Low-intensity preconditioning boosts neurological outcomes

Your competent? doctor will need to EXACTLY PREDICT YOIUR NEXT STROKE within four weeks so you can do this preconditioning. 

Low-intensity preconditioning boosts neurological outcomes

The team led by Prof. Lin Zhu from Guangzhou Sport University have demonstrated that 4-week low-intensity treadmill exercise before the onset of an ischemic stroke can significantly reduce brain injury and improve neurological outcomes.

This study, published in Translational Exercise Biomedicine (ISSN: 2942-6812), an official partner journal of International Federation of Sports Medicine (FIMS), offers a promising, non-pharmacological strategy for the millions of people worldwide at risk of this debilitating condition.

Ischemic stroke, caused by a blockage in blood flow to the brain, remains a leading cause of death and long-term disability worldwide. Although treatments like thrombolysis are available, narrow time windows significantly limit their therapeutic effects. This has led scientists to explore proactive, preventive measures against stroke.

The research team investigated the concept of exercise preconditioning using regular physical activity to build the brain's resilience against a future injury. The study focused on low-intensity exercise, more accessible and sustainable for at-risk populations, particularly the elderly.

Our study provides robust evidence that even low-intensity exercise can precondition the brain to be more resistant to the devastating effects of an ischemic stroke. The beauty of this approach is its practicality, it doesn't require strenuous activity, making it a viable strategy for older adults or those with physical limitations or at risk of stroke."

Lin Zhu, Study Team Leader and Professor, Shanghai Jiao Tong University

The researchers established a transient middle cerebral artery occlusion (tMCAO) mouse model, the standard for simulating human ischemic stroke. Twelve-week-old male mice were divided into three groups: healthy control group (Sham), stroke group (tMCAO), and exercise preconditioning group (Ex+tMCAO) that underwent four weeks of low-intensity treadmill running, 10 m/min for one hour a day, five days a week, before the stroke was induced.

The results were striking. At 24 hours after the stroke, the mice that had exercised showed significantly reduced infarct size. Brain tissue death was markedly lower compared to the non-exercised stroke group. In addition, the exercised mice exhibited a higher density of CD31-positive microvessels, indicating improved formation of new blood vessels in the brain, which is crucial for recovery and supplying oxygen to stressed tissues.

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Exercise preconditioning also dramatically reduced the apoptosis in neurons. At the molecular level, the exercised mice showed significantly lower expression of key pro-inflammatory cytokines and chemokines in the brain, including IL-6, CCL11, CCL2, CXCL1, and Fosl1. These factors are known to exacerbate brain damage by recruiting immune cells and triggering harmful inflammatory cascades. While the exercise group showed a trend toward improved performance on motor coordination tests, like the rotarod test, the improvements were not statistically significant at the 24-hour mark, suggesting that while tissue damage is reduced, functional recovery may take a longer period of time.

Co-corresponding author Prof. Xiaoguang Liu added, "We were excited to see the down-regulation of multiple inflammatory pathways. This confirms that exercise preconditioning not only just act through one mechanism, but also creates a broad, protective environment in the brain by simultaneously boosting repair mechanisms like angiogenesis and suppressing inflammation and apoptosis."

However, the authors acknowledge several limitations. The study was conducted only using young male mice, and female and aged models are needed to validate the results. Furthermore, though gene expression for inflammatory markers was measured, protein-level confirmation is needed to confirm the mechanistic conclusions. 

Despite these limitations, the findings have profound implications for public health. They suggest that encouraging regular, gentle physical activity, such as a brisk walk, could serve as an effective, low-cost preventive medicine against stroke.

This is especially relevant given the rising incidence of stroke in younger adults and the aging global population. Besides, this study also has certain translational significance. Building a "brain reserve" through consistent, manageable exercise could be one of the most effective ways to reduce global burden of ischemic stroke. It transforms the concept of exercise from a rehabilitative tool to a powerful preemptive exercise medicine.

Source:

Shanghai Jiao Tong University

Journal reference:

Chen, P., et al. (2026). Low-intensity treadmill exercise preconditioning alleviates post-ischemic stroke injury in mice by inhibiting ischemia-induced inflammation and apoptosis. Translational Exercise Biomedicine. DOI: 10.1515/teb-2025-0029. https://www.degruyterbrill.com/document/doi/10.1515/teb-2025-0029/html.

Psychedelics Remodel Myelin to Heal PTSD

 Your competent? doctor is already prescribing psychedelics, right?

DMT (8 posts to November 2020)

ecstasy (19 posts to November 2012)

LSD (5 posts to September 2018)

CerAxon (5 posts to January 2012)

citicoline (15 posts to October 2011)

magic mushrooms (10 posts to October 2014) 

psilocybin (14 posts to May 2014)

Psychedelics (25 posts to August 2018)

And knows of the need for myelin repair post stroke!

myelin (79 posts to April 2011)

myelin regeneration (3 posts to August 2024)

myelin repair (5 posts to January 2025)

And knows all about preventing and fixing your PTSD!

Since there is a 23% chance of stroke survivors getting PTSD what is your doctor's treatment plan?

OH NO, your doctor is incompetent in all points! What will you do to correct that problem?

Psychedelics Remodel Myelin to Heal PTSD

Summary: For years, scientists have focused on how psychedelics “rewire” neurons. But a groundbreaking study has found a “missing link” in long-term PTSD recovery: myelin remodeling. Researchers discovered that psilocybin and MDMA do more than just alter brain activity; they trigger the physical repair of myelin—the insulating layer that protects nerve fibers and synchronizes brain signals.

By “re-insulating” the circuits that have been frayed by trauma, these drugs help harmonize the rhythm of brain networks, turning a temporary “psychedelic window” into a permanent structural recovery.

Key Facts

• The “Missing Link”: While psychedelics provide rapid relief, long-term stability requires circuit-level repair. This study identifies adaptive myelination as the key to sustaining those benefits.
• Brain Synchronization: Myelin acts as the brain’s insulation. Remodeling this layer allows disrupted brain circuits (common in PTSD) to synchronize and harmonize their electrical rhythms again.
• Mechanistic Proof: Researchers used a rat model to show that blocking myelin repair prevented the long-term anti-anxiety effects of psilocybin and MDMA, proving that structural repair is necessary for recovery.
• Oligodendrocytes Matter: The study shifts the focus from neurons to oligodendrocytes—the cells that produce myelin—as the “gatekeepers” of long-lasting psychedelic healing.
• Anti-Inflammatory Effects: In addition to repairing insulation, both drugs were found to reduce astrocyte reactivity, lowering brain inflammation associated with chronic stress.

Source: Elsevier

Post-traumatic stress disorder (PTSD) is not only characterized by strongly encoded traumatic memories, but also by disrupted coordination across brain networks.

New research shows that treatment with psychedelic drugs triggers a large-scale reconfiguration of brain network dynamics driven by the remodeling of myelin—the neuronal insulation layer.

The findings from the novel study in Biological Psychiatry show enhancing myelination might be a viable strategy to augment or sustain the therapeutic effects of psychedelic-assisted treatments for PTSD and related disorders.

Psilocybin and 3,4-methylenedioxymethamphetamine (MDMA) produce rapid clinical effects in patients with PTSD. However, durable benefits require circuit-level stabilization.

As the underlying cellular mechanisms remain incompletely understood, the current study identifies myelin as the missing link bridging the short-lived psychedelic experience and longer-term maintenance of healthier neural network dynamics.

The study shows that activity-dependent oligodendrogenesis and myelin remodeling can tune the disrupted timing and persistent response to threat observed in PTSD by synchronizing and harmonizing the rhythm of brain circuits.

John Krystal, MD, Editor of Biological Psychiatry, explains, “The focus of psychedelic and MDMA research has been the effects of these drugs on neurons and neuroplasticity. This work has largely ignored a potentially important role for other cell types in the neurobiology of their therapeutic effects.

“Oligodendrocytes play a number of roles in the brain, which produce the myelin that insulates neurons. Subgroups of oligodendrocytes take up glutamate and contribute to glutamate homeostasis, protecting the brain from neurotoxicity. Another group of oligodendrocytes is involved in immune and inflammatory functions in the brain.”

Researchers used a rat model of contextual fear conditioning and administered repeated low doses of psilocybin or MDMA. They then quantified anxiety-like and exploration behaviors and assessed spatial learning and memory.

The results showed that anxiety-like behaviors were reduced—a shift accompanied by changes in oligodendrocyte biology and multi-omic (genetic) signatures towards myelin remodeling in the dentate gyrus (part of the hippocampus, the brain’s memory center).

“To test whether myelin integrity was simply associated with behavioral change—or actually required for it—we combined the drug interventions with models that either damaged brain insulation (demyelination) or chemically enhanced it (promyelination) to see how these changes affected recovery,” explains lead investigator Mehmet Bostancıklıoğlu, PhD, Department of Physiology, Gaziantep University Faculty of Medicine, Gaziantep, Turkey.

Using high-powered microscopy and genetic analysis, the researchers confirmed both psilocybin and MDMA trigger physical myelin repair. Furthermore, a serotonin receptor 5-HT_2A blockade prevented both the behavioral and myelin-associated effects.

When the team used a different drug (anisomycin) to block the formation of fear memories, anxiety decreased, but the myelin remained unrepaired. This suggests that while memories can be suppressed, biological recovery requires the structural support of myelin.

“Taken together, this moves oligodendrocytes and adaptive myelination from ‘background correlates’ to a mechanistically testable gate on the durability of psychedelic-associated circuit change,” notes Dr. Bostancıklıoğlu.

“The implication of oligodendrocytes in the therapeutic effects of psychedelics and MDMA is important because of their many functions in the brain, including myelin formation, glutamate homeostasis, and neuroinflammation. The dependency of the therapeutic effects of these drugs in animals may suggest that myelin compromise may undermine their efficacy,” adds Dr. Krystal.

“Overall, these data suggest that psychedelics and MDMA, like selective serotonin reuptake inhibitors (SSRIs) and ketamine, may promote the recovery from stress-related damage to myelin, contributing to clinical recovery.”

The study also found that psilocybin and MDMA reduce astrocyte reactivity that can cause inflammation.

The investigators point out that enhancing myelination would not be expected to replace psychotherapy; rather, it could support consolidation and maintenance of healthier network communication after the acute psychedelic session, when the brain is transitioning from destabilization back towards reintegration.

Dr. Bostancıklıoğlu concludes, “We often talk about psychedelics as ‘opening a window’ for brain plasticity. Recent work emphasizes that these drugs can acutely loosen entrenched network patterns and then leave a sub-acute period in which experience can reshape circuits.

“What we show here is that myelin-producing cells may be an underappreciated part of that story—helping translate a transient window into longer-lasting circuit change, at least in a fear-based rat model.”

Key Questions Answered:

Q: Do psychedelics just “mask” traumatic memories?

A: No—this study shows they actually help fix the wiring. Trauma “frays” the insulation (myelin) of your brain’s communication lines, leading to static and mistimed signals. Psychedelics like psilocybin and MDMA trigger the brain to physically re-wrap those wires, allowing for clearer, calmer communication.

Q: Why is “neural insulation” so important for PTSD?

A: In PTSD, the brain’s fear circuits are often “over-active” and poorly timed. Myelin ensures that signals travel at the right speed. By repairing this insulation, the brain can better synchronize its networks, helping to “turn down the volume” on persistent threat responses.

Q: Does this mean I can just take psilocybin and be cured?

A: Not quite. The researchers emphasize that these drugs “open a window” of plasticity. The physical repair of myelin provides the structural support needed for that window to stay open, but it works best alongside therapy to reintegrate those healthier network patterns.

Editorial Notes:

• This article was edited by a Neuroscience News editor.
• Journal paper reviewed in full.
• Additional context added by our staff.

About this PTSD and psychedelics research news

Author: Eileen Leahy
Source: Elsevier
Contact: Eileen Leahy – Elsevier
Image: The image is credited to Neuroscience News

Original Research: Open access.
“MDMA and Psilocybin Regulate Oligodendrocyte-Lineage Cell Numbers and Anxiety-Like Behaviors in a Rat Model of Fear” by Mehmet Bostancıklıoğlu, Davut Sinan Kaplan, Ramazan Bal, Elif Yiğit, Hasan Ulusal, and Ebru Temiz. Biological Psychiatry
DOI:10.1016/j.biopsych.2026.01.016

Low-dose lithium shows promise in slowing verbal memory decline in older adults

 

Your incompetent? doctor already has protocols on uses of lithium for your stroke or TBI, and Alzheimers' prevention, right? Oh no, you DON'T have a functioning stroke doctor, do you?

lithium (19 post to September 2011) So, well over a decade of incompetence! Shooting for a world record, huh!

Low-dose lithium shows promise in slowing verbal memory decline in older adults

In a 2-year randomised, placebo-controlled pilot trial of 80 older adults with mild cognitive impairment (MCI), low-dose lithium carbonate did not meet prespecified significance thresholds for cognitive, neuroimaging, or biomarker outcomes, although it was associated with a slower annual decline in verbal memory compared with placebo.

Results of the study, published in JAMA Neurology, showed that lithium was generally safe and feasible in this population, providing critical effect size estimates to inform larger trials aimed at preventing progression to Alzheimer disease.

“The key point is that lithium doesn’t restore lost memory,” said Ariel G. Gildengers, MD, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania. “What it appears to do -- if the signal holds up -- is slow deterioration. That distinction matters enormously when you’re designing trials and interpreting results.”

To examine the feasibility, safety, and preliminary efficacy of low-dose lithium carbonate in adults aged ≥60 years with MCI, the researchers randomised participants to receive daily lithium or placebo for 2 years, with 80 starting treatment between February 2018 and August 2024. The trial assessed 6 coprimary outcomes, including cognitive performance measures, hippocampal and cortical gray matter volumes, and brain-derived neurotrophic factor levels.

Over the 2-year follow-up, none of the coprimary outcomes reached prespecified significance thresholds. However, lithium-treated participants showed a slower annual decline in verbal memory compared with placebo (0.73 vs 1.42 points per year on the California Verbal Learning Test-II delayed recall; P = .05). Brain volumes declined in both groups, with no significant differences, and serious adverse events were similar between groups. 

When the trial was launched nearly a decade ago, blood‑based tests for Alzheimer’s pathology were not yet available. As a result, participants were enrolled based on clinical symptoms alone, and only a subset turned out to be amyloid‑positive -- a limitation that may have diluted the study’s ability to detect stronger effects.

“If we were designing this study today, we would enroll participants based on amyloid status from the start,” said Dr. Gildengers. “That’s exactly what we’re planning for next.”

“This study tells us that the approach is feasible, safe and worth pursuing, but it also reminds us why careful, adequately powered trials are essential -- especially when the stakes are this high,” he added.

Reference: https://jamanetwork.com/journals/jamaneurology/fullarticle/2845746

SOURCE: University of Pittsburgh

Wearable sensors may detect early disability progression in multiple sclerosis

 With ANY BRAINS AT ALL your stroke medical 'professionals' would immediately use this to objectively diagnose gait abnormalities. And then objectively monitor the recovery. But nothing will occur, we have blithering idiots in stroke!

Wearable sensors may detect early disability progression in multiple sclerosis

A longitudinal study of people with multiple sclerosis (MS) found that declines in daytime physical activity detected through wearable accelerometers were associated with increased risk of disability progression and brain atrophy.

The findings, published in Neurology, suggest continuous activity monitoring may serve as a sensitive, noninvasive biomarker for early disease worsening before clinical symptoms become apparent.

“Timely identification of patients at risk for disease progression is essential to reduce long-term disability, but the current tests for measuring MS disability are not designed to detect small changes,” said Kathryn C. Fitzgerald, Johns Hopkins University, Baltimore, Maryland. “Using a relatively inexpensive and accessible device around the wrist may help us identify early changes in the disease.”

The study enrolled 238 adults aged ≥40 years who underwent annual brain MRI scans and wore wrist-based accelerometers 24 hours per day for 2 straight weeks every 3 months, for up to 3 years. The devices captured several activity metrics, including total activity levels, sedentary time, circadian rhythm parameters, and activity during specific two-hour daytime windows.

Participants had been living with MS for an average of 13 years. At the start of the study, they had an average disability level of 3 on the Expanded Disability Status Scale (EDSS).

Over an average follow-up of 2.9 years, 120 participants experienced confirmed disability progression based on the composite EDSS-plus. Overall physical activity declined by an average of about 2% per year.

Importantly, within-person decreases in daytime activity -- particularly between 8:00 AM and 2:00 PM -- were associated with a significantly higher risk of disability progression. A one-standard deviation decrease in morning or midday activity increased the risk of confirmed progression by roughly 20% to 24%.

MRI analyses also showed that reductions in morning activity were linked to greater brain atrophy, including loss of whole-brain, deep Gray matter, and thalamic volume. While individuals with lower average moderate-to-vigorous activity had smaller brain volumes overall, these between-person differences were not associated with disability progression.

“More research is needed to confirm these findings, but it’s exciting to think that using easily accessible devices could help us predict who is at risk of worsening disease and potentially prevent those changes,” said Ellen M. Mowry, Johns Hopkins University. “Detecting small changes could also help us speed up research on new treatments.”

A limitation of the study is that people who did not have MS were not included, which would help researchers understand how activity levels may change as a part of normal aging. Also, the participants were relatively older and more disabled, so the results may not apply to younger people with MS and those with less disability.

Reference: https://www.neurology.org/doi/10.1212/WNL.0000000000214678

SOURCE: American Academy of Neurology

Quadrupedal Training Approaches in Post-Stroke Rehabilitation: A Scoping Review of Evidence, Mechanisms, and Clinical Applications

 This sounds precisely like the methods Pedro Bach-y-Rita used to fully recover with only a partial brain then our stroke medical 'professionals' can duplicate that! Way back in 1958 so plenty of time to analyze and create 100% recovery protocols!

No knowledge and doing nothing IS PURE INCOMPETENCE!

Pedro Bach-y-Rita (14 posts to May 2011)

Quadrupedal Training Approaches in Post-Stroke Rehabilitation: A Scoping Review of Evidence, Mechanisms, and Clinical Applications

• 

  Jan Arjen Kuipers 1

• 

  Frederick Robert Carrick 1,2,3,4,5

• 

  Monèm Jemni 1,2,6

• 1. Carrick Institute of Neuroscience, Canaveral, Florida, United States

• 2. University of Cambridge Cambridge Institute for Medical Research, Cambridge, United Kingdom

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Abstract

Background: 

Persistent impairments in trunk control, balance, and mobility are frequently observed after stroke, even after standard task-specific rehabilitation. Quadrupedal-derived training (QT)— which involves four-point support, dynamic contralateral tasks, transitional kneeling, and crawling—has attracted clinical interest because it may activate bilateral and spinal sensorimotor networks. Nonetheless, the evidence supporting QT has not been thoroughly systematically mapped. 

Objective: 

To synthesize the extent, characteristics, mechanisms, and clinical applications of quadrupedal-derived training in adult post-stroke rehabilitation. 

Methods: A scoping review was conducted in accordance with the JBI Manual for Evidence Synthesis and the PRISMA-ScR guidelines. It involved searching five databases and additional sources from 2010 to 2025 to find studies on QT in stroke populations, along with mechanistic and translational evidence. The outcomes were pre-mapped to the International Classification of Functioning (ICF) domains. Data on intervention types, total dosage, supervision, progression criteria, safety, and feasibility were gathered. Stakeholder input from stroke survivors, clinicians, and researchers helped shape implementation considerations. 

Results: 

Eighteen studies met the inclusion criteria, including five randomized controlled trials and one case study involving stroke populations, as well as mechanistic and translational research. QT consistently improved trunk control and balance, with effects on functional mobility and certain gait parameters varying depending on the variant and dose. Kneeling-based QT showed greater balance benefits than treadmill-based training in subacute inpatient settings, while static and dynamic four-point variants were mainly used with chronic outpatient groups. No serious adverse events occurred, and adherence was high where recorded. Mechanistic evidence indicates a pathway connecting quadrupedal loading to activation of spinal and interlimb networks, bilateral proximal muscles, and functional improvements. 

Conclusion: 

Quadrupedal-based training is a biologically plausible, resource-efficient, and clinically practical method for improving trunk and balance issues after a stroke. More well-designed studies that include standardized progression, dose–response evaluations, and neurophysiological biomarkers are needed.

Patient-centered goal-setting in stroke rehabilitation: A scoping review

 Patients only have one goal: 100% RECOVERY! And you incompetently don't know that? You're all fired! You're trying to justify your incorrect use of the tyranny of low expectations.

Patient-centered goal-setting in stroke rehabilitation: A scoping review

• 

  Inge Ris 1,2

• 

  Mille Nabsen Marwaa 3

• R

  Rikke Westengaard Nielsen 1

• P

  Palle Larsen 1

• H

  Hanne Kaae Kristensen 1,4

• 1. Health Sciences Research Centre, University College Lillebaelt, Odense, Denmark

• 2. Department of Sports Science and Clinical Biomechanics, Syddansk Universitet, Odense, Denmark

The final, formatted version of the article will be published soon.

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Email

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Abstract

Background: 

Patient-centered goal-setting is an important part of the rehabilitation process. The guidelines for stroke rehabilitation in adults recommend setting goals that are meaningful and relevant for the patient, focusing on activity and participation, and involving the patient. Patient-centered goal-setting is to improve rehabilitation outcomes. However, patient-centered goal-setting occurs partly or not at all. There is also a lack of continuity in goal-setting across sectors. 

Objective: 

This study aimed to identify existing research-based knowledge on procedures used in patient-centered goal-setting processes in stroke rehabilitation. 

Methods: 

A scoping review was conducted by searching PubMed, CINAHL Complete, EMBASE, APA PsycINFO, Scopus, and Cochrane databases for studies involving adults receiving or clinicians delivering stroke rehabilitation and focusing on patient-centered goal-setting processes. The included studies were analyzed using inductive content analyses and linked to five domains in goal-setting processes: person-centeredness, collaboration with healthcare professionals and patients, coordination across sectors, monitoring, and evaluation. 

Results: 

Eighteen studies were included. Inductive content analysis identified elements related to goal-setting processes, mainly occurring at the beginning of the rehabilitation. Linking the studies to five domains revealed gaps in cross-sectoral coordination, monitoring, and evaluation. 

Conclusion: 

Patient-centered goal-setting in stroke rehabilitation is practiced variably, and there is no overall agreement about the procedures to ensure that goal-setting is patient-centered. Therapist-and team-led goal-setting processes are used. Evaluation procedures and cross-sectoral coordination are rarely described.

Summary

Keywords

Cross-sectional study, goal-setting, patient-centered, Scoping review, Stroke, stroke rehabilitation