Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 33,594 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.
What this blog is for:
My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.
In a large prospective cohort of nearly 3,900 older adults followed for up to 11 years, altered daily cortisol patterns were associated with faster cognitive decline, although they were not linked to short-term Alzheimer's disease risk.
The findings, published in JAMA Network Open, suggest that salivary cortisol could serve as an early biomarker of neurocognitive aging and highlight racial differences in stress-related biological patterns that may inform future research and prevention strategies.
“In this cohort study examining salivary cortisol levels and cognitive decline, across the 5 salivary cortisol indices, distinct yet complementary patterns emerged that reflect distinct aspects of diurnal cortisol patterning and associations with cognitive decline,” wrote Ted K. S. Ng, PhD, Rush University Medical Center, Chicago, Illinois, and colleagues. “All indices were associated cross-sectionally with cognitive performance…when participants with the lowest 10% of baseline cognitive performance were excluded, mean cortisol remained significant, underscoring its robustness as an early physiological marker associated with subsequent cognitive decline among cognitively healthy adults.”
For the study, the researchers analysed data from 3,895 Black and White older adults (mean age, 76.7 years) enrolled in the Chicago Health and Aging Project, measuring salivary cortisol at waking, afternoon, and bedtime and following participants for cognitive outcomes over 11 years. Five cortisol indices reflecting daily hormone variability, cumulative exposure, and diurnal change were evaluated in relation to global cognition, cognitive decline, and incident Alzheimer's disease.
Higher cumulative cortisol exposure was associated with faster cognitive decline, with participants in the highest quintile of mean cortisol (β = -0.02; P = .02) and area under the curve (β = -0.02; P = .046) experiencing greater decline over time. In contrast, moderate-to-high intraday cortisol variability was associated with slower cognitive decline (Q3 β = 0.02; P = .04; Q4 β = 0.03; P = .003).
No cortisol measure was associated with incident Alzheimer's disease during follow-up.
Black participants exhibited lower overall cortisol exposure but flatter daily cortisol slopes and lower intraday variability than White participants, although the relationship between cortisol patterns and cognitive decline was similar across racial groups.
“Because cortisol patterns may be responsive to behavioural, pharmacologic, and social interventions, these findings underscore opportunities for precision prevention and equity-informed strategies targeting stress-related cognitive aging,” the authors wrote.
Summary: Researchers unmasked a profound breakdown in the body’s internal garbage clearance system. As we age, tissue-resident macrophages lose their ability to engulf and dispose of expiring white blood cells, specifically short-lived neutrophils. Left un-cleared, these old cells transform into highly toxic, zombie-like “organ aging(2) neutrophils” that damage healthy tissues.
By blocking a single pro-inflammatory receptor known as EP2 exclusively on these long-lived macrophages, the team successfully revived their youthful cellular cleanup capabilities. This targeted intervention halted chronic inflammation and preserved the functional youthfulness of multiple vital organs throughout the body.
Key Facts
The Neutrophil Garbage Crisis: The body produces roughly 100 billion neutrophils daily as frontline immune responders. Because their active lifespans rarely exceed 12 to 24 hours, long-lived tissue-resident macrophages are tasked with continuously clearing these defunct cells. With advanced age, an unrelenting surge of the pro-inflammatory hormone prostaglandin E2 (PGE2) binds to heavily concentrated EP2 receptors on macrophages, shutting down their cellular engulfing (phagocytosis) mechanism.
The Rise of Zombie Neutrophils: Starved of proper macrophage clearance, expiring neutrophils undergo a swift transition into an intensely toxic, senescent state. These zombie cells accumulate within the liver, spleen, bone marrow, and other major organs, where they damage surrounding tissues by leaking destructive chemicals and propagating systemic inflammation.
Widespread Multi-Organ Rejuvenation: Disabling or pharmacologically blocking the EP2 receptor exclusively on tissue-resident macrophages triggered sweeping systemic preservation in aged mice. Rejuvenation and a stark reduction in inflammation metrics were confirmed across a vast network of organs:
Neurological Preservation: Deeply reduced hippocampal inflammation, preventing age-related memory loss and maintaining baseline spatial navigation and cognitive processing speeds.
Metabolic Recovery: Drastically lowered visceral fat accumulation, preserved youthful skeletal muscle mass, and normalized 59 out of 71 age-altered blood proteins, primarily driven by restored liver homeostasis.
Somatic Vitality: Aged mice treated with an experimental EP2 inhibitor looked leaner and exhibited physical speed, balance, and forelimb grip strength matching their youthful counter-cohorts.
Human Translation Confirmed: Transitioning from mice to humans, the Stanford team analyzed comprehensive human hepatic databases. The dataset confirmed that older and diseased human livers exhibit the identical pathological cascade seen in the animal models: a dramatic neutrophil buildup, widespread cellular senescence, and heightened macrophage EP2 receptor activity.
The Precision Medicine Alternative: Dr. Katrin Andreasson emphasizes that while current everyday painkillers (like aspirin or NSAIDs) reduce inflammation by blocking PGE2 production upstream, they are too clumsy, shutting down multiple beneficial prostaglandins and companion receptors. Developing a safe, highly selective drug that targets the EP2 receptor directly, without interfering with broader hormone systems, represents an outstandingly high-priority therapeutic path to extend human health spans.
Source: Stanford
We may age at different rates, but none of us escapes aging. A study in mice and in human cells by Stanford Medicine researchers pins much of the blame on a particular type of immune cell’s increased inability, with advancing age, to gobble up another immune cell type.
So-called tissue-resident macrophages appear to be central coordinators of age-related organ decline. Blocking a single receptor on these cells preserved the youthfulness of multiple organs in mice including the brain, heart, skeletal and heart muscle, liver, spleen, bone marrow, kidney, and colon. The receptor binds specifically to a hormone known to cause inflammation and pain in humans as well as mice.
Targeting the pro-inflammatory EP2 receptor on tissue-resident macrophages restores the clearing of senescent neutrophils, successfully reducing systemic inflammaging to preserve youthfulness across the brain, liver, heart, and skeletal muscles. Credit: Neuroscience NewsIn mice, selectively disabling this receptor exclusively on tissue-resident macrophages prevented chronic-inflammation-driven disorders of age including frailty, excessive fat accumulation and heart trouble; it also substantially slowed cognitive decline, said Katrin Andreasson, MD, the Edward F. and Irene Thiel Pimley Professor in Neurology and Neurological Sciences.
“We’ve been trying to figure out why we age,” Andreasson said. “Now we know at least one big reason for it.”
The study’s findings are described in a paper to be published online July 16 in Science. Andreasson is the senior author, and the lead author is Jessy Tan, PhD, an instructor in neurology.
This discovery clarifies systemic inflammation’s outsized contribution to aging and the debilities that accompany it. And it suggests a pharmaceutical approach that could restrain our organs’ ineluctable march to senescence, extending our overall health spans.
A tale of two cell types
The most abundant white blood cells in our immune system are neutrophils, our bodies’ main first responders. Born in the bone marrow, new neutrophils hop into the bloodstream, where they circulate and, if they come across a bacterial, viral or fungal pathogen, go all medieval on it: They squirt out poison and perform a hara-kiri horror act, spilling their guts out and unloading long, stringy macromolecules that form weblike nets and trap the pathogen.
Perhaps unsurprisingly, neutrophils are extremely short-lived: They’re lucky to survive 24 hours (12 hours is more typical). Some 90% of circulating neutrophils end up in the liver, spleen and bone marrow, awaiting execution and riddance by another batch of immune cells.
This neutrophil clearance is critical. In aged animals, the vast bulk of neutrophils that never see combat undergo a fast transition to senescence, a zombie-like state in which they injure, age and inflame neighboring cells by vomiting toxic chemicals and otherwise behaving like an addled rock star punching holes in a hotel room wall.
The older we get, the more our neutrophil counts rise, with senescent neutrophils constituting an ever higher percentage.
“Senescent neutrophils are killing our tissues,” Andreasson said. “Clearance of these cells is essential for preventing chronic inflammation.”
That’s a job for another type of immune cell called a macrophage. These cells are by turns soldiers, builders, medics and garbage collectors. They comb the tissues for pathogens, chew them up, spurt signaling substances that summon other cells to lend a hand, and pump out growth factors that help repair damaged tissue.
First and foremost, Andreasson said, “They’re the body’s garbage collection crew. A lot of that garbage is defunct cells.” And a lot of those cells are neutrophils — to the tune of 100 billion a day.
Macrophages come in several subtypes. Tissue-resident macrophages are long-lived and ubiquitous. They take up residence in each of the body’s organs during fetal development and remain for their lifetimes in whatever organ they’ve inhabited, adapting their roles to fit that organ.
One of tissue-resident macrophages’ prime responsibilities is to swallow senescent cells. Especially important targets for this operation, the study showed, are some 100 billion neutrophils, produced daily, which start showing signs of senescence within 8 to 12 hours after entering the bloodstream. (Neutrophils that haven’t arrived at senescence yet but have lived long enough and seen enough to put out “kill me now” flags of surrender on their cell surfaces are fair game.)
But tissue-resident macrophages also grow old and tired and dyspeptic. As Andreasson and associates showed in a 2021 Nature paper, over the advancing years these long-lived cells become ever more prone to succumb to aging-associated inflammation and to propagate it.
A distress signal
Immune cells produce hormones called prostaglandins. One of the five varieties of prostaglandin, called PGE2, can exert diverse effects on a cell, depending on which type of surface receptor is expressed on that cell’s surface.
Of the various subtypes of receptors for PGE2, one designated EP2 is highly pro-inflammatory. Tissue-resident macrophages are loaded with EP2.
Infection, injury and toxic chemicals including the ones produced by our aging bodies increase PGE2 output. As the 2021 Nature paper showed, that output grows substantially as we grow older. So does the concentration of EP2 on tissue-resident macrophages.
It’s a one-two punch: PGE2’s pro-inflammatory influence increases with age. The resulting unrelenting inflammatory PGE2 stimulation on tissue-resident macrophages, the new study showed, downshifts these voracious cells’ ability to wolf down neutrophils. Senescent neutrophils then accumulate in tissues and blood.
Andreasson and her colleagues have previously shown that with aging, tissue-resident macrophages undergo a slow decay in their energy metabolism. “Once that starts, there’s a steady decline in a macrophage’s performance,” she said.
In the new study, she continued, “We’ve shown that when tissue-resident macrophages don’t have EP2 on their surfaces anymore or when that receptor is plugged up by a drug, this decline doesn’t happen.”
Block one receptor, rejuvenate many organs
Andreasson’s lab has bioengineered a mouse in which, at a time of the scientists’ choosing, the gene that’s a recipe for EP2 gets deleted — but only in tissue-resident macrophages. The subsequent disappearance of EP2 from these cells, the new study proves, reinvigorated the neutrophil-devouring process that PGE2 undermines.
For their experiments, the Stanford Medicine researchers studied younger normal mice (age 6 to 8 months) corresponding to late adolescence or early adulthood in humans; older normal mice (23 to 25 months), whose human counterparts would be in their 60s or 70s; and otherwise virtually identical older mice whose EP2-encoding gene had been deleted at 4 to 6 months of age (their “teenage” years).
The scientists identified 71 proteins, found in blood, whose levels were significantly altered in older normal mice. Of those proteins, 59 stayed at youthful levels in older mice whose tissue-resident macrophages lacked EP2. Many of these proteins originated in the liver.
“The liver is one of the body’s most tissue-resident-macrophage-enriched organs and a major contributor to aging-related changes in blood chemistry,” Andreasson said. “It’s the central organ determining the body’s metabolic rate.”
Smoldering senescent neutrophils, the study showed, accumulated in normal old mice’s livers, spleens and bone marrow — and, to a lesser extent, in all the many other bodily organs the researchers looked at.
But the organs of older mice lacking EP2 on their tissue-resident macrophages retained the lower neutrophil numbers of youth. These mice looked younger, leaner and more physically fit compared with control littermates. They evidenced less visceral fat and greater muscle mass. Their performance on tests of multiple organs’ function equaled that of young mice.
EP2 deletion reduced inflammation in the blood, liver, colon, heart, kidney and hippocampus (a brain region tightly tied to memory and navigation ability) in the older mice. Their speed, balance and forelimb grip strength resembled that of young animals.
Reducing EP2 action in older mice also preserved their memory capabilities. They could thread their way through a maze or recall previously encountered objects almost as well as younger mice — and far better than similarly old mice in whose tissue-resident macrophages EP2 remained functional.
Seeking drugs to target EP2
There are, today, no approved drugs that selectively shut down EP2 activity, although there are several that target PGE2. Non-steroidal anti-inflammatory painkillers work by blocking PGE2 production, Andreasson said. (That’s how aspirin and similar drugs reduce pain, fever, swelling and redness, the “four horsemen” of inflammation.) But to greater or lesser degrees they all block other vital prostaglandins. Even PGE2 has beneficial properties when it binds to receptors other than EP2, rather than the detrimental inflammatory one examined in this study.
The investigators treated otherwise normal 22-month-old mice for two months with an EP2-inhibiting experimental drug.
This drug reduced total and senescent neutrophil counts in old mice toward youthful levels. In culture dishes, old age diminished — but the EP2-blocking drug likewise significantly restored — the mice’s tissue-resident macrophages’ ability to engulf and digest burnt-out neutrophils.
Finally, the team turned to a large database characterizing goings-on in all cell types in young, old and diseased human livers. This database revealed the same age-related neutrophil buildup, increased neutrophil senescence, tissue-resident-macrophage decline and heightened EP2 activity in older — and even more so, diseased — livers that the Stanford Medicine researchers had seen in mice. It was a first-time observation in human cells, according to Andreasson.
Targeting neutrophil clearance may yield big therapeutic benefits, she said: “We need to develop a safe drug” that incapacitates EP2 without disrupting upstream events such as PGE2 production.
A researcher from the University of Munster in Germany contributed to the work.
Funding: The study was funded by the National Institutes of Health (grants 1RF1AG080742, 1RF1AG070839 and P30AG066515), the American Heart Association, the Phil and Penny Knight Initiative for Brain Resilience (at the Wu Tsai Neurosciences Institute), Stanford University, the Arc Institute, and the Chan-Zuckerberg Biohub. The research was conducted in part at the Neurosciences Preclinical Imaging Community Laboratory at the Wu Tsai Neurosciences Institute.
Key Questions Answered:
Q: Why are neutrophils so helpful in youth but so incredibly destructive to our tissues as we get older?
A: Think of neutrophils as the kamikaze first-responders of the immune system. When you are young and get an infection, they swarm the site, unleash toxic chemicals to melt away pathogens, and deliberately burst open to form weblike nets that trap invaders. Because they are so intensely destructive, they are designed to die within 12 to 24 hours, at which point the body’s macrophage cleanup crews instantly sweep them away. However, as we age, the cleanup crew goes on strike. Left floating in our organs past their expiration date, these un-cleared neutrophils transform into hyper-toxic “zombie cells.” They wander through healthy tissues, punching holes in cell walls, vomiting inflammatory chemicals, and accelerating the physical aging of everything around them.
Q: If we already have anti-inflammatory drugs like aspirin that block this hormone pathway, why can’t we just use those to stop aging?
A: While everyday painkillers like aspirin or ibuprofen do reduce inflammation by shutting down the production of the prostaglandin PGE2, they act like biological sledgehammers rather than precision tools. PGE2 is a complex hormone that does many different jobs depending on which receptor it latches onto. When it hits the EP2 receptor on macrophages, it causes damage and shuts down clearance; however, when it binds to other receptors, it can actually support healing, protect the stomach lining, and assist blood vessel health. Blanket NSAIDs shut down the entire system, causing long-term side effects like ulcers or kidney stress. The Stanford team’s ultimate goal is to develop a hyper-targeted drug that leaves the helpful pathways completely alone, acting like a shield that plugs up only the problematic EP2 receptor.
Q: What makes this discovery a true paradigm shift for the future of longevity and preventative medicine?
A: For decades, the medical community viewed the aging of different organs—like cognitive decline in the brain, fatty buildup in the liver, and frailty in our muscles, as separate, distinct illnesses that required completely different treatments. This study completely upends that reductionist model. By demonstrating that deleting a single receptor on one type of immune cell simultaneously preserved the youthful function of the brain, heart, liver, muscles, colon, and kidneys, Stanford has exposed a universal master key to aging. It proves that we do not necessarily have to treat every organ disease individually; by simply fixing the body’s natural cellular garbage disposal system, we can halt systemic inflammation at its root, unlocking a future where overall human health spans can be extended in unison.
Editorial Notes:
This article was edited by a Neuroscience News editor.
Journal paper reviewed in full.
Additional context added by our staff.
About this aging research news
Author: Bruce Goldman Source: Stanford Contact: Bruce Goldman – Stanford Image: The image is credited to Neuroscience News
'Care'! But you tell us NOTHING ABOUT RESULTS.
They remind us they are faster and shorter treatment times but never tell us
how many 100% recovered. You have to ask yourself why they are hiding
their incompetency by not disclosing recovery results. ARE THEY THAT FUCKING BAD?
The thrombolytic agent tenecteplasewas associated with shorter treatment and transfer times thanalteplasein patients with acuteischemic stroke, a large US registry analysis showed.
“These workflow advantages provide support for broader use of tenecteplase for stroke thrombolysis,” said the investigators led by Steven J. Warach, MD, PhD, of Dell Medical School at The University of Texas at Austin.
Even modest reductions in treatment time may translate into clinically meaningful benefits because earlier reperfusion is strongly linked to improved stroke outcomes(Survivors want 100% recovery OR DON'T YOU CARE ABOUT THAT?), the investigators noted.
The findings were published online on July 13 in JAMA Network Open.
Key Points
Tenecteplase ↓ DTN vs alteplase in AIS; mean difference 3.1 minutes.
30% achieved DTN ≤30 min with tenecteplase vs 20.4% with alteplase.
Tenecteplase also improved DIDO and thrombectomy workflow times.
Hospitals switching from alteplase to tenecteplase showed modest DTN improvement.
Registry data support broader tenecteplase use; nonrandomized confounding remains possible.
Does tenecteplase improve functional stroke outcomes?
Which stroke subgroups benefit most from tenecteplase?
How does tenecteplase affect hemorrhagic transformation risk?
Faster Treatment Across Multiple Workflow Measures
Intravenous (IV) alteplase has long been the standard thrombolytic therapy for acute ischemic stroke, but tenecteplase has gained increasing acceptance because it can be administered as a single IV bolus rather than as a bolus followed by a 60-minute infusion.
Suggested for you
Previous randomized trials have shown tenecteplase has a safety and efficacy profile on par with alteplase, but whether its simpler administration translates into faster real-world treatment workflows has been uncertain.
To investigate, Warach and colleagues analyzed data from the American Heart Association (AHA) Get With The Guidelines-Stroke registry, which captures more than 75% of stroke admissions in the US.
The cohort included 133,228 adults treated with IV thrombolysis for acute ischemic stroke between July 2020 and June 2022 across 2092 hospitals. Of these, 13,988 patients (10.5%) received tenecteplase and 119,240 (89.5%) received alteplase.
Among patients treated at the presenting hospital, the average door-to-needle (DTN) time was 47.0 minutes with tenecteplase compared with 52.7 minutes with alteplase, a mean difference of 3.1 minutes favoring tenecteplase.
Patients receiving tenecteplase were also significantly more likely to achieve key DTN benchmarks. Nearly 30% of patients receiving tenecteplase were treated within 30 minutes compared with 20.4% of those receiving alteplase, whereas 58.3% vs 48.6% met the 45-minute target and 77.5% vs 70.7% achieved treatment within 60 minutes.
Hospitals that transitioned from alteplase to tenecteplase during the study period also experienced modest improvements in average DTN time after making the switch.
The benefits of tenecteplase extended to patients requiring transfer for higher-level care(NOT REOVERY!). Among likely mechanical thrombectomy candidates, mean door-in-door-out (DIDO) time was 108.3 minutes with tenecteplase vs 114.1 minutes with alteplase, an adjusted reduction of nearly 6 minutes. Patients transferred overall also had significantly shorter DIDO times with tenecteplase.
Tenecteplase was also associated with faster endovascular treatment once patients underwent thrombectomy. Compared with alteplase, tenecteplase was associated with shorter door-to-arterial puncture, door-to-device deployment, and door-to-reperfusion times among both transferred patients and those treated at thrombectomy-capable centers.
Support for Broader Use
The researchers acknowledged several limitations. Because it was based on a voluntary, nonrandomized registry, residual confounding cannot be excluded despite statistical adjustment.
The participating hospitals were largely early adopters of tenecteplase and tended to be higher-volume certified stroke centers, potentially limiting generalizability to smaller or less experienced hospitals. In addition, missing workflow data were not imputed and may not have occurred at random.
Despite these limitations, the findings suggest that tenecteplase may improve workflow efficiency for thrombolysis and interfacility transfer, further supporting its broader use in acute ischemic stroke, they concluded.
The study was funded in part by Get With the Guidelines-Stroke, AHA/American Stroke Association. Disclosures for study authors are available with the published article.
You'll have to ask your competent? doctor how close this gets hand recovery to 100%, the only goal in stroke! If your doctor isn't working towards that; THEY NEED TO BE FIRED!
Antara Senior Care has deployed the ExoAtlet II robotic exoskeleton alongside advanced hand and finger retraining devices at its Bannerghatta centre in Bengaluru. This multidisciplinary program is supervised by Physical Medicine and Rehabilitation (PM&R) specialists to aid stroke recovery. Max India is backing this operational scale-up following strong Q4 FY26 results where consolidated revenues expanded 58.1% year-on-year.
For millions of stroke survivors, something as simple as picking up a glass of water or holding a sandwich is a daily challenge. Quentin Sanders wants to make those moments easier through wearable robotic technology designed to restore hand function.
The George Mason University assistant professor is developing a new generation of hand exoskeletons that may help people regain independence after stroke. His lab is testing wearable devices that amplify a user's remaining muscle activity, allowing them to open and close their hand more effectively while remaining affordable enough for broader use.
The latest prototype resembles a lightweight glove that fits over the hand and upper arm. As users attempt to move their hand, the device detects their remaining muscle activity and assists the motion.
"We instruct them to try to open their hand," Sanders explained. "When they try to open their hand, we sense whatever residual activity they have, and then the exoskeleton amplifies that."
One version of the device seeks to use wearable ultrasound technology developed in collaboration with George Mason researcher Siddhartha Sikdar, a professor in the Department of Bioengineering and director of the Center for Medtech Innovation. The system will use wearable ultrasound sensors to monitor how muscles deform as they contract, translating those signals into movement. Another, simpler version uses a button embedded in the glove that users press to control the device.
Whilebrain-controlled devices remain the long-term aspiration for many in the field, Sanders is focused on a more practical solution that builds on the muscle activity people retain after a stroke. "I would say brain-controlled systems are kind of the holy grail. In my lab, we're going one level lower to see if we can use muscle activity to control it."
The need for better rehabilitation tools is growing. Sanders noted that roughly 800,000 people experience a stroke each year in the United States, while millions more live with its long-term effects. Advances in medicine mean more people survive strokes, but many struggle to access the lengthy rehabilitation needed to regain function.
"We're at this point where you're living a long life, but you have this need for rehab," Sanders said. "You need either consistent opportunities for movement or some type of device that can help improve your quality of life."
Commercial hand exoskeletons remain scarce in the United States, and many existing systems cost tens of thousands of dollars. Making the technology more affordable and accessible has become one of the driving goals of his research.
"You've got this large population of people who need these devices who aren't getting them," Sanders said. "I'm hoping we can make this kind of a low-cost, accessible version that people can use to improve some aspect of their life."
Sanders is also working to broaden who can benefit from rehabilitation technologies. Many research studies enroll only patients who meet narrow eligibility criteria, leaving others without solutions tailored to their needs.
"I think that's the other breakthrough people are working on that my lab is working on," he said. "How can we make these devices work for a larger population?"
Scientists have for the first time mapped in exquisite, three-dimensional detail six major conformations of a membrane in the brain related to learning, memory and fear-related behavior.
Researchers used state-of-the-art cryo-electron microscopy housed in OHSU’s South Waterfront Campus to capture the most detailed view yet of a specific type of membrane protein: an acid-sensing ion channel known as ASIC1a.
The findings could form the blueprint for drug development useful in treating stroke, said senior author Isabelle Baconguis, Ph.D., assistant professor in the OHSU Vollum Institute.
“Previous studies show that when you block this channel, it can be
neuroprotective
(Meaning stopping the the neuronal cascade of death in the first week! Neuroprotection is such a bland word, doesn't impart immediacy at all!)
,” Baconguis said. “If you’re able to design a drug that infuses an inhibitor to this channel, it could lengthen the survival of the tissue in cases of stroke.”
Already, scientists in Australia are using a molecule derived from spider venom that explicitly targets ASIC1a to improve outcomes in heart attacks and stroke.
OHSU researchers used recombinant DNA technology to express the human gene to generate human proteins they imaged using cryo-EM. Because acid-sensing ion channels respond to variations of extracellular pH in the central and peripheral nervous systems, researchers were able to capture six distinct conformations by varying their exposure to acidity.
“In our bodies, there are locations where cells undergo different pH conditions, especially in the brain,” Baconguis said. “In neuronal injuries such as stroke, where brain tissue undergoes a drop in pH, these channels can be activated causing tissue damage.”
The images provide a blueprint for designing new drugs capable of inhibiting this one specific acid-sensing ion channel in cases of stroke.
“The sooner you can protect brain tissue from damage, the less severe disability stroke survivors will have,” Baconguis said. “Time is of the essence when it comes to stroke.”
In addition to Baconguis, co-authors include James Cahill, Kimberly A. Hartfield, Ph.D., Craig Yoshioka, Ph.D., of OHSU; Stephan Alexander Pless, Ph.D., Nadine Ritter, Ph.D., and Mette Homann Poulsen, Ph.D., of the University of Copenhagen; and Stephanie Andrea Heusser, Ph.D., of the University of Copenhagen in Denmark and Linköping University in Sweden.
The research was supported by the National Institutes of Health, grant award R24GM154185, RO1GM138862 from the National Institute of General Medical Sciences (NIGMS); and the Lundbeck Foundation, grant award R313-2019-571. Electron microscopy was performed at the Multiscale Microscopy Core, part of OHSU’s university-shared resource cores. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.
We are providing an unedited version of this manuscript to give early access to its findings. Before final publication, the manuscript will undergo further editing. Please note there may be errors present which affect the content, and all legal disclaimers apply.
Abstract
Background
To ensure continuous rehabilitation for patients with hemiparesis due to brain disorders, there is a growing need for simple, accessible systems that enable unsupervised self-training. The occurrence of compensatory trunk movements during the unsupervised exercise may prevent true functional recovery. This study proposes a smartphone-based visual-auditory feedback system designed to detect and suppress compensatory trunk movements in real-time without wearable sensors.
Methods
A pilot cohort (n = 16) was first used to calibrate detection thresholds for compensatory trunk movements. Subsequently, a total of 55 hemiparetic patients were enrolled in a randomized controlled trial and allocated to a Feedback (FB) group (n = 27) or a Non-Feedback (NFB) group (n = 28). Participants performed standardised upper limb rehabilitation tasks using the Rapael Smart Board™, a planar upper limb rehabilitation device. The proposed system utilised a smartphone camera with MediaPipe-based pose estimation to track trunk movements and provided real-time traffic-light feedback based on calibrated thresholds. Outcome measures included trunk path length, trunk deviation, task efficiency, and spatial occupancy, which were evaluated using 3D coordinates reconstructed from depth camera data.
Results
The FB group demonstrated significantly improved postural stability compared to the NFB group, with a 37.9% reduction in trunk path length (p = 0.014) and a 35.3% decrease in spatial occupancy (p = 0.003). Kinematic analysis revealed that the NFB group's shorter hand path lengths were achieved through kinematic redundancy—specifically, the recruitment of trunk degrees of freedom—rather than through selective upper limb motor control. In contrast, the FB group maintained a stable posture near the neutral position, ensuring true upper limb engagement. The usability assessment demonstrated that the system was well received by users and was reliable (Cronbach's = 0.775).
Conclusion
The proposed system, which integrates mobile technology, effectively suppresses compensatory trunk movements and promotes selective motor control, and ensures that rehabilitation outcomes reflect true upper limb joint engagement rather than kinematic redundancy through compensatory trunk recruitment. While certain design considerations remain, particularly related to dynamic recalibration and the use of a fixed auditory feedback window, the system retains strong potential as an automated feedback solution, offering a scalable and accessible pathway for high-quality unsupervised home rehabilitation.
