow of electrons through a semiconductor using two different colors of light. By rotating the polarization of the two optical fields—the direction that the light waves wiggle—the researchers could also control the direction of the electronic current.

 

“This isn’t the way things normally work. When you think about electrons moving through a material, they’re moving because you’ve applied an electrical field and they actually bounce around and drift across the materials. Here, using light, you can actually sort of squirt the electrons in a specific direction without applying an electric field,” said U-M physicist Steven Cundiff, senior author of the team’s report.

 

Although previous work had shown the ability of light to get electrons flowing with light alone, this work goes a step further and shows the light gets electrons flowing in a narrow beam in a specific direction.

 

“The light no longer merely switches the current on; it also aims it,” Cundiff said.

 

Cundiff likens this to a lighthouse, which sweeps a beam of light by rotating its lamp. Here, the beam is made of electrons and that beam can be rotated by rotating the polarization of the two phase-coherent optical fields.

 

The phenomenon relies on quantum interference, which arises when two colors of light drive different absorption pathways to the same final state. The light transfers energy to the semiconductor material in discrete, or quantized, packets called photons, which mobilize the material’s electric charge carriers.

 

In the set-up, the incident light is absorbed by two routes at once, and the routes can be thought of as overlapping ripples, Cundiff said. Those ripples line up and enhance each other for electrons traveling a certain direction, but cancel each other out for electrons moving in other directions.

 

A collaborator on an earlier project, J.E. Sipe of the University of Toronto, had predicted it would be possible to create such an “electron lighthouse.” Now, working with the Lurie Nanofabrication Facility, Gong was able to realize such a device.

 

“The LNF is an amazing facility,” Gong said, adding it was a painstaking process to meld the device’s materials together in a way that didn’t introduce any extraneous electric fields.

 

“That was the biggest puzzle to solve for me, because there isn’t a standard way to do that. So I worked with the LNF staff to play around with different recipes and temperatures to come up with a manufacturing process.”

 

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Author: José R. Pineda got his Ph.D. from University of Barcelona in 2006. Since 2007 he has worked for Institut Curie and The French Alternative Energies and Atomic Energy Commission. Currently he is a researcher of the EHU. He investigates the role of stem cells in physiologic and pathologic conditions.

 

For decades, Alzheimer’s research has been dominated by a seemingly intuitive idea: the disease is largely explained by the accumulation of abnormal proteins in the brain, primarily beta-amyloid and tau. However, while this view has been useful, it has fallen short in explaining certain fundamental aspects. One of the most striking is that Alzheimer’s affects women far more than men. This is not a minor difference: roughly two-thirds of cases occur in women, and the clinical progression tends to be faster and more severe. The work by López-López and colleagues addresses this imbalance from a different angle. Instead of focusing exclusively on protein accumulation, it shifts attention to the brain’s immune system—specifically to a molecular pathway known as interferon signaling. What the study proposes is that the brain’s immune response, far from being a mere bystander, could be a central driver of the disease, and one that operates differently in men and women ¹.

To understand the importance of this idea, it helps to briefly consider what interferons are. They are molecules that form part of the body’s first line of defense against infections, especially viruses. They activate genetic programs that help cells detect and neutralize threats. Under normal conditions, this system is essential for survival. The problem arises when it becomes chronically or inappropriately activated, as is the case in several inflammatory diseases ². So, the study begins with an analysis of human brain tissue from Alzheimer’s patients. Using transcriptomics (techniques that measure the activity of thousands of genes at once) the authors identified a clear pattern: in the brains of women with Alzheimer’s, genes associated with the interferon response were much more strongly activated than in men (Figure 1). This pattern was not explained by differences in disease severity, since both groups showed comparable levels of neuropathological damage. Instead, it points to an intrinsic difference in how the brain responds to the disease. This finding is significant because it suggests that women not only develop Alzheimer’s more often, but may do so through a partially distinct biological pathway. In other words, the same clinical diagnosis may conceal different underlying mechanisms depending on sex.

To move beyond correlation and explore causality, the researchers turned to animal models. They used genetically modified mice (APP/PS1), widely employed in Alzheimer’s research because they develop amyloid plaques similar to those seen in patients. Once again, the same pattern emerged: female mice showed much stronger activation of the interferon pathway, along with increased brain inflammation, neuronal damage, and functional impairment. An especially interesting point is that these differences were not limited to amyloid plaque levels. Indeed, female mice did have more plaques, but the study shows that neuronal damage and inflammation cannot be explained solely by amyloid accumulation. This supports a growing idea in the field: that Alzheimer’s toxicity depends not only on protein buildup, but also on how the brain responds to it. In this context, microglia (the brain’s resident immune cells) become key players. Cell-level analyses revealed that these cells are the main drivers of interferon activation. In essence, microglia detect signals of damage or stress and launch an inflammatory response which, if sustained over time, can ultimately harm neuronal tissue. To test whether this pathway is not only associated with disease but actually contributes to it, the authors performed direct manipulation experiments acutely activating interferon signaling in healthy animals using an immune stimulus. To do that, they did intraperitoneal administration of polyinosinic:polycytidylic acid (poly(I:C)) to induce inflammation, but also they performed crossings between the APP/PS1 mice and a microglia-specific Rela conditional knockout line (AD hiIFN). The result was striking: within hours to days, the brains of these animals began to show changes resembling Alzheimer’s pathology, including altered neuronal activity, synaptic disruption, and markers of axonal damage. This results suggest that activation of this pathway is not a secondary phenomenon, but may be sufficient to induce key features of the disease. In parallel, the researchers performed the inverse experiment: they chronically enhanced interferon signaling in microglia within APP/PS1 mice (an Alzheimer’s disease model). This led to a worsening of neurodegenerative features, even though, paradoxically, amyloid plaque levels did not increase—and in some cases even decreased. This last finding is particularly revealing because it challenges a widespread assumption: that fewer plaques necessarily means a healthier brain. Here, the opposite happens!! The animals had less amyloid burden, yet more neuronal damage and worse function. This points to inflammation, and specifically interferon signaling, as an independent driver of degeneration.

Next, the key question is whether this pathway can be targeted therapeutically. To address this, the study explores a pharmacological intervention aimed at the cGAS–STING pathway (a molecular system that senses cellular damage and triggers interferon production). Using a specific inhibitor (STING inhibitor C-176), the researchers demonstrated by RNA-seq and immunohistochemistry that the treatment was able to reduce interferon signaling in the brain. The results were consistent: inflammation decreased, neuronal integrity was better preserved, and cognitive performance improved in memory tests (very important from the therapeutic and functional perspective). More importantly, these effects were far more pronounced in females, which aligns with the idea that this pathway is more active in them and therefore more impactful when blocked. Notably, these improvements occurred without significant changes in amyloid plaque levels. Once again, the conclusion is clear: modulating the immune response may be as important as, or even more important than, targeting protein aggregates. Taken together, this work proposes a shift in how Alzheimer’s is understood. Rather than viewing it solely as a disease of protein accumulation, it suggests it is also—critically—a disorder of immune dysregulation. More specifically, one in which excessive interferon signaling plays a central role, particularly in women.

The practical implications are twofold. First, it opens the door to therapies that modulate immune pathways in the brain, something already feasible in other diseases using drugs that target similar mechanisms. Second, it highlights the importance of incorporating sex as a biological variable in both research and treatment design. What works in men may not work the same way in women, and vice versa. As with any preclinical study conducted in mice we must be cautious when extrapolating to humans: results in animal models do not always translate directly, and manipulating the immune system carries inherent risks, given its essential role in protecting against infections. However, the value of this work lies not only in its potential clinical applications, but in the conceptual framework it offers.

By identifying interferon signaling as a key factor in sex-specific vulnerability to Alzheimer’s, the study provides a mechanistic explanation for a long-observed but poorly understood phenomenon. Perhaps more importantly, it suggests that intervening in this pathway could alter disease progression even without changing classical amyloid pathology. In a field where many clinical trials have failed by focusing solely on plaque removal, this perspective is not just novel, it may be necessary to explore it in the future.

 

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