Stem Cell Therapy Shows Promise for Stroke Recovery

 The promise has been out there for well over a decade, WHOM will actually solve the problem? NO leadership and NO strategy is the result of our fucking failures of stroke associations!

• stem cells (409 posts to April 2011)

Stem Cell Therapy Shows Promise for Stroke Recovery

University of Miami Miller School of Medicine

Researchers from the University of Miami Miller School of Medicine and collaborating institutions have published a comprehensive review examining the rapidly evolving field of intra-arterial stem cell therapy for ischemic stroke, highlighting its potential to improve recovery for patients who continue to face disability despite major advances in stroke treatment.

Published in the American Heart Association Journal Stroke: Vascular and Interventional Neurology, the review, titled "Progress in Intra-arterial Stem Cell Therapy for Ischemic Stroke – A Review," examines decades of preclinical and clinical research and outlines a roadmap for translating regenerative therapies from the laboratory to the bedside.

Ischemic Stroke, in which blood supply to a part of the brain is cut off by suddenly by a clot blockage, remains one of the leading causes of death and long-term disability worldwide. While clot-busting medications and mechanical thrombectomy have transformed care for acute ischemic stroke, many patients are left with significant neurological deficits despite successful restoration of blood flow. The authors argue that stem cell therapies delivered directly into the brain's circulation via minimally invasive and widely available catheter angiographic techniques may complement existing treatments. The stem cells targeted this way to the stroke injured brain area work by promoting brain repair, reducing inflammation, and enhancing recovery.

"Mechanical thrombectomy has revolutionized stroke treatment, but half of the treated or more patients still do not regain full independence," said Dileep R. Yavagal, M.D., professor of clinical neurology and neurosurgery at the University of Miami Miller School of Medicine and senior author of the review. "Stem cell therapy represents a promising strategy to help the brain recover after injury and may become an important next step in improving outcomes(NOT GOOD ENOUGH!) for stroke patients."

(Likely a much better approach to full recovery is stopping the 5 causes of the neuronal cascade of death in the first week and thus saving hundreds of millions to billions of neurons! So you aren't even thinking of this properly!)

A Targeted Approach

Stem cells can be delivered through several different routes and optimal route in Stroke treatment is not yet established. The review focuses on intra-arterial delivery, an approach in which stem cells are infused directly into arteries supplying the injured region of the brain. Unlike intravenous administration, in which much of the cells are trapped in organs such as the lungs and liver, intra-arterial delivery into the affected artery allow a greater concentration of therapeutic cells to reach stroke-affected tissue. Surgical approaches such through a small hole in the skull are more invasive.

Researchers note that intra-arterial delivery is particularly attractive because it can potentially be performed during the same minimally invasive endovascular procedures and techniques used now as standard of care treatment, mechanical thrombectomy, avoiding the need for a new surgical access or additional intervention.

Preclinical studies, including from Dr. Yavagal's laboratory at the University of Miami Miller School of Medicine Interdisciplinary Stem Cell Institute, reviewed by the authors demonstrate that stem cells may reduce inflammation, promote formation of new blood vessels, support neural repair, and improve neurological outcomes following stroke. Multiple early-stage clinical trials have also established the feasibility and safety of stem cell administration across several delivery routes.

Strong safety record, more research needed

The review analyzes more than two decades of clinical development and notes that more than 40 randomized clinical trials have investigated stem cell therapies for stroke via many different routes of delivery. While safety has been consistently demonstrated, evidence for definitive functional benefit remains under investigation. Several ongoing studies are working to determine optimal cell type, dosing, timing, and patient selection strategies.

"The safety of IA stem cell therapy has been established by several preclinical and clinical studies and will continue to remain a critical endpoint for all future studies," said Roshni Thakkar, Ph.D., co-first author and research assistant professor in the Department of Neurology at the University of Miami. "The next challenge that the field is taking on is to identify the right cells, the right dose, the right patients, and the right time to intervene in order to maximize stroke recovery."

The authors emphasize that future studies should integrate advanced imaging, biological markers, and immune profiling to better understand how stem cells interact with the post-stroke brain and to identify patients most likely to benefit.

"Regenerative medicine has the potential to fundamentally reshape stroke treatment," said Nadia McMillan, M.D., Ph.D., co-first author, senior neuro-endovascular fellow and instructor . "The goal is not only to save brain tissue during a stroke but to help patients regain function and quality of life afterward."

Looking toward the future

According to the review, emerging therapies may eventually include bioengineered stem cells, extracellular vesicles and exosomes, and combination approaches that pair thrombectomy with regenerative treatments. Continued advances could ultimately transform stroke care from a model focused primarily on restoring blood flow to one that also actively promotes brain repair and recovery.

The authors conclude that while significant challenges remain, ongoing clinical trials and rapid advances in regenerative neuroscience provide reason for optimism that stem cell-based therapies may one day become an important adjunct to standard stroke treatment and achieve an outcome free of disability for the vast majority of stroke patients.

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Tags: regenerative medicine , america , investigation , american , Administration , Miami , biological , neuroscience , clinical trials , neurosurgery , University of Miami , blood vessels , inflammation , cell therapy , American Heart Association , quality of life

Parkinsonian gait improvement through vibratory stride parameter feedback

 WHOM will be competent enough to see if this would help gait recovery after stroke?  I'm proving there is NO ONE IN STROKE COMPETENT AT ALL! You're screwed along with your children and grandchildren when they get strokes. 

Parkinsonian gait improvement through vibratory stride parameter feedback

• Paul Kirsch,
• Miriam Helbig,
• Dominic Rupar,
• Simon Baudrexel &
• Christian A. Kell 

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

Hypokinetic gait increases morbidity and mortality of persons with Parkinson’s disease and constitutes a major target symptom for therapy. Feedback on gait quality, e.g. by a physiotherapist, improves stride length and reduces shuffling. Wearable devices measuring gait parameters and providing feedback could improve parkinsonian gait during everyday life when no physiotherapist is available. Here, we report on the efficacy of a new device providing discreet vibratory feedback upon decreased stride length and increased shuffling.

Methods

33 persons with Parkinson’s disease, in two cohorts, received automatic vibratory feedback administered via a newly developed sensor-equipped insole when their stride length and heel strike angle decreased while walking a 730 m walking course. Gait of 14 persons with Parkinson’s disease in the first cohort was investigated in OFF and ON medication state to allow for a comparison of the feedback effect with the effect of medication on stride length, heel strike angle and gait variability. In both cohorts, the effect of feedback on gait parameters was compared against a control walk without stimulation and was subjectively evaluated by the study participants. In the second cohort of 19 participants, the effect of feedback was additionally compared with vibration at random time points to investigate the efficacy of context-adequate feedback.

Results

Both stride length and heel strike angle improved upon feedback to a degree that, on average, was close to the medication effect on parkinsonian gait. Stimulation at random time points showed intermediate values with non-significant improvements in gait parameters compared to control walks. Closed-loop feedback resulted in a less variable gait pattern compared to control walks. Persons with Parkinson’s disease rated the feedback mode as subjectively useful.

Conclusions

Our results demonstrate the use of closed-loop feedback can improve parkinsonian gait and suggest such a device could effectively complement the available approaches in the treatment of persons with Parkinson’s disease.

Trial Registration: This trial was retrospectively registered in the German Clinical Trials Register (DRKS00038516) on 9 December 2025.

Researchers develop artery-on-a-chip platform to predict stroke risk

Much more important would be stopping this risk from occurring. WHOM will you be contacting to get that research done?

Researchers develop artery-on-a-chip platform to predict stroke risk

Predicting an individual's risk of ischemic stroke is difficult because thrombosis embolization-the process of a blood clot detaching from the area where it formed and traveling to and then sticking in another blood vessel-is based on factors that are unique to each person. In a study publishing in the Cell Press journal Cell Biomaterials on July 23, researchers developed a tool to get around this challenge: an artery-on-a-chip platform that can replicate a patient's specific vascular structure and blood flow dynamics, called a "physical twin." 

This idea was born out of a critical clinical gap. We know that even patients at 'low risk' can suffer from severe or fatal strokes. We wanted to find a better way to predict this risk." 

Lining Arnold Ju, Author, University of Sydney, Australia

Ischemic strokes occur when a blood vessel supplying the brain is blocked, usually by a clot or fatty plaque. When vital blood and oxygen are cut off, brain cells die within minutes. For this reason, it's important to find new ways to predict who is at highest risk so that better interventions can be developed. 

"Our work recreates precise, patient-specific carotid artery geometries," says Ju." The physical twin also uses cells that more closely mimic the dynamics of blood flow in these structures. 

The researchers reconstructed carotid arteries from six patients with varying degrees of disease. They used computational fluid dynamics to calculate how blood flowed through each artery, revealing substantial differences in local blood flow despite similar levels of narrowing. After using a laser to create a small injury in the underlying collagen, they also observed strikingly different clotting behaviors depending on the artery's shape. 

Event guide: 10th CAR-TCR Summit eBook Navigate the latest developments in cell therapy at the 10th CAR-TCR Summit Europe.Download the latest edition

"Our findings suggested that three-dimensional vascular shape and local flow disturbances matter far more than simple narrowing," says first author Yunduo Charles Zhao of the Heart Research Institute in Newtown, Australia, who was motivated to shift his research toward predictive stroke diagnosis during his PhD, when his grandmother passed away from stroke. 

"We hope these tools will allow us to study drugs aimed at reducing the risk of stroke and to eventually provide personalized treatments for each patient based on their anatomy." 

The team is currently recruiting stroke patients for a clinical trial to evaluate how this technology can directly benefit underserved stroke patients. They say this technology also has the potential to study other cardiovascular conditions, including peripheral artery disease, deep-vein thrombosis, and aneurisms. 

This work was supported by the National Health and Medical Research Council (NHMRC) of Australia, NSW Cardiovascular Capacity Building Program, MRFF Cardiovascular Health Mission Grants, MRFF Early to Mid Career Researchers Grant, Ramaciotti Foundations; National Heart Foundation, Office of Global and Research Engagement, and University of Sydney Drug Discovery Initiative. 

Source:

Cell Press

Journal reference:

Zhao, Y. C., et al. (2026). Patient-specific carotid artery-on-a-chip 'physical twin' dissects complex flow-dependent VWF mechanopresentation. Cell Biomaterials. DOI: 10.1016/j.celbio.2026.100541. https://www.cell.com/cell-biomaterials/fulltext/S3050-5623(26)00197-2

Feel Fatigued? You Might Need More Of This Critical Mineral

 What is your doctor's EXACT PRESCRIPTION TO PREVENT POST STROKE FATIGUE? Doesn't have one? That is complete fucking incompetence! Your doctor has known of the problem since medical school and HAS DONE NOTHING!

At least half of all stroke survivors experience fatigue Known since March 2017

Or is it 70%? Known since March 2015.

Or is it 40%? Known since September 2017.

WHOM is going to do the further research that will solve this problem? Specific names only.

Feel Fatigued? You Might Need More Of This Critical Mineral

There are a number of reasons you might be feeling fatigued lately—poor sleep, stress, an active toddler perhaps? But one sneaky culprit behind fatigue you may not have considered is a mineral deficiency.

Namely, not getting enough magnesium is associated with a host of undesirable side effects. Here's what to know.

How a magnesium deficiency can contribute to fatigue

Magnesium is an essential mineral that helps keep our bodies functioning at their best, and when you aren't getting enough of it, you'll definitely notice a difference (even if you don't realize it's the lack of magnesium behind your symptoms).

As registered dietitian nutritionist, Natalie Butler, RDN, L.D., previously wrote for mindbodygreen, fatigue and exhaustion are generalized symptoms of a magnesium deficiency. "You may attribute your tiredness to stress, poor sleep, or a host of other reasons and not realize just how much nutrition is playing a role," she says, adding, "This is because magnesium is required for the production of energy. If the body has inadequate access to magnesium, then energy production suffers, leaving you prone to fatigue."

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Not to mention, magnesium also plays an essential role in managing the body's normal inflammatory response. "When magnesium intake is low, inflammatory biomarkers such as high-sensitivity C-reactive protein (hs-CRP), interleukin-6, and fibrinogen1 are significantly affected," Butler notes.

To that end, chronic inflammation is associated with fatigue as well, furthering the importance of making sure your magnesium levels are adequate to keep both inflammation and fatigue in check.

What to do about it

If you think you could be deficient in magnesium, the only way to know for sure is to test your levels with either a blood or urine sample.

But as Butler explains, "While you'll need formal testing to know if you're clinically deficient, you can also add more magnesium-rich foods to your diet or try a magnesium supplement to see if your symptoms improve." After all, she notes, research on chronic fatigue syndrome2 has indicated that magnesium actually provides nutritional support to combat fatigue.

Here's a quick list of some magnesium-rich foods to get you started:

• Dark, leafy greens
• Whole grains
• Nuts & seeds
• Legumes
• Avocados
• Bananas
• Dark chocolate
• Tofu

The takeaway

Fatigue is certainly no fun, especially when you can't figure out why you're feeling exhausted. If that sounds all too familiar, including more magnesium in your routine could be the missing link you're looking for.

Tiny Peptide Shows Powerful Brain Healing After Traumatic Injury

 Ask your competent? doctor EXACTLY WHOM WILL BE TESTING THIS ON STROKE PATIENTS! Doesn't know how to do that? 

TOTAL FUCKING INCOMPETENCE!

This from 2022 would seem to suggest that glycoproteins also occur after stroke and might benefit from this drug also. But why listen to me; not medically trained, unlike your doctor who hasn't a fucking clue how to get you 100% recovered!

Platelet surface receptor glycoprotein VI-dimer is overexpressed in stroke: The Glycoprotein VI in Stroke (GYPSIE) study results January 2022

The latest here:

Tiny Peptide Shows Powerful Brain Healing After Traumatic Injury

Summary: A small peptide called CAQK, composed of just four amino acids, has shown remarkable neuroprotective effects in mouse and pig models of traumatic brain injury. When injected intravenously, CAQK travels directly to damaged brain tissue, where it binds to overexpressed proteins and reduces inflammation, cell death, and tissue damage.

Treated animals displayed improved memory and motor function without toxicity, suggesting strong potential for safe, non-invasive therapy. Researchers plan to seek FDA approval for human clinical trials, marking a major advance toward drug-based treatments for traumatic brain injury.

Key Facts:

• Targeted Repair: CAQK homes in on injured brain areas, reducing inflammation and cell death.
• Non-Invasive Therapy: Delivered intravenously, avoiding risky brain injections.
• Pre-Clinical Success: Improved recovery in mice and pigs without toxicity; human trials planned.

ource: CSIC

Advanced Chemistry of Catalonia (IQAC) of the Spanish National Research Council (CSIC), an institution under the Ministry of Science, Innovation and Universities, has discovered that a small compound—a peptide made up of four amino acids called CAQK—has a significant neuroprotective effect in mouse models of traumatic brain injury.

When administered intravenously shortly after injury in animal models (mice and pigs), CAQK specifically targets the damaged areas of the brain, attracted by a protein that is overexpressed in injured tissue following trauma.

CAQK accumulates in the region marked by this protein and is able to reduce inflammation, cell death, and damage to brain tissue. Moreover, in mice, it improved functional recovery without apparent toxicity.

The results, published in the journal EMBO Molecular Medicine, open new possibilities for treating injured areas of the brain.

The study was led by the company Aivocode (a spin-off of the Sanford Burnham Prebys Institute) in San Diego, California, in collaboration with the Institute for Advanced Chemistry of Catalonia (IQAC-CSIC) and the University of California, Davis.

Aivocode, founded by researchers Aman P. Mann, Sazid Hussain, and Erkki Ruoslahti (authors of the study), plans to soon seek authorization from the U.S. Food and Drug Administration (FDA) to begin Phase I clinical trials in humans.

Although no specific date has been set, the fact that CAQK is a short peptide—easy to produce and with good tissue penetration—makes it a strong candidate for drug development.

Traumatic Brain Injury

Traumatic brain injury (TBI) is brain damage typically caused by blows to the head, such as those resulting from traffic accidents, workplace incidents, or falls. It is estimated to affect around 200 people per 100,000 inhabitants each year.

Currently, treatment focuses on stabilizing the patient by reducing intracranial pressure and maintaining blood flow, but there are no approved drugs to halt brain damage or its secondary effects, such as inflammation or cell death. In addition, the therapies under investigation require direct injections into the brain, an invasive technique that can cause complications.

“The current interventions for treating acute brain injury aim to stabilize the patient by reducing intracranial pressure and maintaining blood flow, but there are no approved drugs to stop the damage and secondary effects of these injuries,” explains Dr. Pablo Scodeller, researcher at IQAC-CSIC and co-author of the study.

The Great Challenge of Neurology

Finding a non-invasive way to treat an injured brain is one of the major challenges in neurology. This study moves in that direction, building on previous work carried out by the researchers in 2016 and published in Nature Communications.

At that time, researcher Aman P. Mann, together with Pablo Scodeller, working in the laboratory of Dr. Ruoslahti (senior author of both studies) at Sanford Burnham Prebys, discovered a peptide—a small chain of amino acids, the building blocks of proteins—that specifically targeted injured areas of the brain in mice.

The peptide, named CAQK, was identified through a large-scale screening technique known as peptide-phage display, which allows the selection of molecules with affinity for specific tissues. In that earlier study, CAQK was used as a “vehicle” to deliver drugs directly to the damaged area.

However, in their new work, the researchers went a step further and demonstrated that the CAQK peptide itself has therapeutic effects.

To evaluate its therapeutic activity, the peptide was first administered intravenously shortly after a moderate or severe traumatic brain injury, and it was observed that the peptide accumulated in the injured brains of mice and pigs (the latter having brains more similar to humans than mice).

Furthermore, it was found that the peptide binds to special molecules called glycoproteins (proteins attached to sugars), which become more abundant after an injury and are part of the extracellular matrix—a supporting network that surrounds brain cells.

Treatment of mice with traumatic brain injury using this peptide resulted in a reduction in lesion size compared to control mice.

“We observed less cell death and lower expression of inflammatory markers in the injured area, indicating that CAQK alleviated neuroinflammation and its secondary effects. Behavioral and memory tests conducted after treatment also showed improvement in functional deficits, with no evident toxicity,” explains the study’s first author, Dr. Mann.

The study’s results demonstrate that the CAQK peptide can help repair the damaged area, highlighting its potential therapeutic applications following trauma.

“What’s exciting is that, in addition to proving highly effective, it’s a very simple compound—a short peptide that is easy to synthesize safely at large scale. Peptides with these characteristics show good tissue penetration and are non-immunogenic,” concludes Scodeller.

Key Questions Answered:

Q: What makes CAQK different from other brain injury treatments?

A: It can be administered intravenously and selectively targets injured brain tissue without invasive procedures.

Q: How does CAQK work?

A: The peptide binds to specific glycoproteins overexpressed after brain injury, reducing inflammation and protecting neurons.

Q: When could human trials begin for using CAQK to treat TBI?

A: Researchers plan to seek FDA authorization soon to start Phase I clinical testing.

About this neuropharmacology and TBI research news

Author: Pilar Quijada
Source: CSIC
Contact: Pilar Quijada – CSIC
Image: The image is credited to Neuroscience News

Original Research: Open access.
“A neuroprotective tetrapeptide for treatment of acute traumatic brain injury”