Health

Study probes 'new normal' for older adults post-COVID

Megan M Rogers — Wed, 18 Mar 2026 18:49:55 +0000

Study probes 'new normal' for older adults post-COVID Megan M Rogers Wed, 03/18/2026 - 12:49

Colorado Arts and Sciences Magazine

Researchers from CU ��ý�� have found that the pandemic reshaped how people age 55 and older interact with their communities while highlighting the importance of "social infrastructure."

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CU researchers study potential links between hearing loss and dementia

Megan M Rogers — Tue, 17 Mar 2026 16:45:55 +0000

CU researchers study potential links between hearing loss and dementia Megan M Rogers Tue, 03/17/2026 - 10:45

Coloradan , Lisa Marshall

A CU ��ý�� lab is exploring how age-related hearing loss rewires the brain—and whether hearing aids can undo the damage.

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Could 3D-printed livers make transplant lists a thing of the past?

Lisa Marshall — Tue, 17 Mar 2026 16:19:38 +0000

Could 3D-printed livers make transplant lists a thing of the past? Lisa Marshall Tue, 03/17/2026 - 10:19

Lisa Marshall

Jonathan Makhoul, a research assistant in the Burdick lab, holds a gel infused with human liver cells and printed with blood-vessel-like channels. Patrick Campbell/CU ��ý��

It weighs 3 to 4 pounds, includes seven different cell types and features an intricate web of blood vessels that help it filter toxins, guard against pathogens, metabolize nutrients and carry out hundreds of other biological functions.

The human liver, experts say, is an architectural wonder. But its complexity has also made it immensely difficult to replicate in the lab.

Now, a multi-institution team, including scientists at the ��ý��, MIT, Harvard and Columbia universities, is taking on the challenge. Supported by a new five-year, up to $25 million award from the Advanced Research Projects Agency for Health (ARPA-H) Personalized Regenerative Immunocompetent Nanotechnology Tissue (PRINT) program, they’re working to develop 3D-printed liver tissue made of human cells and able to be transplanted into anyone without their body rejecting it.

An AI generated illustration of a liver. Adobe Stock photo

“There are many patients out there that either never get a transplant or are stuck on the waiting list for years,” said Jason Burdick, a professor of chemical and biological engineering whose lab at CU’s BioFrontiers Institute will lead the 3D printing part of the project.

“If there were an off-the-shelf alternative, once a patient needs a liver they could get a transplant almost immediately,” he said. “That’s our goal.”

Organs on demand

About 4.5 million U.S. adults have been diagnosed with liver disease, and about 52,000 die annually of liver failure. At any given time, roughly 15,000 people in the U.S. are on the transplant list, with waits ranging from 30 days to more than five years.

Patients who do get a transplant from a cadaver or living donor must take drugs to keep their immune system from rejecting it. Those medications come with their own health challenges, and sometimes the body rejects their new liver anyway.

Above, research associate Matt Davidson looks at a liver organoid under the microscope. Below, Left to Right: Makhoul, research associate Megan Cooke, Professor Jason Burdick and Davidson in the lab.

In 2024, ARPA-H launched the Personalized Regenerative Immunocompetent Nanotechnology Tissue (PRINT) program, an ambitious, fast-track endeavor driven by a single question: “What if we could bioprint any organ on demand?” The PRINT program is led by ARPA-H Program Manager Ryan Spitler, Ph.D.

In January, the agency announced the ImPLANT project team (short for Immunoshielded Printed Liver Assist NeoOrgan for Transplant). Led by Harvard University’s Wyss Institute, the project brings together a dream team of the world’s leading experts in synthetic biology, transplant immunology, vascular engineering and 3D bioprinting to develop life-like replacements for the body’s largest organ.

“We all recognize the moonshot nature of the program and are thankful that ARPA-H is making it possible,” said Chris Chen, M.D., PhD, the ImPLANT project’s principal investigator (PI) at the Wyss Institute.

How to make an organ

Standing at a microscope in the Burdick Biomaterials and Biofabrication lab, research associate Matt Davidson zooms in on a tray of spherical cell clusters known as ‘liver organoids.’

In the room next door, research assistant Jonathan Makhoul switches on a glistening white 3D printer which uses a sharp tool, akin to a sewing machine needle, to print delicate channels deep within a vat of gelatin-like liquid known as a hydrogel.

While these are early days, the effort to manufacture a liver is well underway.

The process goes like this:

Through a technique pioneered at MIT, induced pluripotent stem cells — adult skin or blood cells that have been modified to have the capacity to become any kind of cell— are programmed to become all the different types of liver cells. (Soon, researchers hope to be able to genetically engineer those cells to also evade immune rejection by patients, making them universally compatible.)

Burdick’s team takes clusters of those cells, or liver organoids, and amasses them into larger, tissue-like structures. Then they deploy a novel 3D-printing technique called ‘suspension printing’, pioneered in his lab.

“Rather than building up a three-dimensional structure layer by layer, like most 3D printers do, we can now take a bath of material— in this case organoids suspended within a hydrogel — and print an ink directly into that three-dimensional volume,” said Burdick.

Once the ‘ink’ is washed away and cells migrate to those channel walls, it leaves intricate webs of blood vessels behind.

Producing liver tissue at scale

Ultimately, when a patient needs a new liver, that tissue could then be implanted and sutured in place, its vessels lining up with those connecting it to the rest of the body.

Much like patients seeking a knee replacement today, those seeking a new liver could basically order the part off the shelf.

Of the up to $25 million allocated to the team, about $3.5 million will go to CU ��ý��.

Within a few years, the team hopes to be embarking on animal studies.

Meanwhile, collaborators at Columbia will be developing new bioreactor technologies and manufacturing processes to produce liver cells, organoids and tissues at scale.

If all goes according to plan, clinical trials could be underway within five to 10 years, said Burdick.

“We are all experts in our own fields with many years of research behind us,” said Burdick. “Now that we can combine all of our expertise with enough funding and support to really push the program forward, I’m confident that we can develop new therapies based on 3D printed livers to truly help patients.”

"Research reported in this publication was supported by the Advanced Research Projects Agency for Health (ARPA-H) under Award Number D25AC00322-00. The content is solely the responsibility of the authors and does not necessarily represent the official views of the Advanced Research Projects Agency for Health."

Supported by an up to $25 million federal award, a dream team of experts is working to develop the world’s first off-the-shelf engineered liver tissue.

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Why do we get a skip in our step when we're happy? Thank dopamine

Daniel William Strain — Fri, 27 Feb 2026 19:01:00 +0000

Why do we get a skip in our step when we're happy? Thank dopamine Daniel William… Fri, 02/27/2026 - 12:01

Daniel Strain

Subject "reaches" for a target on a computer screen, while Alaa Ahmed and Colin Korbisch follow the data. (Credit: Jesse Morgan Petersen/CU ��ý�� College of Engineering and Applied Science)

New research by engineers at CU ��ý�� aims to get to the bottom of why, as the saying goes, you get a “skip in your step” when you’re happy.

The study highlights the central role that dopamine, a brain chemical associated with reward, seems to play in making people move faster when they want something. The findings could one day help scientists understand and even diagnose a range of human medical conditions, including Parkinson’s disease and depression.

“Anecdotally, we just feel that this is true,” said senior author Alaa Ahmed, professor in the Paul M. Rady Department of Mechanical Engineering at CU ��ý��. “When you go to the airport to pick up your parents, you may run to greet them. But if you’re picking up a colleague, you’re probably just going to walk.”

In the new study, she and Colin Korbisch, a former graduate student at CU ��ý��, set out to unravel the pathways in the brain that control those sorts of behaviors.

The researchers designed a simple experiment: They asked human subjects to “reach” for a target on a computer screen using a joystick-like device. Those targets dealt out rewards—in this case, a simple flash of light and a beeping sound.

The team discovered that how those rewards exceeded, or failed to meet, expectations changed how the subjects moved, in some cases giving them a little more oomph as they reached.

Colin Korbisch and Alaa Ahmed in the lab. (Credit: Jesse Morgan Petersen/CU ��ý�� College of Engineering and Applied Science)

A subject completes a reaching task in Ahmed's lab. (Credit: Jesse Morgan Petersen/CU ��ý�� College of Engineering and Applied Science)

Those patterns aligned closely with what scientists know about the behavior of dopaminergic neurons—cells in the brain that release dopamine and shape a huge range of human behavior.

The researchers published their findings Feb. 27 in the journal Science Advances.

“Movements are a window to the mind,” Korbisch said. “Normally, you can’t go into the brain and see what the dopaminergic neurons are doing, but movement could reflect those neural computations that are so difficult to disentangle.”

Juice time

Scientists have known for decades that dopamine plays a critical role in helping animals learn.

In the 1990s, for example, neuroscientist Wolfram Schultz conducted seminal studies on dopaminergic activity in primates.

He and his colleagues trained monkeys to expect a reward—maybe a drop of apple juice—when they heard a bell ring. Those same monkeys began to experience a spike in dopamine every time the heard the bell, even before they got their juice.

But when the monkeys heard the bell and didn’t receive any juice, the disappointment also registered in the brain: The animals still experienced an initial spike in dopamine, but that activity dipped when they failed to receive their reward.

Scientists call this pattern a “reward prediction error.” In a sense, the brain is teaching itself which options are worth pursuing, and which can be ignored.

In the current study, Ahmed and Korbisch wanted to see whether those same patterns might affect how we move.

Reach for it

The team had good reason to think they might. Ahmed explained that people with Parkinson’s disease lose many of the dopaminergic neurons in their brains. They also have a lot of trouble moving.

To explore the link between dopamine and movement, the researchers asked human subjects to use the joystick to make a series of reaches toward one of four targets at each corner of a screen. One target gave a reward every time the subjects hit it, while another target never gave rewards. The other two fell in between.

As the team expected, the subjects tended to reach a little faster toward the targets that were more likely to offer a reward.

But the group also discovered something intriguing: If the subjects reached for a target that was unlikely to give a reward, and they unexpectedly got one, their reaching motion suddenly sped up—even after they had already gotten the reward.

This increase in vigor occurred just 220 milliseconds after the subjects heard the beep. The effect was subtle and not something you could spot with the naked eye. But the findings indicate that a pleasant surprise may give people a little extra pep.

The researchers can’t show definitively what is behind that burst of energy. But Ahmed and Korbisch suspect that their subjects were receiving a second jolt of dopamine from the unexpected treat.

When the subjects were certain they were going to get a reward, in contrast, they didn’t seem to get a second surge in dopamine after the beep.

"Importantly, this effect wasn't tied to reward reception alone," Korbisch said. "If the outcome was certain and known to the individual, we saw no further increase in vigor."

Past experience mattered, too. If patients got a string of rewards in a row, they started moving faster overall. If they got nothing but bad luck, they slowed down.

Ahmed noted that many medical conditions affect how people move. People with depression, for example, tend to move more slowly than others. She envisions that, one day, medical professionals could use these sorts of trends to help their patients—following how people move across months or years to track their health.

“If you’ve had a good day, you’ll go faster. If you’ve had a bad day, you’ll move slower,” Ahmed said. “It’s basically that skip in your step.”

Humans tend to move faster when they think they're going to get a reward. A new experiment explores the pathways in the brain that may be behind these patterns.

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Startup brings cancer care technology to Lab Venture Challenge

Megan M Rogers — Thu, 26 Feb 2026 21:54:01 +0000

Startup brings cancer care technology to Lab Venture Challenge Megan M Rogers Thu, 02/26/2026 - 14:54

Doctoral student William Frantz is developing microscopic droplets designed to help doctors track radiation therapy in real time. His pitch at the Lab Venture Challenge highlighted how the technology could make cancer treatment more precise and less harmful, particularly for pediatric patients.

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Karolin Luger wins Vilcek Prize in Biomedical Science

Megan M Rogers — Thu, 05 Feb 2026 16:53:42 +0000

Karolin Luger wins Vilcek Prize in Biomedical Science Megan M Rogers Thu, 02/05/2026 - 09:53

Colorado Arts and Sciences Magazine

The CU ��ý�� biochemist has been awarded for her career dedication to the study of nucleosomes and groundbreaking discoveries.

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The other 'Alzheimer's protein': The quest to prevent toxic tau buildup in the brain

Lisa Marshall — Tue, 03 Feb 2026 22:00:04 +0000

The other 'Alzheimer's protein': The quest to prevent toxic tau buildup in the brain Lisa Marshall Tue, 02/03/2026 - 15:00

Lisa Marshall

In the quest to cure Alzheimer’s, the protein known as beta-amyloid has long taken center stage, driving development of a long list of drugs aimed at breaking up “amyloid plaques” in the brain.

But mounting research shows a lesser-known protein called tau, which forms toxic hairball-like tangles inside neurons, plays an equally vital role in fueling this and other neurodegenerative diseases.

New CU ��ý�� research published in the journal PNAS offers fresh insight into how tau tangles form and spread. In a companion paper, published in the journal Neuron, the researchers propose a new strategy for preventing this process and show the approach can halt or reverse neurodegeneration in mice.

The findings could ultimately pave the way toward a "neuronal vaccine" that stops neurodegeneration before it can spread.

“If we really want to treat Alzheimer’s and many of these other diseases, we have to block tau as early as possible,” said senior author Roy Parker, distinguished professor of biochemistry and director of the BioFrontiers Institute. “These studies are an important step forward in understanding why tau aggregates in cells and how we can intervene.”

A good protein gone bad

First discovered 50 years ago, tau helps brain cells keep their shape and shuttles important molecules around within them. When it malfunctions, tau can turn toxic and spread through the brain killing neurons.

This process underlies more than two dozen neurodegenerative diseases called ‘tauopathies.’ In Alzheimer’s, which affects 7 million people in the U.S., amyloid beta forms plaques that kick-start the spread of tau tangles.

“By the time you treat an Alzheimer’s patient, even if you can completely get rid of amyloid plaque in the brain, it’s often too late because tau has already done its damage and is continuing to spread,” said Parker.

Other "tauopathies" include chronic traumatic encephalopathy (CTE), often found among football players with head trauma; and some forms of frontotemporal dementia, a cruel and fast-moving disease that causes personality changes and memory loss in adults as young as 40.

Roy Parker, director of the BioFrontiers Institute at CU ��ý��.

About one in 1,000 children who get measles will acquire a fatal tauopathy called subacute sclerosing panencephalitis (SSPE) six to 10 years after infection, noted Parker.

“That’s the one that scares me the most, as so many people think measles is not a big deal,” Parker said.

To date, there are no FDA approved drugs to target tau. But Parker’s lab and others are making progress toward that goal.

A 'vaccine' for brain cells

Previous studies looking at postmortem brain tissue of Alzheimer’s patients have found that tau aggregates include unusual proteins containing disordered chains of an amino acid called serine.

This led Parker’s team to wonder whether these “polyserines” somehow drive tau to, essentially, turn bad.

Through a series of experiments described in the PNAS paper, he and his students found that when polyserine makes its way to a budding seed of tau inside a brain cell, it can prompt tau to misfold, clump and spread toxic aggregates to other neurons like a virus.

They also found that when mice with a predisposition to tauopathies have more polyserine on board, they get sicker faster.

“In experiments in human neurons in the test tube, fruit flies, animals and human tissue, we have now shown that overexpression of polyserine increases tau aggregation,” said Parker. “The question now is: How do you target this process to prevent or treat disease?”

In one clever strategy, described in the Neuron paper, they turned polyserine—which naturally gravitates toward tau aggregates—into a sort of Trojan horse.

They administered polyserine, attached to a different protein expressly engineered to bust up tau tangles, to mice. They found that this led to a striking decrease of tau aggregates in the brain, diminished production of new seeds of toxic tau and decreased anxiety and memory deficits in the animals.

“Essentially, if we use this strategy in a mouse that is prone to tau aggregation, it either doesn’t get disease or it slows it way down,” said Parker.

In future work, his lab hopes to get a better sense of why polyserine forms in the first place and what else goes wrong inside cells to turn typically beneficial tau into a lethal threat to neurons.

He imagines a day when his lab’s research can inform development of a preventative treatment, given to people predisposed to tauopathies far earlier in the disease process.

“The holy grail here would be a safe, cheap therapy that is well-tolerated and can be given to people who need it before they have a lot of symptoms,” he said. “Understanding how the cellular environment influences this process, and how to interfere with it, is a huge part of getting there.”

Toxic protein clusters known as tau aggregates underlie dozens of neurodegenerative diseases, or "tauopathies." New research illuminates why they form and spread and how to stop them.

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Tau protein clusters known as tau aggregates underlie dozens of neurodegenerative diseases known as "tauopathies."

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Toxic clusters of the protein tau underlie dozens of neurodegenerative diseases known as 'tauopathies.'

Creating pathways to accessible heart health

Emma Holst — Tue, 03 Feb 2026 17:33:00 +0000

Creating pathways to accessible heart health Emma Holst Tue, 02/03/2026 - 10:33

Emma Holst

February is American Heart Month, a time when people are encouraged to focus on their cardiovascular health.

According to the World Health Organization (WHO), cardiovascular diseases (CVDs) are the leading cause of death globally. Risk factors for poor cardiovascular health include tobacco use, an unhealthy diet, physical inactivity and physiological factors like high blood pressure.

Researchers Sanna Darvish (left) and Sophia Mahoney (right)

At CU ��ý��’s Integrative Physiology of Aging Laboratory led by Doug Seals and Matt Rossman, researchers are studying cardiovascular aging.

Sanna Darvish, a doctoral student of integrative physiology, is working toward reducing CVD risk in underrepresented and ethnic populations. “We hope that by studying vascular dysfunction in vulnerable, underrepresented groups, we can better understand the mechanisms contributing to their exacerbated CVD and identify effective interventions,” explained Darvish.

In a study published in 2024, Darvish and integrative physiology doctoral graduate Sophia Mahoney explored the intersection of ethnicity and race, socioeconomic factors and cardiovascular health.

“I think the public knows men have a high risk of heart attacks, but this is mostly because women and other groups have been historically understudied in biomedical research,” said Darvish. “Most people don’t realize that CVD risk is actually higher in older women compared with older men, and this is exacerbated in Black and Indigenous women.”

One tactic to help combat CVD risk is to stay informed. A conversation with Darvish explored what interventions her research has identified to improve heart health and what steps the laboratory has taken to address accessibility challenges for those from underrepresented groups.

What interventions have you found effective in improving heart health among different populations?

Aerobic exercise is the standard-of-care clinical strategy for reducing CVD in older adults across all racial and ethnic groups. This is emphasized by organizations such as the American Heart Association that recommend 150 minutes of moderate intensity aerobic exercise or 75 minutes of vigorous aerobic exercise per week, plus at least two strength training sessions.

These exercises might include hiking, swimming or yoga. If integrating a workout into your week presents a challenge, remember that some daily activities are also considered forms of exercise. These might include mowing the lawn and gardening, shoveling snow or walking to the store and carrying groceries.

Could you share any trends or patterns you’ve observed regarding exercise and heart health in specific communities?

Most studies have been conducted in largely non-Hispanic white populations. There are a few studies, as outlined in our review paper, that have found that aerobic exercise training improves vascular function among Black Americans, Hispanics, Indigenous Americans, Southeast Asians and Native Hawaiians.

It is important to note that there are many barriers to performing aerobic exercise training, especially in underrepresented groups, including cost, time, limited resources and a lack of motivation and health literacy. These barriers provide justification to identify potential alternative interventions that also improve vascular function but overcome these barriers. Our laboratory is currently studying a few lifestyle and supplement-based interventions that are proving to be effective at improving vascular function in older adults.

What heart health statistics have you found most significant in your work?

Importantly, around age 55–60, women supersede men with higher CVD risk. Accumulating evidence demonstrates this is largely due to menopause and the diminished estrogen production that follows reproductive aging.

I think that increasing education and overall health literacy in the general public about the risks of CVD in women and underrepresented communities is important because many people don’t realize that certain factors, such as menopause or race or ethnicity, do substantially increase the risk for many chronic diseases.

We don’t fully understand the mechanisms of increased CVD risk in these groups. It is our job as researchers to identify those risks and mechanisms so physicians and public health officials can better help their patients live healthier lives.

What challenges have you faced in studying the intersection of socioeconomic factors and cardiovascular health?

Studying underrepresented groups is quite challenging in ��ý�� because we have a relatively homogenous community in terms of race, socioeconomic profile, education status, etc. This makes it difficult to study people who are representative of the U.S. demographic. However, neighboring cities and counties do have more diverse populations, so we do recruit a decent number of people from outside ��ý�� to participate in our clinical trials.

Could you share any steps that CU ��ý�� or your lab has taken to address these challenges?

Recently, our laboratory has emphasized pouring more resources into strategies that may help participation in research be more accessible for individuals of underrepresented groups.

To better accomplish these goals, we have done some reflection as a laboratory and identified specific internal and external methods to improve diversity in our clinical trials. A majority of our lab has completed a training focused on creating inclusive research environments for participants and colleagues, and all lab members complete a mandatory implicit bias training when they join the lab. A large focus of our discussions is dismantling biases we have against the aging community, which is even more discriminatory against aging people of color.

In terms of making our clinical trials more directly accessible, we compensate participants for their time and travel, offer free transportation assistance for those who lack safe and reliable transport, and we offer meal vouchers for participants. We think these steps can be easily adopted by other research groups on campus who are seeking to diversify their clinical research participant cohorts.

Sanna Darvish discusses the interventions her research has identified to improve heart health and the steps the Integrative Physiology of Aging Laboratory has taken to address accessibility challenges for people in underrepresented groups.

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What causes chronic pain? A new study identifies a key culprit

Lisa Marshall — Tue, 27 Jan 2026 23:49:09 +0000

What causes chronic pain? A new study identifies a key culprit Lisa Marshall Tue, 01/27/2026 - 16:49

Lisa Marshall

A neural circuit hidden in an understudied region of the brain plays a critical role in turning temporary pain into pain that can last months or years, according to new ��ý�� research.

The animal study, published in the Journal of Neuroscience, found that silencing this pathway, known as the caudal granular insular cortex (CGIC), can prevent or halt chronic pain.

“Our paper used a variety of state-of-the art methods to define the specific brain circuit crucial for deciding for pain to become chronic and telling the spinal cord to carry out this instruction,” said senior author Linda Watkins, distinguished professor of behavioral neuroscience in the College of Arts and Sciences. “If this crucial decision maker is silenced, chronic pain does not occur. If it is already ongoing, chronic pain melts away.”

The study comes amid what first author Jayson Ball calls a “gold rush of neuroscience.”

With new tools enabling them to genetically manipulate precise populations of brain cells, neuroscientists are now able to identify, with unprecedented granularity, potential targets for new therapies. Such therapies, including infusions or brain-machine interfaces, could someday provide safer and more effective alternatives to opioids.

“This study adds an important leaf to the tree of knowledge about chronic pain,” said Ball, who earned his doctorate in Watkins’ lab in May and now works for Neuralink, a California-based startup that develops brain-machine interfaces for human health.

When touch hurts

About one in four adults have chronic pain, according to the Centers for Disease Control, and nearly one in 10 people say chronic pain interferes with their daily life and work.

Those with nerve-related pain often suffer from a condition called allodynia, an extreme sensitivity in which even light touch hurts.

Acute and chronic pain work differently. Acute pain serves as a temporary warning sign, initiated when an injured tissue—like a stubbed toe—sends a signal to the spinal cord and onward to the brain’s pain center. Chronic pain is more like a false alarm, in which pain signals persist in the brain for weeks, months or years after the initial tissue injury has healed.

“Why, and how, pain fails to resolve, leaving you in chronic pain, is a major question that is still in search of answers,” said Watkins.

In 2011, Watkins’ lab published a study suggesting that the CGIC—a sugar-cube-sized cluster of cells hidden deep within the folds of a portion of the human brain called the insula—plays an important role in allodynia. Human studies have also shown that chronic pain patients have an over-active CGIC.

But for a long time, the only way to manipulate the CGIC was to remove it—an impractical approach for human treatments.

For the new study, the team used novel fluorescent proteins to observe which cells in the central nervous system light up when a rat sustains a sciatic nerve injury. The team then used cutting-edge “chemogenetic” tools to switch on or off genes inside specific populations of neurons.

The researchers discovered that while the CGIC plays a minimal role in processing acute pain, it plays a vital role in making pain persist.

According to the study, the CGIC signals the brain’s pain processing center, or somatosensory cortex, which in turn tells the spinal cord to keep the pain going.

“We found that activating this pathway excites the part of the spinal cord that relays touch and pain to the brain, causing touch to now be perceived as pain, as well,” said Ball.

Disabling the chronic pain circuit

When the team turned off cells within this pathway immediately after injury, the rat’s pain from injury was short-lived. In animals already experiencing chronic allodynia, disabling this pathway made the pain cease.

“Our research presents a clear case that specific brain pathways can be directly targeted to modulate sensory pain,” said Ball.

It’s still unclear what prompts the CGIC to start sending chronic pain signals. And more research is necessary before these lessons learned could be applied to help humans.

But Ball imagines a not-too-distant future in which medical professionals treat pain with injections or infusions that target specific brain cells without the systemic side effects and dependency risk that come with opioids. He also believes brain-machine interfaces, either implanted in or attached to the skull, could play a similar role in treating severe chronic pain. Numerous startups are now rushing to get to market first, he said.

“Now that we have access to tools that allow you to manipulate the brain, not based just on a general region but on specific sub-populations of cells, the quest for new treatments is moving much faster,” he said. “I’m betting my career that in the near future we are going to see amazing medical uses for these technologies.”

New research shows that a little-known brain pathway plays a critical role in making pain last after tissue heals. The findings could help pave the way for new brain-machine interfaces and medications that ease suffering without the use of opioids.

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CU ��ý�� joins Medtronic in strategic partnership to drive breakthrough health innovations

Megan M Rogers — Thu, 22 Jan 2026 21:06:29 +0000

CU ��ý�� joins Medtronic in strategic partnership to drive breakthrough health innovations Megan M Rogers Thu, 01/22/2026 - 14:06

The University of Colorado (CU) and Medtronic, a global leader in health care technology, have entered into a strategic research agreement to accelerate the development of transformative health technologies. CU was selected from a nationwide search for its strength in advancing disruptive innovation.

“This is an incredible collaboration across the breakthrough innovation ecosystem at CU ��ý��, clinical excellence at CU Anschutz, and enhancements in patient care delivered by Medtronic,” said Bryn Rees, associate vice chancellor for innovation and partnerships at CU ��ý��. “We are excited to contribute to improving health care through this university-industry alliance."

The long-term partnership will focus on artificial intelligence, robotics and sustainability, aiming to move technologies from lab to bedside faster and deliver real benefits to patients worldwide. The collaboration spans CU ��ý��, CU Anschutz and CU Denver, leveraging each campus’s unique expertise.

“Together, we will explore new frontiers critical to the future of health care,” said Jim Peichel, chief technology officer at Medtronic.

The alliance launched at a summit on the CU Anschutz campus, where priority research projects were identified. CU Anschutz brings deep clinical research capabilities, while CU ��ý�� contributes cutting-edge innovation and entrepreneurial strength.

Learn more about CU ��ý��’s innovation initiatives.

CU ��ý�� and two other CU campuses have been chosen from a nationwide search to partner with Medtronic—a global leader in health care technology—in a strategic research agreement aimed at accelerating transformative health innovations.

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Health

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