Wonders of Bioelectricity in Health Care!

Neuroprosthetics to Restore Sight

Last year, two intriguing experiments restored vision by stimulating neuroelectrical signals. One is closer to the clinic, while the other seems like it could restore a more natural ability to see.

Age-related macular degeneration (AMD) is a progressive disease that affects about 5 million people around the world. It is the leading cause of permanent vision loss. It destroys the light-sensitive cells in the macula, the central part of the retina that allows you to focus on objects directly in front of you, like the words on this page. My grandmother had AMD, and even as her peripheral vision stayed intact, AMD increasingly reduced the area directly in front of her eyes. It was maddening. She could see, but she could no longer look. In my grandmother’s day, the only option was a big machine that could enlarge her newspaper or crossword puzzles, like the old projectors used in 20th-century classrooms to display transparencies against the wall. These big machines didn’t work. But now there are little machines that might.

A trial designed by an international European research collaboration tested a photovoltaic retina implant microarray (PRIMA) system in 32 people with macular degeneration. ¹ This system consists of special glasses and an ultrathin 2 × 2 mm silicon array surgically implanted under the retina. A small camera mounted on the glasses turns incoming photons from the outside environment into patterns of near-infrared light, which it projects onto the implant. The implant, in turn, converts these patterns into electrical impulses that stimulate the (still intact) cells further downstream in the visual processing pipeline. The normal flow of visual information resumes.

After one year, 27 of the patients were able to use their central vision to read five lines down an eye chart (some had not been able to see it at all before being implanted). Though it takes effort, concentration, and training to use, one participant told the BBC it was “out of this world” to be able to read and do crosswords again (https://www.bbc.co.uk/news/articles/c0qpz39jpj7o).

The next generation of these kinds of implants may take this idea much further. Researchers at Northwestern University used a technique called optogenetics, which makes cells sensitive to light, to create a full “eye bypass.” ² Instead of replacing nonfunctioning parts of the eyeball, it bypassed the organ entirely to deliver electrical pulses directly into the brain’s cortex. The soft electrode sat under the scalp, where it beamed patterns of light through the skull into neurons that had been modified by optogenetics to send an electrical signal when they’re hit by light.

Unlike the retinal implant, the Northwestern experiment was in mice, which limited the scientists’ ability to evaluate how robustly the picture they saw matched the external world. You can’t ask a mouse how much further down the eye chart it can read. Furthermore, optogenetics relies on gene therapy, which not everyone is comfortable signing up for.

Nonetheless, these approaches address the issue from the same perspective—all sensory information, at the end of the day, just boils down to electrical impulses crackling into and out of your brain. While the first PRIMA implant may be available in the clinic in the next few years, the roadmap for the Northwestern approach is not yet in sight. But the idea that we can harness the electrical underpinnings of perception is now mainstream, and the advances are only coming faster.

Tools That Let People Who Can’t Speak Express Themselves—and Tools That Know When Not to

Are all our senses, movements, and conscious experiences ultimately reducible to a particular spatiotemporal pattern of electrical signals traded between the neurons of the body and the brain? This interpretation is known as the “neural code”: Crack the brain’s fundamental electrical language, proponents argue, and a brain–computer interface (BCI) should be able to decipher a person’s inner voice, intentions, and desires.

Many unpleasant consequences might spring to mind, but explorations of the neural code have dramatic implications for future therapies. Last year, two clinical trials showed that a BCI could restore the ability to speak at a natural pace after it had been lost to neurodegenerative disease or catastrophic accident.

Speech neuroprosthetics have been in development for a long time. Since 2010, it has been possible to detect words as people imagine saying them—such as “yes,” “no,” “thirsty,” “hungry,” “hello,” and “goodbye”—using a variety of devices that can eavesdrop on electrical activity in the language-related areas of the motor cortex. ¹

The technology has evolved rapidly since then, from decoding words to sentences to real-time conversations, which have been turned into text output, synthesized voices, and even animated avatars vocalizing on a computer screen. Thanks to AI, the decoders keep getting faster. By 2023, they had reached 62 words per minute (typical human speech is around 160).^2,3

But speed is not everything and couldn’t address two other limitations of BCIs: a disorienting “tape delay” between thinking the words and their output, and a flatness of affect. These tools have not been able to translate the “metadata” of language, like tone, emphasis, and cadence.

Researchers with the BrainGate 2 project were looking for ways to make synthetic speech more continuous and more expressive. A trial volunteer with amyotrophic lateral sclerosis (ALS) tested their approach, an algorithm that could both detect the neural activity linked to the “metadata” and provide continuous closed-loop auditory feedback. The BCI streamed the interpreted speech within 10 ms of detecting it, allowing the volunteer to modulate his BCI voice with nuance. Not only did it let him change intonation to ask a question, but he even sang. ⁴

However, the same advances that bring speech prosthetics closer to the clinic also intensify privacy concerns. If a BCI articulated every word that flitted through your mind, it would be the equivalent of a form of technological Tourette’s. So, a collaboration led by researchers at Stanford University sought to give people with BCIs assurance that they could trust their decoders to only speak the words they wanted to and keep out of their other private thoughts.

The researchers tested their approach with the help of four volunteers whose ability to speak had been lost to ALS or brainstem stroke. A decoder was trained on the neural activity in the “speech hotspot” regions where inner speech, silent reading, and passive listening are represented. The algorithm was able to tease out the difference between intentionally articulated mental speech and the private inner monologue that is not for public consumption. ⁵ It was also possible to assign a keyword that the volunteer could mentally articulate in their mind to lock the system.

Before speech neuroprosthetics can be marketed, the technology will need to learn one of our oldest axioms: that silence is golden.

A New Tool to Observe the Developing Brain from the Start

It’s been a real head-scratcher: how does a brain—billions of neurons that orchestrate an organism’s every thought and action—create itself out of essentially nothing?

The biggest obstacle to observing brain development is the opaque barrier of the skull. Only two existing tools can overcome this limitation, and both come with steep tradeoffs: fMRI is a noninvasive way to track brain activity by measuring changes in blood flow—but its resolution is often too low to yield useful information. Hard electrode wires can penetrate through bone and into the brain, where they offer high resolution—but they do so much damage in the process that the organism with the implant does not survive for long. Aside from being grim, this limits any scientific insights to a short time window.

Jia Liu and his colleagues at Harvard wanted a better and more permanent way to eavesdrop on the full neurodevelopmental journey, from start to finish. ¹ There was an intriguing opportunity in an early stage of brain development.

Before the central nervous system forms, it starts as a far simpler structure known as the neural tube. The neural tube has its own precursor: An initially flat anatomical feature called the neural plate. Eventually, the sides of this flat plate fold over and close in to form the tube; the front end matures into the brain while the rest becomes the spinal cord.

This offered an opportunity. Could the team embed something on that plate? In theory, it would grow into the developing brain and stay there with a front row-seat to the entire metamorphosis.

But to take advantage of that, the group couldn’t use traditional electronics. The usual hard materials would shred the expanding brain. They needed to find something that matched the brain’s Young’s modulus (this is a measure of a material’s softness and conformability—the brain matches that of soft tofu).

But soft materials posed their own problem: they are too squishy to be compatible with the nanofabrication process, as the materials tend to swell, causing the high-resolution patterns etched on them to become unusable.

After a long search, Liu’s group identified a perfluropolymer whose tofu-like Young’s modulus matched the brain but which also held its shape enough to be reliably fabricated. They used it to build a soft, stretchable mesh microelectrode array.

Then they applied principles from the Japanese art of folding paper, called kirigami, to design a device that would unfold with the growing brain without destroying or interfering with its processes.

They delicately placed this onto the tadpole embryo’s neural plate. As it unfolded into the neural tube, the electrode ribbon was subsumed into the growing brain, where it stretched and bent with the proliferating tissue, all the while continuously reporting on the brain’s electrical activity. No immune response, no damage, and at least one of the tadpoles lived to a ripe old age.

A few insights emerged immediately, including the presence of a link between electrical activity in the brain and limb regeneration—something previously theorized but never observed.

Liu and his colleagues are now working on ways to make this implant work in mammals. Here, the skull is only the first problem—an added complication is the womb, which will require in vitro fertilization and a creative approach to power sourcing.

This is only one example of the rapid evolution of brain implants away from traditional electronic materials. From silk to crustacean chitosan, researchers investigate diverse sources to make them as biocompatible as any biological material. A recent new material blurs the boundaries significantly. Former Neuralink startup Science Corp is working on chips that integrate living (lab-grown) human neurons into their chips. ² The neurons in the device stretch their dendrites out of the hardware and into the brain. They are betting that the ultimate biocompatible material for brain implants will be brain tissue.

Turning the Body’s Electrochemistry into Drug-Free Cancer Immunotherapy

Manganese is an essential trace metal crucial to biological functions, from metabolism to the nervous and digestive systems. In recent years it has emerged as a promising adjunct to immunotherapy for cancer. Now researchers have put it at the center of a game-changing new approach to immunotherapy that would let you skip the actual drugs.

In nanoparticle form, manganese has proven especially effective at delivering immunotherapy drugs through cell membranes to target tumors. ¹ But it’s not just a courier—it also brings its own firepower, because manganese activates the body’s own immune signaling cascade. Among other things, this can break through the barrier of the tumor microenvironment, which normally blinds the immune system to the presence of cancer.

Promising, but a major challenge has been keeping those manganese ions in your body long enough to do all that. After intravenous injection, they tend to only stick around for 2 days before making their way out of the body. This is not the only problem with administering cancer drugs systemically: If they accumulate in sufficient quantities to be toxic to the tumor, they often also have unhealthy effects on the body.

So, instead of introducing them into the bloodstream, which would distribute them throughout the whole system, a group of scientists from institutions in China and Australia designed an implantable biobattery that would dispense magnesium ions only at the site of the tumor. ²

Biobatteries are emerging as interesting new medical design choices. Instead of using traditional electrolytes, they conscript a person’s own bodily fluids into that role. But if electrical implants already face a hard time in the hostile environment of biology, the tumor microenvironment poses an even greater challenge, thanks to its acidity, high redox potential, and hypoxic conditions.

But the researchers figured out a way to turn the tumor’s hostile microenvironment to their own advantage—their zinc and manganese dioxide biobattery used this corrosive fluid as an electrolyte, which oxidized the solid manganese dioxide cathode into free manganese ions. Now, it was the tumor that faced a hostile environment, thanks to the ionic by-products of the battery discharge.

When the researchers implanted these batteries under the skin of mice that had been engineered with a malignant strain of breast cancer, the ions accumulated in the tumor, where they damaged its cellular machinery. This triggered immunogenic cell death, a noisy way to die that alerts the immune system, which increases the secretion of macrophages, pro-inflammatory cytokines, and other responders. The tumor could no longer hide from the body. The effect was a kind of drug-free cancer immunotherapy. As a result of their boosted immune systems, growth of the tumors in the implanted mice grew 99.6% less quickly than those in the control groups.

The researchers are working on translating their success into other kinds of cancer. More preclinical and clinical trials are in the planning stages.

If this device can work as well in humans as it did in mice, it would turn a tumor from a life-threatening problem into a manageable chronic condition, which is a goal that other cancer researchers have also begun to pursue in a long-running rethink of “the war on cancer.”

Harnessing the Body’s Electrical Pathways to Ease Pain

The search for a painkiller that works goes back to the Sumerians, who first isolated opium from poppies.

But their early efforts foreshadowed the dilemma of targeting pain without unintended consequences. From the cardiovascular risks that shadowed anti-inflammatory COX 2 inhibitors to the opioid epidemic, plenty of cautionary tales in pain medicine underscore the danger of the cure becoming worse than the disease.

However, new approaches have emerged from the study of bioelectricity. Pharmacology is getting closer to pain relief that targets the problem precisely, thanks to research that exploits the body’s electric signals to press the mute button on pain—and nothing else.

In 2025, the Food and Drug Administration approved the first new pain medication in four decades. Suzetrigine inhibits Na_v1.8, a voltage-gated sodium channel instrumental to the firing of pain-signaling neurons in the peripheral nervous system. The Yale researchers who isolated this variant recognized that it played no essential role in the regulation of brain or heart signals. ¹ Therefore, interfering with it could block pain without wreaking cardiovascular or neurological havoc. It was the first nonopioid drug ever approved to manage acute pain.

It’s not a perfect solution. It worked for acute postoperative pain but has yet to be effective against the chronic kind that plagues people suffering from shingles, cancer, diabetic neuropathy, and other ailments. It’s thought 30% of the global population deals with this kind of constant pain.

The researchers who developed suzetrigine are now working to extend Na_v1.8 research to tackle chronic pain. In the meantime, however, there is another electrical alternative: electroacupuncture.

Unlike the surface patches used in the popular Transdermal Electrical Nerve Stimulation, electroacupuncture (EA) is delivered via needles that are slipped under the skin and then attached to electrodes to charge, like tiny jumper cables. EA seems to be effective against chronic pain. And, last year, a team led by researchers from the Chinese Academy of Sciences found evidence that it does something more: It can also help against chronic pain’s devastating effects on mental health. ²

It’s not hard to see why relentless physical discomfort leads to debilitating anxiety and depression. One proposed neurological mechanism is that the stress of pain creates feedback loops that cause microglia, the brain’s immune cells, to cannibalize their own synapses, creating inflammation which is linked to anxiety and depression. Inhibiting this microglial hyperactivity, the researchers thought, would disrupt this vicious cycle.

And that’s exactly what EA did—in mice, it should be noted—successfully reducing behaviors linked to anxiety and depression. The findings are in line with (human) trials that suggest EA reduces both physiological and psychological pain. They also provide a biological mechanism to explain why. Human neuroimaging trials will be needed to show it all translates, but one thing is clear: Electrical measures are letting us tease apart the many ways pain hurts us.

Weak Magnetic Fields Can Change Your Cells

Does magnetism affect biology? For big, powerful magnetic fields, the answer is a resounding yes, and that has translated into useful medical treatments, including Transcranial Magnetic Stimulation. You sit under a very strong magnet, and its field changes the electrical firing of your neurons. These changes have been harnessed to treat depression, obsessive-compulsive disorder, and migraines.

Magnets can also be diagnostic tools, which you know if you’ve ever had an MRI, a medical imaging technique in which you basically climb into a giant magnet. Its enormous field forces all your body’s protons into alignment. The wobbling of those protons back to their original orientation translates into images of living tissue that are far clearer than anything you’d get from an X-ray or CT scan. So far, so uncontroversial.

A much more contentious question has been whether biological tissues are affected by weak magnetic fields. Really weak—we’re talking fridge magnet strength.

According to what we know about biochemistry, the answer should be no. The tiny amount of energy a weak magnetic field puts into a warm, messy biological system should be lost in the background noise. The exception is certain animals and bacteria that have materials in their bodies that may make them sensitive to Earth’s magnetic field (whose strength makes a fridge magnet seem like an MRI machine).

And yet, in previous experiments, weak magnetic fields did influence bits of biology when they shouldn’t have.

But how would this possibly work? One potential mechanism is an idea from quantum physics: The “radical pair mechanism” has emerged as an intriguing candidate for how a weak magnetic field might cut through the noise of macrobiological systems.

The radical pair hypothesis has to do with how unpaired electrons interact in chemical reactions that involve molecules called free radicals. These are characterized by having one renegade electron in their outermost shell. When two such molecules pair up, their renegade electrons pair off in one of two ways: One configuration allows chemistry to proceed as normal. But the other essentially presses a giant stop button on the chemical reaction assembly line. This mechanism, well-established in chemistry, explains how a weak magnetic field can change the state of a tiny particle, leading to a cascade that affects larger molecular interactions.

What about biology? In 2026, researchers at the University of Waterloo, in Ontario, Canada, found that the application of a weak magnetic field led to detectable changes to tiny structures inside cells. ¹

Cells contain many different types of structures. Some are little factories; others are more like scaffolding. The scaffolding in a cell is not like the static stuff construction workers use to fix up a building. Instead, it’s a highly dynamic material that rapidly self-assembles and self-disassembles, making it available on-demand exactly and only where needed.

Through clever magnetic manipulation, the Waterloo researchers were able to slow down the chemical reactions that break down those scaffolding structures. This aligned with the radical pair hypothesis in quantum biology and provided evidence for the idea that weak magnetic fields can cause measurable effects at atomic scales in biology.

Maybe this all seems a little niche, but magnetobiology will only become more relevant. For one thing, the future of space travel may depend on a better understanding of how our bodies are affected by weak magnetic fields and the reactions they instantiate. All life evolved under the protection of Earth’s immense magnetosphere. The shield it provided against the searing solar wind may have been a big reason life was able to take root. But there hasn’t been much research into what else the magnetosphere might be doing for us. We should find out! We don’t want to be in a situation where we only realize what we’re missing when our astronaut explorers are halfway to Jupiter’s moons.

Electrical Mitochondria

If you’re like most people, you grew up with a simple mental model of mitochondria as little power packs in the cell, dispensing the little energy pellets that biology uses to do its work. But a more complex and unexpected picture has emerged from research undertaken over the past few years. It strains some of the most unshakeable dogmas in biology.

It’s not a new insight that mitochondria bind biology to electrical activity. In 1978, Peter Mitchell won a Nobel Prize for his discovery that mitochondria use energy from electrons ripped from food to create an electrochemical gradient—similar to a battery—that drives the generation of adenosine triphosphate. ATP is the energy currency used by plants and animals to drive everything from DNA synthesis to intercellular electrical communications. But while this role as the cell’s “energy transformer” has long been considered mitochondria’s primary purpose, new research has made it clear that there’s far more to them.

Mitochondria seem to do startling things depending on the cells they’re embedded within. Some can affect the epigenome, others flit between cells to perform first aid on other struggling mitochondria. The research suggests that mitochondria also have a hand in regulating neuronal excitability, neurotransmitter release, and inflammation.

But getting a broader picture of their activities has been difficult. Traditionally, mitochondria are examined inside their individual cells. The imagining techniques that can observe them up close fail to capture their activities across many different tissues.

So, an international research group set out to reconcile microscopic anatomy with the panoramic scale of neuroimaging. In 2025, the researchers, hailing from Columbia, UCLA, and the French National Center for Scientific Research, published a “mitochondrial brain map”. ¹

They found that different types of mitochondria specialize according to the needs of the parts of the brain they cluster in. In the very energy-hungry gray matter, which is responsible for most of your ability to process and interpret information, they found a cluster of a special type of mitochondria that has become particularly good at energy transformation.

Their surprising ability to specialize was just one of the newly discovered roles mitochondria play that make them crucial to your health. The ability to specialize is a consequence of another newly discovered ability of mitochondria: they can communicate with each other. It is through these social collaborations that mitochondria are able to transduce the body’s various hormonal, chemical, and other signals into their own electrical membrane potential. This simple and powerful signal can help other organelles make decisions about the overall state of the cell and can even influence a cell’s decision about whether to die by apoptosis. It increasingly seems that mitochondrial signals are instrumental in shaping a person’s subjective experience of themselves, including fatigue levels, mood, and stress. ²

Indeed, the body’s mitochondrial collective, as one of the authors has suggested, might be seen as a kind of biological motherboard https://www.scientificamerican.com/article/why-mitochondria-are-more-like-a-motherboard-than-the-powerhouse-of-the-cell/). In electronic devices—smartphones, televisions, and laptops—the motherboard is the hub that connects all the hardware parts (like the memory and the processors) to the others and to the power source. Without it, the components are just a collection of pieces. Only with it do they become a functioning, coherent whole.

This is one aspect of an understanding of biology that is still struggling to emerge. Life is more than a bunch of molecular machines floating in a chemical soup. It also runs on patterns that can’t always be understood by identifying the right gene or the relevant protein. Like iron filings outlining and showing evidence of things unseen—the electromagnetic field around a magnet—the behavior of mitochondria may only be the first step to understanding biology through a deeper electromagnetic lens.

Electricity versus Fungus

Fungi (mold, mushrooms, and yeast) are intricately entwined with nearly every organism and ecosystem on earth. They’ve certainly altered the course of our human civilization—their yeast makes our bread and our beer, and their self-defense chemicals underpin our antibiotics. Researchers are probing their enzymes for more breakthrough discoveries, from antiaging drugs to alternative fuels.

All this has come from studying only a tiny fraction of the vast unknown fungal kingdom with which we share the planet. Only 3–5% of the estimated 5 million species have been catalogued.

This ignorance is becoming a problem. Growing evidence suggests that human interactions with the fungal kingdom are changing them, and their relationship to us, in dangerous ways. The number of fungal diseases is growing thanks to myriad factors including global trade, climate change, and overuse of antifungal drugs. The new diseases are much more dangerous than the harmless athlete’s foot most people normally associate with fungal infections.

Treating them won’t be easy. Genetically, humans and fungi are surprisingly similar (more so than fungi and plants). Therefore, anything that hurts one will hurt the other, which is why, for example, every effective antifungal drug damages your liver. Conversely, any medicine that doesn’t hurt you probably won’t bother them much either, which is why so many supposed “antifungal treatments” fall down on the job. Scarier diseases, ineffective treatments—no wonder some researchers think the next global pandemic will emerge from the fungal kingdom.

But all is not lost. Electricity could become an effective frontline treatment. Electrical stimulation, according to the authors of a review published last year in Cell Reports Physical Science, “has widespread effects on various fungal targets.” ¹

Beyond its direct effects, electrical stimulation also counteracts resistance to conventional antifungal agents, good news for the azoles and polyenes whose efficacy has been flagging. Its ability to manipulate fungal membrane potential, alter the structure of the cell wall, and interrupt ATP supply all enhance drug permeability, thereby making fungi vulnerable once more to conventional antifungal drugs—without hurting us in the process. Thirty minutes of micro- to milliampere-level direct current stimulation, the authors report, is effectively fungicidal against Saccharomyces cerevisiae and Candida albicans. The second is the unsavory character responsible for yeast infections, while the first (normal brewer’s yeast) has recently acquired an opportunistic taste for humans. A recent case study from Brazil highlights how such pathogenic fungi can colonize people who are already immunosuppressed and kill them. ²

Of particular interest is electroporation. Electroporation is most familiar in laboratory settings as a gentle way to punch temporary holes in a cell’s membrane to insert, for example, DNA during gene therapy. But cranking up the electrical intensity turns electroporation into something that would better be called “electroperforation”—a highly effective nonthermal sterilization method.

In theory, electrical stimulation provides a much-needed workaround to the inconvenient fact that fungi are so much like us. But that’s not the only reason it’s promising—not only might it hurt them without hurting us, but the process might also even boost our health. Many trials suggest electrical stimulation can, with the right parameters, accelerate healing in human wounds, further amplifying the effectiveness of an antifungal zap.

Anyway, watch this space. Electrical medicine may yet help us stave off the fungal apocalypse!