Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 33,056 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.
Tokyo, May 14 (Jiji Press)--A team including Takashi Shichita, a professor at the Institute of Science Tokyo's Medical Research Laboratory, has developed a drug candidate to suppress a type of protein that causes the rehabilitation-induced partial recovery of motor functions lost from a stroke to end after only about two months.
People who lost the abilities to move their hands or feet, or to speak due to the deaths of some nerve cells in their brains from the cerebral infarction can regain the functions to a certain extent through rehabilitation. The recovery normally lasts for about two months.
The recovery is possible because surviving nerve cells repair the neuron networks, with microglia, or cells in charge of brain immunity, helping the restoration process by secreting a protein called insulin-like growth factor 1, or IGF1.
In a genetic manipulation experiment using mice, Shichita and other members of the team discovered that microglia stopped secreting IGF1 after a while following a stroke due to the function of another protein, ZFP384. The same mechanism was confirmed in the brains of dead stroke patients.
The team developed the drug candidate to block the production of ZFP384. After injecting the drug into mice, the team found that microglia continued to secrete IGF1 and helped maintain the recovery of brain functions.
This is different than all the other stem cell research I've seen where stem cells aren't even monitored after transplantation and exosomes are the reason for improvement! But why go thru all the trouble of stem
cells if exosomes are the reason for the benefits? Which must be why no
one seems to be monitoring stem cell survival. Ask your competent? doctor for clarification!
Scientists have discovered that transplanted stem cell-derived brain cells may do far more than simply survive after a stroke.
A stem cell treatment helped mice recover from strokes by rebuilding damaged brain connections, restoring blood vessels, and improving movement, according to new research from the University of Zurich and the University of Southern California. The findings raise hopes that future therapies could one day repair stroke damage that is currently considered permanent.
Stroke remains one of the world’s leading causes of long-term disability. When blood flow to part of the brain is cut off, oxygen-starved cells die within minutes. Unlike skin or bone, the brain has only a limited ability to replace lost tissue, leaving many survivors with lifelong paralysis, speech problems, or memory loss.
Scientists have spent years searching for ways to help the brain rebuild itself. In the new study, researchers used neural progenitor cells, early-stage cells capable of developing into different types of brain tissue. The cells were created from induced pluripotent stem cells, which are adult human cells reprogrammed into a stem cell-like state.
The team transplanted these cells into the brains of mice one week after a stroke. That timing turned out to be critical. Earlier transplants survived poorly because the injured brain was still overwhelmed by inflammation and toxic chemical signals. Waiting several days allowed conditions to stabilize enough for the transplanted cells to take hold.
What happened next surprised the researchers.
New Neurons and Rebuilt Connections
Over five weeks, the transplanted cells survived, spread through nearby brain tissue, and matured mostly into functioning neurons. Many became GABAergic neurons, specialized inhibitory brain cells that help regulate neural activity and are heavily depleted after stroke. These cells are essential for balancing brain signaling, preventing excessive excitation, and coordinating movement.
Where the fuck is the protocol you delivered to all stroke hospitals? Oh, you DID NOTHING OFTHE SORT! You're fired for extreme incompetence! The goal is to get survivors 100% recovered; NOT TO GET YOU PUBLISHED YOU FUCKING BASTARDS!
Your compeuppance is going to be a real bitch when you realize you could have solved stroke when still working; I'll have zero sympathy for your predicanent!
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
Millions of people around the world experience post-stroke hemiparesis, making it difficult to move one side of the body. Hemiparesis impairs an individual’s muscle strength and coordination which limits gait speed, efficiency, and endurance and contributes to reduced community participation. These limitations in strength and control also negatively impact balance, leading to a high prevalence of instability, falls, and fall-related injuries. Assistive technologies like powered exoskeletons that apply torques to the hips in the sagittal plane (hip flexion and extension) and frontal plane (hip abduction and adduction) may benefit both gait efficiency and stability in hemiparetic populations.
Methods
In this study, we investigate the impact of exoskeleton-delivered frontal and sagittal plane hip torque in eight individuals with hemiparesis. Participants completed two-minute walking bouts on an instrumented treadmill with no exoskeleton, and then with the exoskeleton applying phase-based flexion and extension assistance. They then completed a series of abduction torque trials, in which they walked with the exoskeleton-supplied sagittal-plane assistance for 10 strides, and then sagittal-plane assistance and constant abduction torque for 10 strides. The abduction torque series consisted of four levels of abduction torque, each repeated 5 times, in random order.
Results
Compared to steady-state walking without the exoskeleton, the application of sagittal plane torques significantly increased propulsive forces at push-off for the non-paretic limb by 0.83 ± 0.32% BW (p = 0.0373) and had little impact on step width or margin of stability. In the transient period following onset, hip abduction torques significantly increased step width by 0.053 ± 0.011 m (adjusted p < 0.025) and margin of stability for the paretic and non-paretic limb by 0.039 ± 0.006 m (adjusted p < 0.025) and 0.014 ± 0.004 m (adjusted p = 0.01), respectively. These outcomes are correlated with the level of abduction assistance.
Conclusion
These results provide initial evidence supporting the use of a hip exoskeleton to impact foot placement, margin of stability, and propulsion in individuals with hemiparesis, which may benefit both gait efficiency and stability.
A self-administered, in-home, finger-stick blood test detected Alzheimer's disease (AD) biomarkers that correlated with cognitive performance in older adults — a finding that could open the door to large-scale dementia risk screening outside of clinical settings.
The cross-sectional observational validation study of 174 participants (mean age, 66 years; 54% female) showed capillary blood levels of p-tau217 correlated with episodic memory, attention, and executive function, while glial fibrillary acidic protein (GFAP) correlated with working memory and executive function, as measured by computerized cognitive tests.
When researchers combined the p-tau217 results with composite memory scores, they identified a high-risk group — about 9% of participants — who performed significantly worse across cognitive and functional measures.
The approach is designed to move AD biomarker testing out of specialist clinics and into the community, where most people with early cognitive concerns are never evaluated.
"This is the whole reason for doing the capillary blood sampling — to allow it to be scalable, to allow it to be done at a community level, which is where it's likely to be most usefully employed," study investigator Anne Corbett, PhD, professor in dementia research at the University of Exeter Medical School, Exeter, England, told Medscape Medical News.
The study builds on the DROP-AD trial, which validated capillary blood sampling for AD biomarkers in 337 participants.
As reported previously by Medscape Medical News, that study demonstrated strong concordance between capillary and venous samples — but collection was still supervised in clinical settings. In the current study, participants collected samples entirely at home and returned them by mail.
In the UK, only 1 in 1000 people with early cognitive decline receive a specialist evaluation. Corbett said the study deliberately set its memory threshold at 1 SD below age-matched norms — milder than the 1.5 SD cutoff for mild cognitive impairment — to catch people earlier in the disease course.
"When you look at the new generation of disease-targeted treatments, they are looking for preclinical mild cognitive impairment with biomarkers," she said. "That's even more relevant in the US, where some of these drugs are already in use."
Participants were either cognitively normal (n = 146) or had mild to moderate dementia (n = 28). Each collected 70 μL of capillary blood using a Capitainer dried blood spot device. Cards were dried at room temperature and mailed without cooling.
Capillary p-tau217 correlated with episodic memory (r = 0.299; P < .001), attention (r = 0.197; P = .019), and executive function (r = 0.191; P = .021). GFAP correlated with working memory (r = 0.183; P = .034) and executive function (r = 0.182; P = .046).
Both biomarkers discriminated between participants with and without dementia, though with modest accuracy (p-tau217 AUC = 0.656, P = .012; GFAP AUC = 0.688, P < .001). The high-risk group identified through the dual-threshold approach showed large effect sizes across cognitive and functional domains (Cohen d > 1.0).
In a subgroup of 40 participants with paired venous samples, capillary-venous correlations were strong (p-tau217: r = 0.711-0.743; GFAP: r = 0.700-0.790).
An unexpected finding was that only 6% of participants were positive for both biomarkers. GFAP-positive participants were nearly five times more likely to report a history of heart disease (odds ratio, 4.14; P = .016), while p-tau217 positivity had no cardiovascular association, suggesting the two markers may identify distinct at-risk populations.
"We didn't expect quite such a separation," Corbett said. She described the finding as exploratory and said her group planned to examine whether the two groups showed different cognitive trajectories.
Corbett estimated a timeline of 4 to 5 years before the approach could enter clinical pathways and said her group was launching a study this summer to prototype the technology in a real-world NHS context.
Foundational Research
Commenting for Medscape Medical News, Suzanne Schindler, MD, PhD, associate professor of neurology at Washington University School of Medicine, St. Louis, Missouri, said the study addressed a real problem but that the data supported feasibility, not clinical readiness.
"This isn’t ready for clinical practice, but it's laying groundwork for future studies," Schindler said.
She noted the cohort lacked a dedicated mild cognitive impairment (MCI) group, making it difficult to assess the tool's effectiveness in a population it seemed designed to reach. "They likely will be able to identify some of the individuals at highest risk and lowest risk, but there's going to be a lot of people that aren't stratified," said Schindler, who was not involved in the study. "It has value for the extremes, but for those folks in the middle, it's not going to stratify them."
Schindler differentiated this approach from a previous direct-to-consumer blood biomarker test by Quest Diagnostics that drew criticism for high false-positive rates. That test used the amyloid-beta 42-to-40 ratio, which was less specific, and was framed as a clinical tool. The current study's higher-specificity cutoff and triaging framing made it less concerning, she said.
She noted that blood biomarker testing is recommended only for symptomatic individuals, in part because approved treatments target people who already have cognitive impairment. But trials are underway testing anti-amyloid therapies in people with no symptoms.
"If that happens, we will then have a need to screen people who are cognitively unimpaired," she said, a scenario that would make scalable, home-based testing far more urgent.
Marwan Sabbagh, MD, professor of neurology and Moreno Family Chair for Alzheimer's Research at the Barrow Neurological Institute, Phoenix, Arizona, who was also not involved in the research, said the sample needed to be much larger and more diverse. "You need a bigger spread. … You need more MCI," Sabbagh told Medscape Medical News.
But Sabbagh did see major potential in getting at-risk individuals into the clinical pathway more quickly than what’s traditionally done.
"A typical 70-year-old goes to primary care, and primary care may or may not screen them, may or may not evaluate them, and may or may not refer them," he said. Capillary testing could compress that timeline dramatically — flagging at-risk individuals through an online cognitive test, sending a kit in the mail, and returning a result in days rather than months.
He added that capillary testing could eventually replace venous plasma testing as a gating mechanism before PET scans, but he said the field was not ready for a direct-to-consumer model.
"This could become part of the annual Medicare wellness visit," Sabbagh said. "I'm not sure we're ready to jump to a direct-to-consumer model."
The study was funded by the National Institute for Health and Care Research Invention for Innovation program and the NIHR Exeter Biomedical Research Centre. Disclosure information for study authors is available in the original study publication. Schindler reported no relevant financial relationships.
Can you walk while successfully doing another activity at the same time?
Known as dual-task gait performance, a 2023 paper found struggling to do this has been linked to a risk of falls and cognitive decline in adults aged 65 and over.
The researchers found that most people begin to struggle with the test in their 60s, and that after that point, participants’ cognitive health seemed to influence their performance most.
Another paper suggested a dual-task gait test could help to predict cognitive impairment better than single-task gait speed measurement.
But what is a dual-task gait test, and why might it matter? Here’s what Dr Donald Grant, a GP and senior clinical advisor at The Independent Pharmacy, told us.
What are dual-task gait tests?
These involve walking while doing another activity at the same time (hence the “dual” task). Often, the second task is distracting, e.g. counting back from 1,000 in sevens.
What do dual-task gait speeds say about how a person is ageing?
We know that older adults’ gait, or walking style and speed, can say a lot about how they’re ageing.
But when you add a cognitive or physical distraction to that, Dr Grant said, dual task walking tests “can give us a useful insight into how an individual’s brain and body are working together”.
He added: “As we age, our cognitive abilities can be impacted, making these tasks less automatic, requiring more active thinking.
“When people start to struggle with dual-task examinations, it could indicate cognitive ageing, which is perfectly natural as people get older. This means it can become more challenging to divide attention between thinking and movement simultaneously, which may increase people’s risk of falls.”
The doctor said “walking is more than a physical movement” as it requires clear thinking, coordination and strong mobility, “so dual task tests can help identify any early signs of concern”.
Dual-task walking tests are only one way to gauge how an individual is ageing
Despite being a “great functional assessment tool, as they accurately measure how well a person can perform everyday tasks simultaneously,” Dr Grant said dual-task walking tests aren’t the be-all and end-all.
“These walking tests can provide a good snapshot of overall health, but they’re never used to actively diagnose potential health concerns. They can help form part of a larger assessment, allowing medical professionals to better understand an individual’s mobility and cognitive abilities,” he said.
But to measure ageing, GPs tend to look at a combination of factors, such as pre-existing health conditions, physical function and cognitive abilities, he added
The expert ended: “Simple observations, such as memory tests, plus speed, balance or mobility examinations, can all help build a picture of how someone is functioning day to day.”
You need this testing post stroke so your
competent? doctor can initiate dementia prevention protocols! Your
doctor doesn't have them? Tough luck, you were handed an incompetent
doctor!
Send
me hate mail on this: oc1dean@gmail.com. I'll print your complete
statement with your nameand title(If you can't stand by your name don't bother replying anonymously) and my response in my blog. Or are you afraid
to engage with my stroke-addled mind? I would like to know why you
haven't created dementia prevention protocols, and what is your definition of
competence in stroke? Swearing at me is allowed, I'll return the favor.
With your chances of getting dementia post stroke, your competent?
doctor needs to be monitoring this and provide dementia prevention
solutions. Over a decade to accomplish that! Was it done? NO? So, you DON'T have a functioning stroke doctor, do you? YOUR DOCTOR IS RESPONSIBLE FOR PREVENTING THIS!
Dr David Vauzour, lead researcher of the paper published in Gut Microbes, said: “Even in people who had only just begun noticing mild memory changes, there were clear shifts in both their gut bacteria and the metabolites they release into the bloodstream”.
What might gut changes say about dementia risk?
The researchers looked at stool samples from 150 adults aged 50 and over. Some were healthy, while others had mild cognitive impairment (MCI), sometimes seen as a precursor to dementia.
There was also a third group of people who performed normally on cognitive tests but who said they felt like something “wasn’t quite right” with their memory or cognition.
All participants gave the researchers both fasting blood samples (which were used to identify 33 key molecules made in our gut) and stool samples (used to identify the gut bacteria of participants).
“We explored whether specific combinations of these gut and diet-derived chemicals could separate the healthy from those experiencing early cognitive decline,” Dr Vazour said.
“What we found was really striking. Even in people who had only just begun noticing mild memory changes, there were clear shifts in both their gut bacteria and the metabolites they release into the bloodstream.”
They built a machine-learning model on just six of these metabolites. It was able to classify people into the three groups with 79% accuracy, and could tell cognitively healthy adults apart from those with mild cognitive impairment with over 80% accuracy.
The chemical changes seen in participants’ blood samples seemed to be linked to the bacteria present (or absent) in their stool, which Dr Vaxour said adds “weight to growing evidence that the so‑called gut–brain axis ― the communication network between our digestive system and the brain ― may play an important role in cognitive ageing”.
Researchers hope to use these findings to build a diagnostic tool
The study’s co-author, Dr Simon McArthur from Queen Mary University of London, has high hopes for the findings.
“While we’re not yet at the point of providing a diagnostic test, our work suggests we may be able to use dietary and microbial information to help catch the presence of dementia earlier in life, potentially even before significant brain damage has occurred,” he said.
“We hope this work will pave the way for simple, non-invasive blood tests capable of identifying people at higher risk of memory decline years before dementia is typically diagnosed.”
For his part, Dr Vauzor added, “If particular gut bacteria or the chemicals they produce contribute to early cognitive decline, treatments involving diet, probiotics, microbiome‑based therapies, or personalised nutrition could one day form part of dementia prevention strategies.” However, writing for the Science Media Centre, Prof Eef Hogervorst, a Professor of Biological Psychology at Loughborough University, wasn’t as convinced.
He said, “It is an interesting finding and a very well-written paper with good theory and impressive statistical analyses, but with small groups and no follow-up, I think the conclusion that this can be an early diagnostic marker for cognitive decline and even dementia may be a little overstated.”
Are your doctor and hospital competent? enough to ensure human testing occurs? If you don't get it started now your grandchildren won't get the benefits on their stroke recovery.
Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand action! You do know incompetent doctors and hospitals can be fired!
Summary: Researchers developed a groundbreaking technology called LinCx, a custom-built biological “wire” designed to bypass broken or disrupted brain connections.
The study demonstrates a method for creating precise electrical synapses between specific neurons, offering a potential alternative to long-term medication or external brain stimulation for treating neurological disorders.Key Research Findings
Cellular Precision: Unlike drugs or broad electrical stimulation that affect large populations of cells, LinCx allows for the creation of new electrical connections between carefully chosen, individual neurons.
The “Bypass” Mechanism: Instead of repairing damaged synapses, the technology installs a new electrical “bypass” between neurons, strengthening communication without modifying existing native connections.
Protein Engineering: The “wires” are based on engineered proteins from fish that naturally form electrical synapses. These molecules are redesigned to dock only with a specific engineered partner, preventing unintended connections with native brain proteins.
Behavioral Impact:
In Mice: Targeted connections strengthened communication within specific circuits, reshaped brain-wide activity, and altered social interactions and stress responses.
In Worms: The addition of new connections successfully altered temperature-seeking behaviors.
Closing the Gap: LinCx overcomes the limitations of prior tools—like optogenetics—which often require external stimulation or result in unintended “crosstalk” between cell types.
Source: Duke University
Broken or disrupted circuits in the brain contribute to many neurological disorders. A new custom-built biological “wire” developed at Duke University School of Medicine points the way toward a new treatment approach — bypassing broken brain connections, rather than relying on long-term medication or external stimulation.Researchers led by Kafui Dzirasa, MD, PhD, developed a technology called LinCx that allows scientists to create new electrical connections between carefully chosen neurons. Unlike existing tools that often influence many cells at once, this approach enables selective, long‑lasting changes in how defined brain circuits function.
The LinCx technology creates a selective electrical bypass between defined neurons, allowing for long-lasting changes in brain circuit function without external hardware. Credit: Neuroscience NewsThe study is published in Nature on May 13, 2026.
“By introducing a way to plug in new electrical connections with cellular‑level precision, our study marks a major step forward in the ability to edit brain circuitry and understand how neural networks give rise to behavior,“ said Dzirasa, the A. Eugene and Marie Washington Presidential Distinguished Professor of Psychiatry & Behavioral Sciences, Behavioral Medicine & Neurosciences.
Rather than repairing faulty synapses, the technique installs a new electrical “bypass” between specific neurons, strengthening communication without directly modifying existing connections.
The technology is based on proteins originally found in fish that naturally form electrical synapses. Using protein engineering, the researchers redesigned these molecules so they dock only with a matching engineered partner and not with native brain proteins. Laboratory screening, including a newly developed fluorescence‑based assay, identified pairs with high specificity that reliably passed electrical signals between cells.
In mice, targeted electrical connections strengthened communication within specific circuits, reshaped brain‑wide activity patterns, and produced measurable changes in behavior, including social interaction and stress responses.
The team demonstrated the system’s versatility in both worms and mice. In worms, adding new connections altered temperature‑seeking behavior. In mice, targeted electrical connections strengthened communication within specific circuits, reshaped brain‑wide activity patterns, and produced measurable changes in behavior, including social interaction and stress responses.
“For decades, neuroscience has lacked tools that can precisely control communication between specific cell types,” Dzirasa said.Drugs, electrical stimulation, and optogenetics typically affect broad populations of cells, while prior attempts to use electrical synapses often resulted in unintended connections. LinCx overcomes these limitations and may be able to improve on these tools without requiring external stimulation.
“We will next test whether LinCx is powerful enough to override synaptic deficits induced by lifelong genetic disruptions,” he said.
Other Duke authors: Elizabeth Ransey, Gwenaëlle E. Thomas, Ryan Bowman, Elise Adamson, Kathryn K. Walder-Christensen, Hannah Schwennesen, Caly Ferguson, Stephen D. Mague, Nenad Bursac.
Funding: The Burroughs Wellcome Fund, the Ernest E. Just Life Science Institute, the Hartwell Foundation, Hope for Depression Research Foundation, Howard Hughes Medical Institute, and the National Institutes of Health.
Key Questions Answered:
Q: How do you “plug in” a new wire in a living brain?
A: Scientists use protein engineering to create matching molecular “partners.” When these proteins meet at specific neurons, they dock together to form a functional electrical bridge (an electrical synapse) that allows signals to pass directly between the cells.
Q: Could this be used to “re-wire” human personalities?
A: While the study showed changes in social and stress behaviors in mice, the immediate goal is medical: overriding the synaptic deficits caused by genetic disruptions or neurological disorders. The precision of the tool is designed to restore healthy function rather than arbitrarily “edit” traits.
Q: Will this replace brain implants like Deep Brain Stimulation (DBS)?
A: It points toward a future where we don’t need external electrodes or hardware. Because LinCx is a purely biological intervention, it could potentially treat broken circuits internally and permanently.Editorial Notes:
This article was edited by a Neuroscience News editor.
Journal paper reviewed in full.
Additional context added by our staff.
About this neurotech research news
Author: Fedor Kossakovski Source: Duke University Contact: Fedor Kossakovski – Duke University Image: The image is credited to Neuroscience News
Original Research: Open access. “Long-term editing of brain circuits using an engineered electrical synapse” by Elizabeth Ransey, Gwenaëlle E. Thomas, Elias M. Wisdom, Agustin Almoril-Porras, Ryan Bowman, Elise Adamson, Kathryn K. Walder-Christensen, Jesse A. White, Dalton N. Hughes, Hannah Schwennesen, Caly Ferguson, Kay M. Tye, Stephen D. Mague, Longgang Niu, Zhao-Wen Wang, Daniel Colón-Ramos, Rainbo Hultman, Nenad Bursac & Kafui Dzirasa. Nature DOI:10.1038/s41586-026-10501-y
