Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective 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.

Showing posts with label nonrepeatable. Show all posts
Showing posts with label nonrepeatable. Show all posts

Sunday, December 28, 2025

Engineered Protein Reveals Hidden Incoming Signals Between Neurons

 

 Haven't our competent? stroke researchers already put together various methods of listening in on neuron signals? How else are we going to make neuroplasticity repeatable unless we know the signals sent between neurons?

But the stroke leaders would already have ensured that listening to brain signals using one of these already occurs. Add sarcasm tag here.

1. Use nanowires to listen in on single neurons

2. Or lay a grid across the cortex to listen in.

3. Electronic tattoo decodes brainwaves January 2025

But we have NO stroke leaders, nothing will get done until we get survivors in charge.

Leaders solve problems, they don't run away from them.

The latest here:

Engineered Protein Reveals Hidden Incoming Signals Between Neurons

Summary: Researchers have engineered a next-generation glutamate sensor, iGluSnFR4, capable of detecting the faintest incoming synaptic signals between neurons—signals that, until now, have been nearly impossible to record in living brain tissue. By capturing these whisper-quiet inputs, scientists can finally observe how neurons weigh thousands of glutamate messages and transform them into an electrical output, the core computation behind memory, learning, and emotion.

This breakthrough opens new paths for studying disorders marked by disrupted glutamate signaling and gives researchers a powerful tool to test how potential therapies actually affect synaptic communication. The work represents a major step toward decoding the brain’s internal language and mapping how neural circuits truly operate.

Key Facts

  • New Input Detection: iGluSnFR4 is the first protein sensor sensitive enough to reliably record incoming glutamate signals at single synapses in real time.
  • Decoding Computation: The sensor reveals how neurons integrate thousands of chemical inputs to generate electrical output, illuminating core neural computations.
  • Disease Impact: Disorders such as Alzheimer’s, autism, schizophrenia, and epilepsy involve disrupted glutamate signaling; this tool provides a way to pinpoint those disruptions directly in neural circuits.

Source: Allen Institute

Scientists have engineered a protein able to record the incoming chemical signals of brain cells (as opposed to just their outgoing signals).

These whisper-quiet incoming messages are the release of the neurotransmitter glutamate, which plays a critical role in how brain cells communicate with one another but until now has been extremely difficult to capture.

Why it matters

  • Understanding the brain’s code: Scientists can now study how neurons compute—how they take thousands of input signals and—based off those—produce an output signal that could underlie decision, thought, or memory, decoding long-held mysteries about the brain.
  • New avenues for disease research: Disrupted glutamate signaling is linked to Alzheimer’s, schizophrenia, autism, epilepsy, and more. These sensors could help uncover the root causes of these conditions.
  • Smarter drug development: Drug companies can test how new treatments affect actual synaptic activity—speeding up the search for better therapies.

The special protein that researchers at the Allen Institute and HHMI’s Janelia Research Campus have engineered is a molecular “glutamate indicator” called iGluSnFR4 (pronounced ‘glue sniffer’).

It’s sensitive enough to detect the faintest incoming signals between neurons in the brain, offering a new way to decipher and interpret their complex cascade of electrical activity that underpins learning, memory, and emotion.

iGluSnFR4 could help decode the hidden language of the brain and deepen our understanding of how its complex circuitry works. This discovery allows researchers to watch neurons in the brain communicate in real time. 

The findings have just been published in Nature Methods and could transform how neuroscience research is done as it pertains to measuring and analyzing neural activity.

The brain’s hidden language uncovered

To understand the significance of this discovery, it helps to understand how the brain works: billions of neurons “talk” to each other by sending pulses of electricity down their branch-like axons.

When the electrical signals reach the end of the axons, they can’t jump the gap to the next brain cell, known as a synapse. Instead, they trigger the release of chemical messengers called neurotransmitters (glutamate being the most common and critical for memory, learning, and emotion) into the synapse that causes the next brain cell to fire in sequence.

It’s like a row of falling dominos, but vastly more complex: Each neuron receives inputs from thousands of other neurons, and specific patterns and combinations of those input neurons firing is what makes the next (receiving) neuron fire. With this new discovery, scientists can now identify the critical patterns and combinations of input neuron activity that cause the next neurons to fire. 

Until now, detecting these incoming signals in living brain tissue was nearly impossible. Older technologies were either too slow or not sensitive enough to pick up the action at the single-synapse level. Now researchers can hear the entire conversation rather than fragments of it.

“It’s like reading a book with all the words scrambled and not understanding the order of the words or how they’re arranged,” said Kaspar Podgorski, Ph.D., a lead author on the study and senior scientist at the Allen Institute.

“I feel like what we’re doing here is adding the connections between those neurons and by doing that, we now understand the order of the words on the pages, and what they mean.”

Before these protein sensors existed, researchers could only record the outgoing signals from brain cells, leaving half of the communications equation (the cells’ inputs) a mystery. The incoming signals were always too faint and fast to capture, until now.

“Neuroscientists have pretty good ways of measuring structural connections between neurons, and in separate experiments, we can measure what some of the neurons in the brain are saying, but we haven’t been good at combining these two kinds of information. It’s hard to measure what neurons are saying to which other neurons,” said Podgorski.

“What we have invented here is a way of measuring information that comes into neurons from different sources, and that’s been a critical part missing from neuroscience research.”

“The success of iGluSnFR4 stems from our close collaboration started at HHMI’s Janelia Research Campus between the GENIE Project team and Kaspar’s lab. That research has extended to the phenomenal in vivo characterization work done by the Allen Institute’s Neural Dynamics group,” said Jeremy Hasseman, Ph.D., a scientist with HHMI’s Janelia Research Campus.

“This was a great example of collaboration across labs and institutes to enable new discoveries in neuroscience.”

This discovery removes a significant barrier in modern neuroscience: the inability to clearly monitor and make sense of how brain cells receive information. With this powerful new tool available to researchers through Addgene, some of the brain’s deepest mysteries may soon be revealed.

Key Questions Answered:

Q: What breakthrough did scientists achieve with iGluSnFR4?

A: They engineered a protein sensor sensitive enough to record neurons’ incoming glutamate signals in real time, something previously impossible in living brain tissue.

Q: Why does capturing incoming signals matter for understanding the brain?

A: Incoming synaptic inputs determine how neurons compute and decide whether to fire, giving researchers access to the patterns that underlie learning, memory, emotion, and decision-making.

Q: How could this change disease research and drug development?

A: Because disrupted glutamate signaling is implicated in disorders like Alzheimer’s, autism, schizophrenia, and epilepsy, this sensor lets scientists directly observe synaptic dysfunction and test how treatments alter real neural communication.

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 and neuroscience research news

Author: Peter Kim
Source: Allen Institute
Contact: Peter Kim – Allen Institute
Image: The image is credited to Neuroscience News

Original Research: Open access.
Glutamate indicators with increased sensitivity and tailored deactivation rates” by Kaspar Podgorski et al. Nature Methods


Saturday, September 23, 2017

Agreed Definitions and a Shared Vision for New Standards in Stroke Recovery Research: The Stroke Recovery and Rehabilitation Roundtable Taskforce

I still don't see this as helping because they could agree on using the Rankin scale which has zero objectivity. I see the need for objective damage diagnosis like 3d scans of the dead and damaged areas mapped to external disabilities.  Until we get to those two points none of this stroke research is repeatable. You can have 9 different reasons for the same external disability and there is no way one intervention will correct all nine. And since they are hiding the paper behind a paywall, we can't tell how bad it is and get our non-existent stroke leadership to correct it.
1. Penumbra damage to the motor cortex.
2. Dead brain in the motor cortex.
3. Penumbra damage in the pre-motor cortex.
4. Dead brain in the pre-motor cortex.
5. Penumbra damage in the executive control area.
6. Dead brain in the executive control area.
7. Penumbra damage in the white matter underlying any of these three.
8. Dead brain in the white matter underlying any of these three.
9. Spasticity preventing movement from occurring.
http://journals.sagepub.com/doi/abs/10.1177/1545968317732668
First Published September 21, 2017 Research Article


The first Stroke Recovery and Rehabilitation Roundtable established a game changing set of new standards for stroke recovery research. Common language and definitions were required to develop an agreed framework spanning the four working groups: translation of basic science, biomarkers of stroke recovery, measurement in clinical trials and intervention development and reporting. This paper outlines the working definitions established by our group and an agreed vision for accelerating progress in stroke recovery research.

Saturday, August 26, 2017

Examining a new functional electrical stimulation therapy with people with severe upper extremity hemiparesis and chronic stroke: A feasibility study

No clue what the objective diagnosis of impairment was so this research is impossible to repeat. What a waste.  Fugl-Meyer is uselessly subjective and has zero discrimination. Chedoke-McMaster has exactly the same problems. Some day there will objective 3d measurements of dead and damaged areas, only then will research become repeatable. Can't tell if any patients had spasticity.
http://journals.sagepub.com/doi/abs/10.1177/0308022617719807
First Published August 21, 2017 Research Article



Upper extremity impairment post-stroke is common and results in decreased occupational engagement. For those with chronic stroke and severe hemiparesis, few treatment options are available. MyndMove™ is a functional electrical stimulation technology programmed to stimulate up to eight muscle groups in reach and grip patterns. A pre–post, cohort, feasibility study was conducted to inform the design of a randomized controlled trial examining the effectiveness of MyndMove™ therapy.

Individuals enrolled had chronic severe upper extremity hemiparesis following a stroke (> 6 months) with Chedoke-McMaster Stroke Assessment Stage 1–2 (arm and hand) and a Fugl-Meyer Upper Extremity score less than 19. Treatment with Myndmove™, consisting of 20 one-hour sessions, 3–5 times per week over 4–6 weeks was provided.

Of 25 enrolled participants, 24 (96%) completed treatment. Fifty-eight percent (14/24) of the participants demonstrated improvement equal to or exceeding the minimal clinically important difference of five on the Fugl-Meyer Upper Extremity test. Mean change from baseline Fugl-Meyer Upper Extremity overall score was 7.1 (SD 5.0) (p < 0.001). Mean time to complete treatment was 40 days (SD 6.0).

MyndMove™ therapy is feasible to deliver within outpatient settings and may be a suitable function-based treatment option for severe chronic stroke upper extremity impairment.

Tuesday, August 15, 2017

Effect of Core Stability Training on Trunk Function, Standing Balance, and Mobility in Stroke Patients

I see nothing here that suggests they used any type of repeatable protocol or had objective diagnosis of deficits prior to starting.  As such this research is worthless,  being nonrepeatable
http://journals.sagepub.com/doi/full/10.1177/1545968316675431#articleShareContainer

A Randomized Controlled Trial

First Published November 7, 2016 Research Article


Background. Trunk function is important for standing balance, mobility, and functional outcome after stroke, but few studies have evaluated the effects of exercises aimed at improving core stability in stroke patients.  
Objective. To investigate the effectiveness of core stability training on trunk function, standing balance, and mobility in stroke patients.  
Methods. An assessor-blinded, randomized controlled trial was undertaken in a stroke rehabilitation ward, with 32 participants randomly assigned to an experimental group or a control group (n = 16 each). The experimental group received 400 minutes of core stability training in place of conventional programs within total training time, while the control group received only conventional programs. Primary outcome measures were evaluated using the Trunk Impairment Scale (TIS), which reflects trunk function. Secondary outcome measures were evaluated by pelvic tilt active range of motion in the sagittal plane, the Balance Evaluation Systems Test–brief version (Brief-BESTest), Functional Reach test, Timed Up-and-Go test (TUG), and Functional Ambulation Categories (FAC). A general linear repeated-measures model was used to analyze the results.  
Results. A treatment effect was found for the experimental group on the dynamic balance subscale and total score of the TIS (P = .002 and P < .001, respectively), pelvic tilt active range of motion (P < .001), Brief-BESTest (P < .001), TUG (P = .008), and FAC (P = .022).  
Conclusions. Core stability training has beneficial effects on trunk function, standing balance, and mobility in stroke patients. Our findings might provide support for introducing core stability training in stroke rehabilitation.

Saturday, December 24, 2016

Promoting Therapists’ Use of Motor Learning Strategies within Virtual Reality-Based Stroke Rehabilitation

Well fuck, with any smarts at all these therapists would be pointing to a stroke protocol they are using for this and how the efficacy was. Without a protocol, none of this research is repeatable.
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0168311


Abstract

Purpose

Therapists use motor learning strategies (MLSs) to structure practice conditions within stroke rehabilitation. Virtual reality (VR)-based rehabilitation is an MLS-oriented stroke intervention, yet little support exists to assist therapists in integrating MLSs with VR system use.

Method

A pre-post design evaluated a knowledge translation (KT) intervention incorporating interactive e-learning and practice, in which 11 therapists learned how to integrate MLSs within VR-based therapy. Self-report and observer-rated outcome measures evaluated therapists’ confidence, clinical reasoning and behaviour with respect to MLS use. A focus group captured therapists’ perspectives on MLS use during VR-based therapy provision.

Results

The intervention improved self-reported confidence about MLS use as measured by confidence ratings (p <0.001). Chart-Stimulated Recall indicated a moderate level of competency in therapists’ clinical reasoning about MLSs following the intervention, with no changes following additional opportunities to use VR (p = .944). On the Motor Learning Strategy Rating Instrument, no behaviour change with respect to MLS use was noted (p = 0.092). Therapists favoured the strategy of transferring skills from VR to real-life tasks over employing a more comprehensive MLS approach.

Conclusion

The KT intervention improved therapists’ confidence but did not have an effect on clinical reasoning or behaviour with regard to MLS use during VR-based therapy.