3 hours agoKelly Morgan

People who eat more ultra-processed foods like soft drinks, chips and cookies may have a higher risk of having memory and thinking problems and having a stroke than those who eat fewer processed foods, according to a new study published in the May 22, 2024, online issue of Neurology®, the medical journal of the American Academy of Neurology. The study does not prove that eating ultra-processed foods causes memory and thinking problems and stroke. It only shows an association.
Ultra-processed foods are high in added sugar, fat and salt, and low in protein and fiber. They include soft drinks, salty and sugary snacks, ice cream, hamburger, canned baked beans, ketchup, mayonnaise, packaged breads and flavored cereals. Unprocessed or minimally processed foods include meats such as simple cuts of beef, pork and chicken, and vegetables and fruits.
“While a healthy diet is important in maintaining brain health among older adults, the most important dietary choices for your brain remain unclear,” said study author W. Taylor Kimberly, MD, PhD, of Massachusetts General Hospital in Boston. “We found that increased consumption of ultra-processed foods was associated with a higher risk of both stroke and cognitive impairment, and the association between ultra-processed foods and stroke was greater among Black participants.”
For the study, researchers looked at 30,239 people age 45 or older who self-identified as Black or white. They were followed an average of eleven years.
Participants filled out questionnaires about what they ate and drank. Researchers determined how much ultra-processed food people ate by calculating the grams per day and comparing it to the grams per day of other foods to create a percentage of their daily diet. That percentage was calculated into four groups, ranging from the least processed foods to the most processed foods.
Of the total participants, researchers looked at 14,175 participants for cognitive decline and 20,243 participants for stroke. Both groups had no history of cognitive impairment or stroke.
By the end of the study, 768 people were diagnosed with cognitive impairment and 1,108 people had a stroke.

For those in the cognitive group, people who developed memory and thinking problems consumed 25.8% of their diet in ultra-processed foods, compared to 24.6% for those who did not develop cognitive problems.
After adjusting for age, sex, high blood pressure and other factors that could affect risk of dementia, researchers found that a 10% increase in the amount of ultra-processed foods eaten was associated with a 16% higher risk of cognitive impairment.
They also found that eating more unprocessed or minimally processed foods was linked with a 12% lower risk of cognitive impairment.
For those in the stroke group, people who had a stroke during the study consumed 25.4% of their diet in ultra-processed foods, compared to 25.1% for those who did not have a stroke.
After adjustments, researchers found greater intake of ultra-processed foods was linked to an 8% increase in risk of stroke, while greater intake of unprocessed or minimally processed foods was linked to a 9% decreased risk of stroke.
The effect of ultra-processed food consumption on stroke risk was greater among Black participants, with a 15% relative increase in risk of stroke.
“Our findings show that the degree of food processing plays an important role in overall brain health,” Kimberly said. “More research is needed to confirm these results and to better understand which food or processing components contribute most to these effects.”
A limitation of the study was that only participants who self-identified as Black or white were included in the study, so results may not be generalizable to people from other populations.
The study was funded by the National Institute of Neurological Disorders and Stroke, the National Institute on Aging, National Institutes of Health and Department of Health and Human Services.

Eosinophils are specialized cells of our immune system. They are identified by their distinctive granules that stain red when treated with an acidic reagent, eosin, which gave them their name. Eosinophils are typically rare in our blood and tissues, accounting for about 3% of our white blood cells. Their biological roles are poorly understood, but recent studies suggest that eosinophils are involved in regulating our fat metabolism, repairing certain tissues, and helping us fight different infections and cancers.
Despite their potential beneficial actions, eosinophils generally have a bad reputation among doctors. In common diseases such as allergic asthma and rhinosinusitis, eosinophils are abnormally numerous in the blood and tissues, a condition known as eosinophilia. Eosinophilia is a clinical sign that aids in diagnosing these “eosinophil-associated” diseases and guides their treatment. It is known that eosinophilia is driven by increased production of eosinophils by the bone marrow. Since the 1990s, it has also been known that a specific signalling protein, the cytokine Interleukin-5 (IL-5), is essential for eosinophilia. This led to the development and market introduction of precision therapies targeting IL-5 with monoclonal antibodies to treat severe forms of eosinophilic diseases. However, the effects of IL-5-blocking treatments on eosinophils remain poorly described.
The Laboratory of Cellular and Molecular Immunology (LCMI) of the University of Liege, under the direction of Fabrice Bureau and Christophe Desmet, aimed to better understand the origin of eosinophils and eosinophilia, and the effects of treatments targeting eosinophils. As Christophe Desmet explains, “these questions previously suffered from a too rudimentary definition of the eosinophil development pathway in our bone marrow.” Two doctoral students from the laboratory, Joseph Jorssen and Glenn Van Hulst, combined their talents in bioinformatics and flow cytometry with the help of the Genomics and Flow Cytometry platforms of the GIGA Institute to finely characterize, using different approaches to analyse the surface protein and messenger RNA composition of eosinophils at various stages of their development. Although the mouse remains a reference model, collaboration with the Hematology Department of Liege University Hospital and GIGA also allowed for a very detailed and updated mapping of eosinophil development in human bone marrow, and to observe its conservation through evolution.
This detailed characterization work provides the community with simple-to-use methods and freely accessible bioinformatics data that will greatly facilitate future studies of eosinophils. Using these resources, the same study showed that IL-5 does not act as previously believed by researchers and clinicians. Most thought that IL-5 promoted the maturation of cells destined to become eosinophils and that IL-5-targeting treatments blocked this maturation. “Our study actually supports the opposite hypothesis,” explains Christophe Desmet: IL-5 slows down the maturation of developing eosinophils, allowing them to multiply longer. By stimulating this “transit amplification,” IL-5 promotes eosinophilia, and by inhibiting this process, IL-5-targeting treatments reduce it.
This study thus provides resources, methods, and perspectives to understand the origin of eosinophils, the effects of current precision therapies, and the regulation of eosinophil development and numbers in normal and disease conditions.

Engineers at the University of California San Diego have developed a wearable ultrasound patch that can offer continuous, non-invasive monitoring of blood flow in the brain. The soft and stretchy patch can be comfortably worn on the temple to provide three-dimensional data on cerebral blood flow — a first in wearable technology.
A team of researchers led by Sheng Xu, a professor in the Aiiso Yufeng Li Family Department of Chemical and Nano Engineering at the UC San Diego Jacobs School of Engineering, published their new technology on May 22 in Nature.
The wearable ultrasound patch marks a significant leap from the current clinical standard, called transcranial Doppler ultrasound. This method requires a trained technician to hold an ultrasound probe against a patient’s head. The process has its downsides, however. It is operator-dependent, so the accuracy of the measurement can vary based on the operator’s skill. It is also impractical for long-term use.
Xu’s team developed a device that overcomes these hurdles. Their wearable ultrasound patch offers a hands-free, consistent and comfortable solution that can be worn continuously during a patient’s hospital stay.
“The continuous monitoring capability of the patch addresses a critical gap in current clinical practices,” said study co-first author Sai Zhou, a materials science and engineering Ph.D. candidate in Xu’s lab. “Typically, cerebral blood flow is monitored at specific times each day, and those measurements do not necessarily reflect what may happen during the rest of the day. There can be undetected fluctuations between measurements. If a patient is about to experience an onset of stroke in the middle of the night, this device could offer information that is crucial for timely intervention.”
Patients who are undergoing and recovering from brain surgery can also benefit from this technology, noted Geonho Park, another co-first author of this study who is a chemical and nano engineering Ph.D. student in Xu’s lab.
The patch, roughly the size of a postage stamp, is constructed from a silicone elastomer embedded with several layers of stretchy electronics. One layer consists of an array of small piezoelectric transducers, which produce ultrasound waves when electrically stimulated and receive ultrasound waves reflected from the brain. Another key component is a copper mesh layer — made of spring-shaped wires — that enhances signal quality by minimizing interference from the wearer’s body and environment. The rest of the layers consist of stretchable electrodes.

During use, the patch is connected through cables to a power source and computer. To achieve 3D monitoring, the researchers integrated ultrafast ultrasound imaging into the system. Unlike standard ultrasound, which captures about 30 images per second, ultrafast imaging captures thousands of images per second. This high frame rate is necessary for collecting robust data from the piezoelectric transducers in the patch, which would otherwise suffer from low signal intensity due to the strong reflection of the skull.
The data are then post-processed using custom algorithms to reconstruct 3D information such as the size, angle and position of the brain’s major arteries.
“The cerebral vasculature is a complex structure with multiple branching vessels. You need a device capable of capturing this three-dimensional information to get the whole picture and obtain more accurate measurements,” said Xinyi Yang, another co-first author of this study and materials science and engineering Ph.D. student in Xu’s lab.
In this study, the patch was tested on 36 healthy volunteers for its ability to measure blood flow velocities — peak systolic, mean flow and end diastolic velocities — in the brain’s major arteries. Participants engaged in activities affecting blood flow, such as hand-gripping, breath-holding and reading. The patch’s measurements closely matched those obtained with a conventional ultrasound probe.
Next, the researchers plan to collaborate with clinicians at UC San Diego School of Medicine to test the patch on patients with neurological conditions that impact cerebral blood flow. Xu has co-founded a startup company called Softsonics to commercialize this technology.
This work was supported by the National Institutes of Health (1R21EB025521-01, 1R21EB027303-01A1, 3R21EB027303-02S1, 1R01EB033464-01, 1R01HL171652-01).

According to the US Centers for Disease Control and Prevention, at least 5.8 million Americans are currently living with Alzheimer’s disease, which is the most common form of dementia. There is no cure for Alzheimer’s, in part because scientists do not yet have a full understanding of what causes the disease. But a new study from Scripps Research is shedding light on the molecular drivers that could contribute to Alzheimer’s progression.
In the study, published in Advanced Scienceon May 21, 2024, the researchers used a new technique for studying single, living brain cells affected by Alzheimer’s disease. By measuring the electrical activity of single neurons and the protein levels within those neurons, the scientists discovered new molecules linked to Alzheimer’s. The hope is these molecules could be targeted by drugs to treat or slow the progression of the neurodegenerative disease in the future.
Close collaboration among Scripps Research’s professors, including clinical neurologist Stuart Lipton, MD, PhD, protein expert John Yates, III, PhD, and bioinformaticist Nicholas Schork, PhD, (who is also the deputy director and distinguished professor of quantitative medicine at The Translational Genomics Research Institute, or TGen) enabled the scientists to develop this biotechnology feat.
“It was mind-boggling to me that we could take one cell, measure its electrical activity on the order of one-millionth of one-millionth of an ampere, and then look at thousands of proteins within that same cell to allow us to find the proteins that drive Alzheimer’s-related abnormal electrical activity,” says senior author Lipton, who is also the Step Family Foundation Endowed Professor and co-director of the Neurodegeneration New Medicines Center at Scripps Research. “But the beauty of this method is that it lets us uncover novel targets for Alzheimer’s disease and related dementias.”
Previous research by Lipton and others has shown that certain neurons become overactive in the brains of people with Alzheimer’s, sending electrical signals that are stronger or more frequent than usual. Evidence suggests that this overactivity (also known as hyperexcitability) contributes to the cognitive decline associated with Alzheimer’s.
In the new work, Lipton and colleagues developed a system in which scientists can take precise measurements of individual brain cells and then compare those affected by Alzheimer’s with healthy cells. Lipton’s group, who has previously developed methods for precisely measuring the electrical activity of neurons, teamed up with Yates to use mass spectrometry to identify levels of over 2,250 proteins in each nerve cell. Mass spectrometry can identify and quantify proteins from cells, but these analyses have traditionally been done on bulk collections of cells. Recent advances are permitting measurements at the single-cell level.
In the new system, known as single cell (sc)Patch-Clamp/Proteomics, a tiny glass tube filled with a salt solution is used as an electrode to measure the electrical activity of a cell, and then extract the cell for protein studies with mass spectrometry.

“This approach allows us to connect perturbations of electrical functions to molecular events in neurons, which is an exciting application of proteomics,” says Yates.
The scientists analyzed the electrical patterns and protein levels of about 150 neurons and then used computational tools — applied by Schork — to find associations between hyperexcitability and abnormal protein levels. They pinpointed nearly 50 proteins that were present at higher or lower levels in hyperexcitable Alzheimer’s cells compared to healthy cells.
“Some of these proteins were already known to be associated with Alzheimer’s, but many were not,” says Lipton.
The proteins were involved in many diverse functions of neurons, including control of electrons in free radicals (redox modulators), energy metabolism and inflammation. Fifteen of the proteins stood out as having particularly high or low levels in Alzheimer’s neurons, and Lipton’s group is planning follow-up studies on some of these molecules.
He also plans to expand the use of scPatch-Clamp/Proteomics for drug screens — testing whether potential Alzheimer’s drugs fix both the hyperexcitability of neurons and the abnormal protein levels. He is correlating these findings with experiments on larger groups of brain cells obtained from patients with Alzheimer’s known as cerebral organoids, or “mini-brains.”
“One cell doesn’t always tell the whole story,” Lipton explains. “Some of the dysfunction in Alzheimer’s has to do with how cells interact with each other, so if we can repeat this kind of study in a mini-brain organoid, we may make additional discoveries.”
Lipton notes this method could be applied to drug discovery efforts for additional brain-related diseases.
“This new approach to personalized medicine — based upon protein expression and electrical activity of a single Alzheimer’s neuron — could revolutionize drug discovery not only for this disease but other neurological diseases, which has lagged far behind other therapeutic areas,” he adds.

Women with breast cancer who exclusively ate a whole-foods, plant-based diet lost weight, improved cholesterol levels and other key metabolic factors, had less fatigue, and perceived that they felt sharper mentally and generally more well.
The outcomes are from a small study by researchers at the University of Rochester Medical Center and Wilmot Cancer Institute. Study participants were individuals with stage 4 breast cancer, who will be on lifelong treatment.
These patients are typically excluded from dietary studies, but with their survivorship numbers growing, it presented an opportunity to make an impact both short- and long-term, said research leader Thomas M. Campbell, MD, an assistant professor of Family Medicine at URMC and an expert on using plant-based diets to improve health.
What Did the Clinical Trial Require?
The study included 30 patients who were on stable treatment and could tolerate food.
Researchers randomly divided participants into two groups: One received standard care, and the intervention group ate meals provided by the research team for eight weeks. The diet consisted solely of fruits, vegetables, whole grains (including whole grain pasta), legumes (beans), potatoes, and nuts and seeds. Participants agreed to avoid animal-based foods (meat, eggs, and dairy), and all oils and added solid fats. They also took a daily multivitamin.
Weekly assessments occurred, and the study reported 95 percent compliance.

“It’s exciting to see that these major dietary changes were feasible, well-tolerated, and acceptable to the clinical trial participants,” Campbell said.
No calorie restriction was involved. Individuals were encouraged to eat as often as they wanted of food that was “on plan.”
How A Clean, Plant-Based Diet Makes a Difference
The women started with an average BMI of 29.7, which is borderline obese. The patients in the whole-foods plant-based group lost one-two pounds per week for eight weeks, without mandated exercise.
This is significant because individuals with breast cancer often gain weight during treatment, which is risky. Why? Too much body weight increases insulin levels and hormones (estrogen and testosterone) in the blood, which can fuel cancer.
Another encouraging study result: researchers saw a reduction in blood samples of IGF-1, a growth factor that has been associated with many common cancers, as well as less inflammation.

“Although we cannot say anything yet about whether the diet can stop cancer progression from this small study, we saw preliminary results that suggest favorable changes within the body, which is very positive,” Campbell said.
To better understand the implications for cancer growth, the team is collaborating with Isaac Harris, PhD, at Wilmot, in a bench-to-clinic investigation recently funded by the American Cancer Society.
Scientists know that cancer cells rely on amino acids to survive, and the patients who followed the plant-based diet had changes in their blood levels of amino acids. Harris is studying the effect of amino acid composition on cancer cell survival, and the effect of the amino acids on various cancer drugs.
The journal Breast Cancer Research and Treatment published the primary study, which is believed to be the first of its kind. The breast cancer trial had enough significant results that two additional papers were also published from the dietary intervention: a second study in the same journal, and a third study in Frontiers in Nutrition, all in March 2024.
How to Start Making Healthy Changes
Patients should first consult with their oncologists or healthcare providers before making major dietary changes, Campbell said. This is especially important for people who take blood thinners or insulin medications.
Examples of food provided in the breast cancer clinical trial included peanut soba noodles, steel cut oatmeal, banana flax muffins, sweet potato enchiladas, and Mediterranean white bean soup.
To get started with plant-based recipes and meal ideas that are simple and affordable, Campbell recommends these websites: plantyou.com, shaneandsimple.com, and monkeyandmekitchenadventures.com.
Several factors influence a person’s motivation to eat healthier, Campbell added, including family support, taste preferences, and cooking ability.
Whether a person makes dramatic changes overnight, or simply decides to swap out an occasional meal in favor of a plant-based recipe can be a good choice: “You only need five-10 plant-based recipes that are easy, tasty, and convenient enough that you will make them regularly to have a substantial overhaul in your diet,” he said.
Higher food costs are often cited as a reason to shirk a plant-based diet, but in 2023 co-author Erin Campbell, MD, published a separate study showing that the diets leading to the biggest health improvements — including Dietary Approaches to Stop Hypertension or the DASH diet, which is also plant-based — were the same or cheaper in terms of food costs compared to standard American diets with ultra-processed foods and restaurant take-out.

A study co-led by researchers at UCLA Health has found distinct brain connectivity patterns in six-week-old infants at risk for developing autism spectrum disorder (ASD). The authors say their findings suggest that differences in brain responses likely emerge much earlier than ASD-related behaviors can be identified and also indicate that these brain patterns themselves may lead to the emergence of ASD-related behaviors by altering the brain changes that typically guide social development. Their results were published in Nature Communications Biology.
The study prospectively evaluated 53 infants, 24 of whom had a higher likelihood of developing ASD due to having at least one older sibling with an ASD diagnosis while 29 had no family history of ASD or any other developmental disorders. Prior research has shown that the likelihood for developing ASD is approximately 20% in infants with a sibling with ASD.
The focus of the research was on the Salience Network, a collection of brain regions that work together to detect and filter important stimuli from the environment and direct attention accordingly. The network plays a crucial role in identifying which stimuli are worthy of attention, thereby facilitating appropriate responses.
The researchers found that the high-likelihood infants showed stronger connections between the Salience Network and sensorimotor regions of the brain, areas involved in processing sensory information and movement. Meanwhile, the infants with a typical likelihood of developing ASD exhibited stronger connections between the Salience Network and prefrontal regions, which are crucial for social attention and interactions. In addition, infants with stronger connectivity to sensorimotor regions had weaker connectivity to prefrontal regions, suggesting that greater attention to basic sensory information comes at the expense of attention to socially relevant information.
Importantly, these early brain patterns seen at 6 weeks predicted behavior at age one year. Infants with greater connectivity with sensory regions showed great sensory over-responsivity at age one, an impairing condition that is common in autism whereby individuals show extreme responses to typical environmental sounds or sensations. In contrast, infants with more connectivity with social attention regions showed better ability to share attention with others at age one, an important precursor to developing the social and communication skills that are often impaired in autism.
The authors say these early brain connectivity patterns could help explain the reduced social attention and atypical sensory processing commonly seen in ASD. “Although our modest sample size and the single timepoint for evaluating Salience Network connectivity are limitations in the current study, the overall results strongly suggest that atypical patterns of Salience Network connectivity may reflect a developmental vulnerability,” they write. “This is a possibility that should be examined in large-scale longitudinal studies that heavily sample brain and behavioral measures during the first postnatal years.”
“An emerging theory in autism research is that differences in sensory processing may precede the more classic social and communication symptoms of autism, and this data supports that theory in showing that very early brain differences related to how attention is allocated may predict both sensory and social behaviors in toddlers,” said Shulamite Green, Ph.D., assistant professor at the David Geffen School of Medicine at UCLA and corresponding author. “In other words, more attention to extraneous sensory stimuli in the environment could make it difficult to attend to social cues, and this difference in attention could really affect how the brain develops across the first year of life and beyond.”
“What I find compelling about these converging findings in such young babies is that they provide both a mechanistic and theoretical account for the lack of the typical attentional biases for social stimuli seen in older infants and toddlers who later receive an ASD diagnosis,” added Mirella Dapretto, Ph.D., co-author and associate director of the Semel Institute for Neuroscience and Human Behavior.

Breastmilk can promote equitable child health and save healthcare costs by reducing childhood illnesses and healthcare utilization in the early years, according to a new study published this week in the open-access journal PLOS ONE by Tomi Ajetunmobi of the Glasgow Centre for Population Health, Scotland, and colleagues.
Breastfeeding has previously been found to promote development and prevent disease among infants. In Scotland — as well as other developed countries — low rates of breastfeeding in more economically deprived areas are thought to contribute to inequalities in early childhood health. However, government policies to promote child health have made little progress and more evidence on the effectiveness of interventions may be needed.
In the new study, researchers used administrative datasets on 502,948 babies born in Scotland between 1997 and 2009. Data were available on whether or not infants were breastfed during the first 6-8 weeks, the occurrence of ten common childhood conditions from birth to 27 months, and the details of hospital admissions, primary care consultations and prescriptions.
Among all infants included in the study, 27% were exclusively breastfed, 9% mixed fed and 64% formula fed during the first 6-8 weeks of life. The rates of exclusively breastfed infants ranged from 45% in the least deprived areas to 13% in the most deprived areas.
The researchers found that, within each quintile of deprivation, exclusively breastfed infants used fewer healthcare services and incurred lower costs compared to infants fed any formula milk. On average, breastfed infants had lower average costs of hospital care per admission (£42) compared to formula-fed infants (£79) in the first six months of life and fewer GP consultations (1.72, 95% CI: 1.66 — 1.79) than formula-fed infants (1.92 95% CI: 1.88 — 1.94). At least £10 million of healthcare costs could have been avoided if all formula-fed infants had instead been exclusively breastfed for the first 6-8 weeks of life, the researchers calculated.
The authors conclude that breastfeeding has a significant health and economic benefit and that increasing breastfeeding rates in the most deprived areas could contribute to the narrowing of inequalities in the early years.

For people with paralysis or amputation, neuroprosthetic systems that artificially stimulate muscle contraction with electrical current can help them regain limb function. However, despite many years of research, this type of prosthesis is not widely used because it leads to rapid muscle fatigue and poor control.
MIT researchers have developed a new approach that they hope could someday offer better muscle control with less fatigue. Instead of using electricity to stimulate muscles, they used light. In a study in mice, the researchers showed that this optogenetic technique offers more precise muscle control, along with a dramatic decrease in fatigue.
“It turns out that by using light, through optogenetics, one can control muscle more naturally. In terms of clinical application, this type of interface could have very broad utility,” says Hugh Herr, a professor of media arts and sciences, co-director of the K. Lisa Yang Center for Bionics at MIT, and an associate member of MIT’s McGovern Institute for Brain Research.
Optogenetics is a method based on genetically engineering cells to express light-sensitive proteins, which allows researchers to control activity of those cells by exposing them to light. This approach is currently not feasible in humans, but Herr, MIT graduate student Guillermo Herrera-Arcos, and their colleagues at the K. Lisa Yang Center for Bionics are now working on ways to deliver light-sensitive proteins safely and effectively into human tissue.
Herr is the senior author of the study, which appears in Science Robotics. Herrera-Arcos is the lead author of the paper.
Optogenetic control
For decades, researchers have been exploring the use of functional electrical stimulation (FES) to control muscles in the body. This method involves implanting electrodes that stimulate nerve fibers, causing a muscle to contract. However, this stimulation tends to activate the entire muscle at once, which is not the way that the human body naturally controls muscle contraction.

“Humans have this incredible control fidelity that is achieved by a natural recruitment of the muscle, where small motor units, then moderate-sized, then large motor units are recruited, in that order, as signal strength is increased,” Herr says. “With FES, when you artificially blast the muscle with electricity, the largest units are recruited first. So, as you increase signal, you get no force at the beginning, and then suddenly you get too much force.”
This large force not only makes it harder to achieve fine muscle control, it also wears out the muscle quickly, within five or 10 minutes.
The MIT team wanted to see if they could replace that entire interface with something different. Instead of electrodes, they decided to try controlling muscle contraction using optical molecular machines via optogenetics.
Using mice as an animal model, the researchers compared the amount of muscle force they could generate using the traditional FES approach with forces generated by their optogenetic method. For the optogenetic studies, they used mice that had already been genetically engineered to express a light-sensitive protein called channelrhodopsin-2. They implanted a small light source near the tibial nerve, which controls muscles of the lower leg.
The researchers measured muscle force as they gradually increased the amount of light stimulation, and found that, unlike FES stimulation, optogenetic control produced a steady, gradual increase in contraction of the muscle.
“As we change the optical stimulation that we deliver to the nerve, we can proportionally, in an almost linear way, control the force of the muscle. This is similar to how the signals from our brain control our muscles. Because of this, it becomes easier to control the muscle compared with electrical stimulation,” Herrera-Arcos says.

Fatigue resistance
Using data from those experiments, the researchers created a mathematical model of optogenetic muscle control. This model relates the amount of light going into the system to the output of the muscle (how much force is generated).
This mathematical model allowed the researchers to design a closed-loop controller. In this type of system, the controller delivers a stimulatory signal, and after the muscle contracts, a sensor can detect how much force the muscle is exerting. This information is sent back to the controller, which calculates if, and how much, the light stimulation needs to be adjusted to reach the desired force.
Using this type of control, the researchers found that muscles could be stimulated for more than an hour before fatiguing, while muscles became fatigued after only 15 minutes using FES stimulation.
One hurdle the researchers are now working to overcome is how to safely deliver light-sensitive proteins into human tissue. Several years ago, Herr’s lab reported that in rats, these proteins can trigger an immune response that inactivates the proteins and could also lead to muscle atrophy and cell death.
“A key objective of the K. Lisa Yang Center for Bionics is to solve that problem,” Herr says. “A multipronged effort is underway to design new light-sensitive proteins, and strategies to deliver them, without triggering an immune response.”
As additional steps toward reaching human patients, Herr’s lab is also working on new sensors that can be used to measure muscle force and length, as well as new ways to implant the light source. If successful, the researchers hope their strategy could benefit people who have experienced strokes, limb amputation, and spinal cord injuries, as well as others who have impaired ability to control their limbs.
“This could lead to a minimally invasive strategy that would change the game in terms of clinical care for persons suffering from limb pathology,” Herr says.

18 minutes agoPria Rai & Manish Pandey