New brain imaging technique offers hope for better stroke rehabilitation

 Which means the followup research needs to be how to get dendritic branching and axon pathfinding going to reconnect the areas of the brain. WHOM IS GOING TO DO THAT?

axon pathfinding (42 posts to March 2012)

dendritic branching (42 posts to February 2012)

Doesn't anyone in stroke have two functioning neurons to see the path forward to survivor recovery except for me?

The latest here:

New brain imaging technique offers hope for better stroke rehabilitation

• Download PDF Copy

 Reviewed

Georgetown University Medical CenterMar 3 2025

A new Georgetown University Medical Center study in collaboration with MedStar Health and the National Institutes of Health exploring a new brain imaging technique is bringing stroke experts a step closer to better tailoring rehabilitation.

Neurologists often use MRI images of the brain's white matter to glean information about a person's ability to recover, but a new imaging technique added to MRI allows clinicians to better see the condition of white matter tracts leading to the limbs, an observation usually only seen after death during an autopsy.

A white matter tract called the corticospinal tract provides the main wiring that goes from your brain down to your spinal cord to help power your arms and legs. If those cables are severed or atrophied, the person is not going to be able to regain meaningful use of their arms and legs – they wouldn't have much motor strength."

Matthew A. Edwardson, MD, study leader, associate professor of neurology at Georgetown University School of Medicine and vascular neurologist and a member of the stroke team atMedStar Georgetown University Hospital

The imaging technique used by Edwardson and his colleagues is called diffusion tensor-based morphometry (DTBM). It combines directional information about the structures in the brain with the shape and size of the structures being imaged. Previously it was difficult to separate the white matter cables from the gray matter using morphometry approaches because they did not include the directional information. This two-part technique allows researchers to map and quantify changes over time in the white matter tracts.

"To our knowledge, this is the first study to allow us to measure atrophy of these tracts in stroke survivors," says Edwardson, a member of the Center for Brain Plasticity and Recovery, a joint collaboration between Georgetown University and MedStar National Rehabilitation Network.

He and colleagues from the National Institutes of Health (NIH) describe their findings in March 3, 2025 in the journal Neurology ("Association between changes in white matter volume detected with diffusion tensor-based morphometry and motor recovery after stroke").

"Now, we can see if the cables have shrunk in size which would indicate that a stroke has caused enough damage to the brain to lead to the wiring becoming atrophied," says Edwardson. "That observation is strongly correlated with how well somebody will recover. If there's a lot of atrophy in the brain in those cables, they're not going to have much ability to recover their arm function after a stroke."

Spectroscopy Applications in the Environment eBook eBook Compilation of the top interviews, articles, and news in the last year. Download the latest edition

Edwardson says further studies would be needed before the observations could be used to tailor stroke rehabilitation.

"It would be helpful for the therapist to know at the time of admission to inpatient rehabilitation whether there's some likelihood of their patient regaining function," he says. "If it is determined that the patient isn't likely to recover meaningful motor use, then the therapist could change their strategy to perhaps focus on the unimpaired side with strategies to compensate for the disability."

Along with Edwardson co-authors of the publication are Amritha Nayak, ME, M. Okan Irfanoglu, PhD; and Carlo Pierpaoli, MD, PhD; of NIH's National Institute of Biomedical Imaging and Bioengineering; and . Marie Luby, PhD; and Lawrence L. Latour, PhD; of NIH's National Institute of Neurological Disorders and Stroke.

The authors report having no personal financial interests related to the study.

Funding was received from the National Center for Advancing Translational Sciences (UL1TR000101), and Georgetown's Clinical and Translational Science Award.

Source:

Georgetown University Medical Center

Journal reference:

Edwardson, M. A., et al. (2025) Association Between Changes in White Matter Volume Detected With Diffusion Tensor–Based Morphometry and Motor Recovery After Stroke. Neurology. doi.org/10.1212/WNL.0000000000213408.

New Alzheimer’s Breakthrough Targets Plexin-B1 Protein

 You'll want your competent? doctor to make sure followup research occurs because of your increased risk of dementia post stroke. Do you even have a competent doctor?My definition of competence is having EXACT 100% RECOVERY PROTOCOLS. None of this guideline shit!

Your risk of dementia, has your doctor told you of this?

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018

The latest here:

New Alzheimer’s Breakthrough Targets Plexin-B1 Protein

Summary: Researchers identified a novel way to potentially slow or halt Alzheimer’s progression by targeting the plexin-B1 protein. Their study shows how reactive astrocytes and plexin-B1 play crucial roles in clearing amyloid plaques. This discovery opens new pathways for Alzheimer’s treatments and emphasizes the importance of cellular interactions.

Key Facts:

• Key Protein: Targeting plexin-B1 protein can enhance the brain’s ability to clear amyloid plaques.
• Cellular Interactions: Reactive astrocytes help control the clearance of harmful deposits in the brain.
• Innovative Treatments: The study opens new pathways for developing treatments for Alzheimer’s disease.

Source: Mount Sinai Hospital

Researchers at the Icahn School of Medicine at Mount Sinai have made a significant breakthrough in Alzheimer’s disease research by identifying a novel way to potentially slow down or even halt disease progression.

The study, which focuses on the role of reactive astrocytes and the plexin-B1 protein in Alzheimer’s pathophysiology, provides crucial insights into brain cell communication and opens the door to innovative treatment strategies.

It was published in Nature Neuroscience on May 27. 

The research team emphasizes that while their findings mark a significant advance in the fight against Alzheimer’s, more research is needed to translate these discoveries into treatments for human patients. Credit: Neuroscience News

This groundbreaking work is centered on the manipulation of the plexin-B1 protein to enhance the brain’s ability to clear amyloid plaques, a hallmark of Alzheimer’s disease. Reactive astrocytes, a type of brain cell that becomes activated in response to injury or disease, were found to play a crucial role in this process.

They help control the spacing around amyloid plaques, affecting how other brain cells can access and clear these harmful deposits.

“Our findings offer a promising path for developing new treatments by improving how cells interact with these harmful plaques,” said Roland Friedel, PhD, Associate Professor of Neuroscience, and Neurosurgery, at Icahn Mount Sinai and a senior author of the study.

The research was driven by the analysis of complex data comparing healthy individuals to those with Alzheimer’s, aiming to understand the disease’s molecular and cellular foundations.

Hongyan Zou, PhD, Professor of Neurosurgery, and Neuroscience, at Icahn Mount Sinai and one of the study’s lead authors, highlighted the broader implications of their findings: “Our study opens new pathways for Alzheimer’s research, emphasizing the importance of cellular interactions in developing neurodegenerative disease treatments.”

One of the study’s most significant achievements is its validation of multiscale gene network models of Alzheimer’s disease.

“This study not only confirms one of the most important predictions from our gene network models but also significantly advances our understanding of Alzheimer’s. It lays a solid foundation for developing novel therapeutics targeting such highly predictive network models,” said Bin Zhang, PhD, Willard T.C. Johnson Research Professor of Neurogenetics at Icahn Mount Sinai and one of the study’s lead authors.

By demonstrating the critical role of plexin-B1 in Alzheimer’s disease, the research underscores the potential of targeted therapies to disrupt the disease’s progression.

The research team emphasizes that while their findings mark a significant advance in the fight against Alzheimer’s, more research is needed to translate these discoveries into treatments for human patients.

“Our ultimate goal is to develop treatments that can prevent or slow down Alzheimer’s progression,” Dr. Zhang added, outlining the team’s commitment to further exploring the therapeutic potential of plexin-B1.

Funding: This study is supported by the NIH National Institute on Aging (NIA) grants U01AG046170 and RF1AG057440 and is part of the NIA-led Accelerating Medicines Partnership – Alzheimer’s Disease (AMP-AD) Target Discovery and Preclinical Validation program.

This public private partnership aims to shorten the time between the discovery of potential drug targets and the development of new drugs for Alzheimer’s disease treatment and prevention.

About this Alzheimer’s disease research news

Author: Jennifer Gutierrez
Source: Mount Sinai Hospital
Contact: Jennifer Gutierrez – Mount Sinai Hospital
Image: The image is credited to Neuroscience News

Decoding hand and wrist movement intention from chronic stroke survivors with hemiparesis using a user-friendly, wearable EMG-based neural interface

Are you going to do followup research that will create protocols that deliver wrist and hand recovery? WHY NOT? If not, I'd have you all fired for incompetence! We have to remove a lot of dead wood in stroke, there must be some suitable researchers out there actually trying to solve stroke to 100% recovery, but they are not sticking their necks out for fear of the incompetent leadership in stroke.

Laziness? Incompetence? Or just don't care? NO leadership? NO strategy? Not my job? Not my Problem?

Decoding hand and wrist movement intention from chronic stroke survivors with hemiparesis using a user-friendly, wearable EMG-based neural interface

• Eric C. Meyers,
• David Gabrieli,
• Nick Tacca,
• Lauren Wengerd,
• Michael Darrow,
• Bryan R. Schlink,
• Ian Baumgart &
• David A. Friedenberg 

Journal of NeuroEngineering and Rehabilitation volume 21, Article number: 7 (2024) Cite this article

• Metrics details

Abstract

Objective

Seventy-five percent of stroke survivors, caregivers, and health care professionals (HCP) believe current therapy practices are insufficient, specifically calling out the upper extremity as an area where innovation is needed to develop highly usable prosthetics/orthotics for the stroke population. A promising method for controlling upper extremity technologies is to infer movement intention non-invasively from surface electromyography (EMG). However, existing technologies are often limited to research settings and struggle to meet user needs.

Approach

To address these limitations, we have developed the NeuroLife^® EMG System, an investigational device which consists of a wearable forearm sleeve with 150 embedded electrodes and associated hardware and software to record and decode surface EMG. Here, we demonstrate accurate decoding of 12 functional hand, wrist, and forearm movements in chronic stroke survivors, including multiple types of grasps from participants with varying levels of impairment. We also collected usability data to assess how the system meets user needs to inform future design considerations.

Main results

Our decoding algorithm trained on historical- and within-session data produced an overall accuracy of 77.1 ± 5.6% across 12 movements and rest in stroke participants. For individuals with severe hand impairment, we demonstrate the ability to decode a subset of two fundamental movements and rest at 85.4 ± 6.4% accuracy. In online scenarios, two stroke survivors achieved 91.34 ± 1.53% across three movements and rest, highlighting the potential as a control mechanism for assistive technologies. Feedback from stroke survivors who tested the system indicates that the sleeve’s design meets various user needs, including being comfortable, portable, and lightweight. The sleeve is in a form factor such that it can be used at home without an expert technician and can be worn for multiple hours without discomfort.

Significance

The NeuroLife EMG System represents a platform technology to record and decode high-resolution EMG for the real-time control of assistive devices in a form factor designed to meet user needs. The NeuroLife EMG System is currently limited by U.S. federal law to investigational use.

Introduction

Stroke is a leading cause of long-term disability in the United States, affecting more than 800,000 people per year [1]. Unilateral paralysis (hemiparesis) affects up to 80% of stroke survivors, leaving many to struggle with activities of daily living (ADLs) including the ability to manipulate objects such as doors, utensils, and clothing due to decreased upper-extremity muscle coordination and weakness [2]. Restoration of hand and arm function to improve independence and overall quality of life is a top priority for stroke survivors and caregivers [3]. Intensive physical rehabilitation is the current gold standard for improving motor function after stroke. Unfortunately, 75% of stroke survivors, caregivers, and health care providers report that current upper extremity training practice is insufficient [4]. The development of user-centric neurotechnologies to restore motor function in stroke survivors could address these unmet clinical needs through a range of different mechanisms, such as improving motivation, enhancing neuroplasticity in damaged sensorimotor networks, and enabling at-home therapy.

Assistive technologies (AT) hold potential to restore hand function and independence to individuals with paralysis [5]. ATs, including exoskeletons and functional electrical stimulation (FES), can assist with opening the hand and also evoke grips strong enough to hold and manipulate objects [6]. Additionally, these systems have been used therapeutically during rehabilitation to strengthen damaged neural connections to restore function [7]. A wide variety of mechanisms to control ATs have been investigated including voice [8], switch [9], position sensors [10], electroencephalography (EEG) [11], electrocorticography (ECoG) [12], intracortical microelectrode arrays (MEA) [13], and electromyography (EMG) [14]. Unfortunately, no single system has simultaneously delivered an intuitive, user-friendly system with a high degree-of-freedom (DoF) control for practical use in real-world settings [4].

Recent advances in portable, high-density EMG-based (HDEMG) systems have the potential to overcome several of these barriers and deliver an intuitive and entirely non-invasive AT control solution [15, 16]. While various EMG-based ATs exist, including the commercially available MyoPro Orthosis [15], most of these systems use a small number of electrodes and rely on threshold-based triggering [14]. Consequently, these systems have limited DoF control which constrains their practical use. Conversely, HDEMG systems consisting of dozens of electrodes and leveraging machine learning approaches to infer complex movement intention can provide high DoF control, significantly expanding functional use cases as well as increasing the proportion of the stroke population that could benefit from these technologies [16,17,18,19]. Currently, HDEMG systems are primarily research systems and are not optimized for usability, including being difficult to set up, requiring manual placement of electrodes, and being non-portable and bulky, which can hinder the successful translation of technologies [4].

To address these limitations, we developed the NeuroLife^® EMG System to decode complex forearm motor intention in chronic stroke survivors while simultaneously addressing end user needs. The EMG system was designed to be used as a control device for various end effectors, such as FES systems and exoskeletons. Additionally, the system was specifically designed to meet user needs in domains previously identified as high-value for stroke survivors: donning/doffing simplicity, device setup and initialization, portability, robustness, comfortability, size and weight, and intuitive usage [4]. The sleeve is a wearable garment consisting of up to 150 embedded electrodes that measure muscle activity in the forearm to decode the user’s motor intention. A single zipper on one edge of the sleeve allows for a simplified and streamlined donning and doffing by the user and/or a caregiver. The sleeve design facilitates an intuitive setup process as embedded electrodes that span the entire forearm are consistently placed, eliminating the need for manual electrode placement on specific muscles. The lightweight stretchable fabric, similar to a compression sleeve, was chosen to enhance comfort for long-term use. The sleeve connects to backend Intan hardware housed in a lightweight, 8 × 10″ signal acquisition module appropriate for tabletop upper-extremity rehabilitation. Overall, these design features help address critical usability factors for ATs [4].

In this work, we demonstrate that our EMG system can extract task-specific myoelectric activity at high temporal and spatial resolution to resolve individual movements. Based on EMG data collected from seven individuals with upper extremity hemiparesis due to stroke, trained neural network machine learning models can accurately decode muscle activity in the forearm to infer movement intention, even in the absence of overt motion. We demonstrate the viability of this technique for online decoding, as two subjects used the system for closed-loop control of a virtual hand. This online demonstration is a promising step towards using HDEMG sleeves for high DoF control of ATs based on motor intention. Finally, we present usability data collected from study participants that highlight the user-centric design of the sleeve. These data will be used to inform future developments to deliver an effective EMG-based neural interface that meets end user needs.

More at link.

Groove Rhythm in Exercise Boosts Brain Function

 Does your doctor have enough functioning brain cells to get this research implemented for your benefit?  This also means your competent? doctor has to get you 100% recovered to be able to do aerobic exercises. But first your doctor is required to get this research proven in stroke survivors.

Groove Rhythm in Exercise Boosts Brain Function

Summary: A new study has found that combining aerobic exercise with groove rhythm (GR) music can significantly enhance executive function in the brain.

Conducted with 48 healthy participants aged 18-26, the research revealed that exercising to GR not only increased enjoyment but also activated the left dorsolateral prefrontal cortex (DLPFC) more than standard exercise. Participants who felt their bodies resonate with the GR experienced an elevated sense of excitement and demonstrated improved attention, concentration, and judgment.

This discovery is particularly relevant in Japan, where less than 30% of the population regularly exercises, suggesting that GR-enhanced exercise could offer a more enjoyable and cognitively beneficial approach to fitness.

Key Facts:

1. Exercising to groove rhythm music enhances executive function in the prefrontal cortex.
2. Participants reported increased excitement and body resonance with the rhythm during GR exercise.
3. The study suggests GR-based exercise as a potential tool for improving brain function and making exercise more enjoyable.

Source: University of Tsukuba

Listening to rhythmic music, particularly music with a pronounced groove, elicits a heightened sense of excitement, prompting individuals to instinctively move their bodies in sync with the rhythm. This natural inclination to move in harmony with music is referred to as groove.

Notably, aerobic exercise, even at low-intensity levels, stimulates the dorsolateral prefrontal cortex (DLPFC) of the brain, thereby improving executive functions such as attention, concentration, and judgment.

Building upon previous research, it was discovered that individuals with a high affinity for groove rhythm (GR) experienced increased executive function in the prefrontal cortex simply by listening to GR.

Consequently, the research team explored the potential synergy of combining GR with exercise to amplify the enjoyment and cognitive benefits of physical activity.

In this study, 48 healthy participants aged 18-26 engaged in 3 min of very-light intensity aerobic exercise set to GR. The results revealed that participants who reported their bodies “resonating with the rhythm” during exercise, coupled with a subjective sense of “increased excitement,” demonstrated enhanced executive function in the prefrontal cortex and increased activation in the left DLPFC compared to standard very light-intensity exercise. These results were reasonable considering that music preferences vary among individuals.

In Japan, where less than 30% of the population maintains a regular exercise routine, the development of inclusive exercise programs is crucial. Based on the findings of this research, investigating the impact of groove rhythm-based exercise is expected to introduce “enriched-exercise” as an enjoyable, motivating, and efficient approach for enhancing brain function.

Funding:

This work was supported in part by Japan Society for the Promotion of Science (JSPS) Grant [16H06405 (HS), 18H04081 (HS), and 18J10631 (TF)]; the Japan Science and Technology Agency (JST) Grant [JPMJMI19D5 (HS)]; Meiji Yasuda Life Foundation of Health and Welfare Grant (TF), and a grant from the Advanced Research Initiative for Human High Performance (ARIHHP), University of Tsukuba.

About this music, exercise, and neuroscience research news

Author: KAMOSHITA Kimio
Source: University of Tsukuba
Contact: KAMOSHITA Kimio – University of Tsukuba
Image: The image is credited to Neuroscience News

Inhibition of Notch 1 signaling in the subacute stage after stroke promotes striatal astrocyte-derived neurogenesis

Well shit this was already confirmed in August 2018. Why didn't you do the followup research that would deliver these results in human testing? Your mentors and senior researchers incompetently didn't know about this earlier research and thus didn't instruct you to actually solve the problem for survivors? How many times do I have to point out stroke incompetence before the offending parties are removed?

Inhibition of Notch1 Signaling at the Subacute Stage of Stroke Promotes Endogenous Neurogenesis and Motor Recovery After Stroke August 2018

The latest here:

Inhibition of Notch 1 signaling in the subacute stage after stroke promotes striatal astrocyte-derived neurogenesis

Xiao-Zhu Hao1, Cheng-Feng Sun1, Lu-Yi Lin1, Chan-Chan Li1, Xian-Jing Zhao1, Min Jiang2, Yan-Mei Yang1, *, Zhen-Wei Yao1, *

AbstractInhibition of Notch1 signaling has been shown to promote astrocyte-derived neurogenesis after stroke. To investigate the regulatory role of Notch1 signaling in this process, in this study, we used a rat model of stroke based on middle cerebral artery occlusion and assessed the behavior of reactive astrocytes post-stroke.We used the γ-secretase inhibitor N-[N-(3,5-diuorophenacetyl)-1-alanyl]-S-phenylglycine t-butylester (DAPT) to block Notch1 signaling at 1, 4, and 7 days after injury. Our results showed that only administration of DAPT at 4 days after stroke promoted astrocyte-derived neurogenesis, as manifested by recovery of white matter fiber bundle integrity on magnetic resonance imaging, which is consistent with recovery of neurologic function. These findings suggest that inhibition ofNotch1 signaling at the subacute stage post-stroke mediates neural repair by promoting astrocyte-derived neurogenesis.Key Words: astrocyte; diffusion kurtosis imaging; magnetic resonance imaging; middle cerebral artery occlusion; N-[N-(3,5-diuorophenacetyl)-1-alanyl]-S-phenylglycine t-butylester; neural repair; neurogenesis; neuron; Notch1 signaling; subacute stagehttps://doi.org/10.4103/1673-5374.363179Date of submission: October 18, 2021Date of decision: February 16, 2022Date of acceptance: October 11, 2022Date of web publication: December 21, 2022IntroductionImpaired neural tissue can be supplemented by endogenous neurogenesisafter stroke. One third of endogenous neurogenesis derives from proliferatedsubventricular neural stem cells, and two thirds from striatal reactiveastrocytes, both of which are negatively regulated by Notch1 signaling(Arvidsson et al., 2002; Li et al., 2010). Notch1 signaling exerts various effectsat different times and locations during neurogenesis, which explains theconflicting results from studies involving interventions at different time points;therefore, timely control of Notch1 signaling is important for promoting theproduction of new neurons (Oya et al., 2009; Wang et al., 2009b; Li et al.,2012; Zhao et al., 2012). In our previous study, we found that the number ofneuroblasts increased in the subacute stage after stroke, and that inhibition ofNotch1 signaling during this period with the γ-secretase inhibitor N-[N-(3,5-diuorophenacetyl)-1-alanyl]-S-phenylglycine t-butylester (DAPT) promotedneuroblast and neuron generation (Hao et al., 2018). However, the temporalprofile of Notch1 signaling activity in astrocytes and whether DAPT treatmentin the subacute stage after stroke can promote transdifferentiation ofastrocytes into the neural linage remained unclear.The Notch1 signaling system comprises the Notch1 receptor and the Notch1ligand (Oya et al., 2009; Wang et al., 2009a, b), which receive and send theNotch1 signal, respectively. Astrocytes can concurrently express both theNotch1 receptor and the Notch1 ligand (Lebkuechner et al., 2015). Notch1signaling has been reported to stimulate proliferation and migration ofresident astrocytes in the subventricular zone (SVZ) and striatum into theperi-infarct area after stroke (Shimada et al., 2011). A recent study indicatedthat striatal astrocytes enter the neurogenic program 3 days after stroke, asNotch1 signaling decreases, and that inhibition of Notch1 signaling at thistime point promotes this process (Magnusson et al., 2014). Two other studiesindicated that striatal astrocytes become neuroblasts 1 week after strokeand transdifferentiate into neurons, and that synapses form 2 weeks later(Arvidsson et al., 2002; Duan et al., 2015). Thus, promoting striatal astrocyte-derived neurogenesis through inhibition of Notch1 signaling in the subacutestage after cerebral ischemia is a promising area for investigation.The central nervous system is a complex neural network. Only newbornneurons have been reported to establish new connections and undergomyelination, which would be beneficial effects for the recovery of damagedbrain tissue (Tanaka et al., 2003; Jiang et al., 2006). In vivo imaging toolsneed to be developed to monitor the functional effects of newborn neuronswithin the existing or newly built neural circuitry and their contribution tobrain function after stroke (Deng et al., 2010). Diffusion kurtosis imaging (DKI)parameters, such as mean kurtosis (MK), axial kurtosis (Ka) and radial kurtosis(Kr), provide detailed information about microstructural deformation andreorganization that indirectly illustrates functional recovery (Hao et al., 2018;Shen et al., 2019; Wei et al., 2019).In this study, we first elucidated the temporal profile of both astrocytictransdifferentiation into neurons and Notch1 activation in astrocytes andthen attempted to analyze the effects of DAPT administered at different timepoints on astrocyte-derived neurons. More importantly, we used magneticresonance imaging (MRI) to evaluate neurogenesis-related microstructuralchanges in the damaged brain in vivo.

Beneficial Effect of Astragalosides on Stroke Condition Using PC12 Cells under Oxygen Glucose Deprivation and Reperfusion

 It's been 8 years has your doctors and hospital done nothing to get followup research done in humans?

Do you prefer your  doctor and hospital incompetence NOT KNOWING? OR NOT DOING?

Beneficial Effect of Astragalosides on Stroke Condition Using PC12 Cells under Oxygen Glucose Deprivation and Reperfusion

Published: 08 May 2014

• Bi-Ying Chiu,
• Ching-Ping Chang,
• Jia-Wei Lin,
• Jung-Sheng Yu,
• Wen-Pin Liu,
• Yao-Chin Hsu &
• Mao-Tsun Lin 

Cellular and Molecular Neurobiology volume 34, pages 825–837 (2014)Cite this article

• 851 Accesses

• 33 Citations

• Metrics details

Abstract

Astragalosides (AST) are reported to be neuroprotective in focal cerebral ischemic models in vivo. In this study, the direct effect of AST against oxygen and glucose deprivation (OGD) including neuronal injury and the underlying mechanisms in vitro were investigated. 5 h OGD followed by 24 h of reperfusion [adding back oxygen and glucose (OGD-R)] was used to induce in vitro ischemia reperfusion injury in differentiated rat pheochromocytoma PC12 cells. AST (1, 100, and 200 µg/mL) were added to the culture after 5 h of the OGD ischemic insult and was present during the reoxygenation phases. A key finding was that OGD-R decreased cell viability, increased lactate dehydrogenase, increased reactive oxygen species, apoptosis, autophagy, functional impairment of mitochondria, and endoplasmic reticulum stress in PC12 cells, all of which AST treatment significantly reduced. In addition, AST attenuated OGD-R-induced cell loss through P38 MAPK activation a neuroprotective effect blunted by SB203580, a specific inhibitor of P38 MAPK. Our data suggest that both apoptosis and autophagy are important characteristics of OGD-R-induced PC12 death and that treating PC12 cells with AST blocked OGD-R-induced apoptosis and autophagy by suppressing intracellular oxidative stress, functional impairment of mitochondria, and endoplasmic reticulum stress. Our data provide identification of AST that can concomitantly inhibit multiple cells death pathways following OGD injuries in neural cells.

This is a preview of subscription content, access via your institution.

 

An Unexplored Role for MMP-7 (Matrix Metalloproteinase-7) in Promoting Gut Permeability After Ischemic Stroke

 WHOM is going to do the followup research? WHOM is the stroke leader ensuring this gets done?

An Unexplored Role for MMP-7 (Matrix Metalloproteinase-7) in Promoting Gut Permeability After Ischemic Stroke

Jonathan Larochelle

,

Changjun Yang

,

Lei Liu

and

Eduardo Candelario-Jalil

Originally published29 Jul 2022https://doi.org/10.1161/STROKEAHA.122.040144Stroke. 2022;0:10.1161/STROKEAHA.122.040144

Abstract

Poststroke infections are common complications of stroke and are highly associated with poor outcomes for patients. Stroke induces profound immunodepression coupled with alterations to autonomic signaling, which together render the body more susceptible to infection from without (nosocomial/community-acquired infection) and from within (commensal bacterial infection). Critical to the hypothesis of commensal infection is the phenomenon of poststroke gut permeability and gut dysbiosis. Few studies have provided adequate explanations for the mechanisms underlying the molecular alterations that produce a more permeable gut and perturbed gut microbiota after stroke. A dysregulation in the production of matrix MMP-7 (metalloproteinase-7) may play a critical role in the progression of gut permeability after stroke. By cleaving junctional and extracellular matrix proteins, MMP-7 is capable of compromising gut barrier integrity. Because of MMP-7’s unique abundance in the small intestine and its capacity to be induced in states of bacterial invasion and inflammation, along with its unique degradative capability, MMP-7 may be crucially important to the progression of gut permeability after ischemic stroke.

 

 

 

 

 

 

 

 

 

 

Footnotes

The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.

For Sources of Funding and Disclosures, see page XXX.

Correspondence to: Eduardo Candelario-Jalil, PhD, Department of Neuroscience, University of Florida, McKnight Brain Institute, 1149 SW Newell Dr, Gainesville, FL 32610. Email ecandelario@ufl.edu

Hemispheric asymmetry in myelin after stroke is related to motor impairment and function

 So you've described a problem, WHAT THE FUCK IS THE CURE?  No cure, useless research. Followup research needed or at least update the stroke strategy.

Hemispheric asymmetry in myelin after stroke is related to motor impairment and function

 Hemispheric asymmetry in myelin after stroke is related to motor
impairment and function
Bimal Lakhania, Kathryn S. Haywarda,b,c, Lara A. Boyda,⁎
aDepartment of Physical Therapy, University of British Columbia, Vancouver, BC V6T 1Z3, Canada
bStroke Division, Florey Institute of Neuroscience and Mental Health, University of Melbourne, Melbourne, VIC 3084, Australia
cNHMRC Centre of Research Excellence in Stroke Rehabilitation and Brain Recovery, Australia
a b s t r a c ta r t i c l e i n f o
Article history:
Received 19 October 2016
Received in revised form 3 January 2017
Accepted 10 January 2017
Available online 16 January 2017
The relationships between impairment, function, arm use and underlying brain structure following stroke remain unclear. Although diffusion weighted imaging is useful in broadly assessing white matter structure, it has limited utility in identifying specific underlying neurobiological components, such as myelin. The purpose of the present study was to explore relationships between myelination and impairment, function and activity in individuals with chronic stroke. Assessments of paretic upper-extremity impairment and function were administered, and 72-hour accelerometer based activity monitoring was conducted on 19 individuals with chronic stroke. Participants completed a magnetic resonance imaging protocol that included a high resolution T1 anatomical scan and a multi-component T2 relaxation imaging scan to quantify myelin water fraction (MWF). MWF was automatically parcellated from pre- and post-central subcortical regions of interest and quantified as an asymmetry ratio (contralesional/ipsilesional). Cluster analysis was used to group more and less impaired individuals based on Fugl-Meyer upper extremity scores. A significantly higher precentral MWF asymmetry ratio was found in the more impaired group compared to the less impaired group (p b 0.001). There were no relationships between MWF asymmetry ratio and upper-limb use. Stepwise multiple linear regression identified precentral MWF asymmetry as the only variable to significantly predict impairment and motor function in the upper extremity (UE).
These results suggest that asymmetric myelination in a motor specific brain area is a significant predictor of upper-extremity impairment and function in individuals with chronic stroke. As such, myelination may be utilized as a more specific marker of the neurobiological changes that predict long term impairment and recovery from stroke.
© 2017 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license

Immunocytes Rapid Responses Post-ischemic Stroke in Peripheral Blood in Patients With Different Ages

 WHOM is going to do all the followup research needed to make this usable? With NO strategy to update and NO leadership to see research thru to the end, NOTHING WILL OCCUR.

Immunocytes Rapid Responses Post-ischemic Stroke in Peripheral Blood in Patients With Different Ages

Haiyue Zhang¹, Jingwei Guan¹, Hangil Lee², Chuanjie Wu¹, Kai Dong¹, Zongjian Liu³, Lili Cui¹, Haiqing Song¹, Yuchuan Ding² and Ran Meng^1,4*

• ¹Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, China
• ²Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI, United States
• ³Department of Rehabilitation, Beijing Rehabilitation Hospital, Capital Medical University, Beijing, China
• ⁴Advanced Center of Stroke, Beijing Institute for Brain Disorders, Beijing, China

Objectives: To explore the alterations in immune cell composition in peripheral blood in patients with acute ischemic stroke (AIS) based on their age group.

Methods: Patients with imaging confirmed AIS were enrolled from April 2019 to January 2020 and were divided into three groups according to their ages: <55 years (group-A), 55–65 years (group-B), and >65 years (group-C). Blood samples were collected immediately when the patients were admitted to our ward prior to any intervention. Flow cytometry was used to analyze immune cell composition in peripheral blood.

Results: A total of 41 eligible patients were included for final analysis. Among the three groups, the proportions of CD56⁺ CD16dim NK cells were least to greatest in group-B, group-A, then group-C, respectively. With increasing age, there was a decrease in the proportion of CD3⁺ T-cells (group-A vs. group-C, P = 0.016) and CD3+CD4+ T-cells (group-C vs. group-A, P = 0.008; group-C vs. group-B P = 0.026). Meanwhile, no significant differences in proportions of monocytes and B cells were observed.

Conclusions: The compositions of immune cells in peripheral blood of AIS patients were distinct when divided by age groups. Differences in immune cell ratios may affect clinical outcomes and foreshadows possible need for customized treatment of AIS in different age groups.

Introduction

Ischemic stroke is a general term for necrosis of brain tissue caused by stenosis, occlusion, or insufficiency of arteries that supply blood to the brain (e.g., carotid and vertebral arteries). It accounts for approximately 87% of all strokes. Acute ischemic stroke (AIS) is a life-threatening disease with high morbidity and mortality worldwide (1–3). The pathophysiology of AIS involves immune cell activation, inflammation, and programmed cell death; of these, immune responses play a pivotal role given their contribution to both tissue damage and repair (1, 4, 5). More specifically, during the acute stage, ischemia-induced immune response damages the brain; in the sub-acute stage, Treg cells and macrophages protect and repair the brain (6–9).

Aging is an important factor that affects immune response, thereby influencing clinical outcomes (10, 11). Although the elderly are among the most vulnerable to AIS, the influence of aging and consequent changes to immune response in AIS has not been studied well. Theoretically, as people grow older, ischemia-induced immune response may be modified and weakened, which may result in poorer outcomes. To elucidate the impact of aging on immune response to AIS, we analyzed the alterations in immune cell composition in peripheral blood of AIS patients based on their age groups. The results of this study may become references for predicting outcomes and designing customized treatment.

More at link.