DMT Shows Promise in Protecting the Brain After Stroke

 

 Didn't your competent? doctor start prescribing this years ago? Oh no, incompetence reigned because your doctor doesn't follow stroke research!

Which proves your board of directors is so incompetent they can't recognize crapola in their hospital staff that needs to be removed! YOU need to reconstitute the hospital!

DMT (20  posts to November 2020)

DMT Shows Promise in Protecting the Brain After Stroke

Summary: New research shows that DMT, a natural psychoactive compound found in plants and the human brain, can protect against stroke damage in animal and cell models. Treatment with DMT reduced infarct size, brain swelling, and inflammation, while also repairing blood-brain barrier function.

The compound acted through Sigma-1 receptors to limit microglial activation and support astroglial cells, creating a dual protective effect. These findings suggest DMT could one day serve as an adjuvant therapy for stroke, expanding treatment options and improving recovery outcomes.

Key Facts

• Barrier Protection: DMT restored blood-brain barrier integrity after stroke.
• Inflammation Control: It reduced cytokine production and microglial activation.
• Therapeutic Potential: Could complement limited existing stroke treatments.

Source: HUN-REN BRC

DMT, or dimethyltryptamine is a natural psychoactive molecule found in many plants and mammals.

According to an article published in Science Advances, researchers from the HUN-REN BRC Institute of Biophysics and Semmelweis University Heart and Vascular Centre found that DMT reduces the harmful effects of stroke in animal models and cell culture experiments. 

This psychoactive compound also inhibited the production of inflammatory cytokines in brain endothelial cells and peripheral immune cells, while reduced the activation of brain microglia cells through Sigma-1 receptors. Credit: Neuroscience News

A solution from nature in the spotlight

DMT is also present in the human brain, and it is currently undergoing clinical trials to aid recovery of brain function after stroke. However, its exact mechanism of action had not been fully understood until now. “It is amazing how we can always turn to Nature to find ingenious solutions for health problems” says co-lead author Mária Deli from the HUN-REN BRC.

The blood-brain barrier as a therapeutic target

 “We found that DMT significantly reduced infarct volume and edema formation in a rat stroke model”, explains co-first author Marcell László.

In both animal experiments and cell culture models, the authors showed that DMT treatment restored the structure and function of the damaged blood-brain barrier and improved the function of astroglial cells.

This psychoactive compound also inhibited the production of inflammatory cytokines in brain endothelial cells and peripheral immune cells, while reduced the activation of brain microglia cells through Sigma-1 receptors.

DMT could serve as therapeutic adjuvant to existing stroke treatments 

“The therapeutic options currently available for stroke are very limited. The dual action of DMT, protecting the blood-brain barrier while reducing brain inflammation, offers a novel, complex approach that could complement existing treatments”, says Judit Vigh, co-first author of the work.

Since current stroke therapies do not always result in full recovery, a DMT-based treatment may represent a promising new alternative, mainly in combination with existing methods.

The recent findings from researchers in Szeged and Budapest, Hungary, support the development of a therapy that goes beyond the limitations of conventional stroke treatment. Clinical trials on the use of DMT and investigation on its long-term effects are currently ongoing.

About this neuroscience research news

Author: Anett Nagy-Demcsák
Source: HUN-REN BRC
Contact: Anett Nagy-Demcsák – HUN-REN BRC
Image: The image is credited to Neuroscience News

Original Research: Open access.
“N,N-dimethyltryptamine mitigates experimental stroke by stabilizing the blood-brain barrier and reducing neuroinflammation” by Maria A. Deli et al. Science Advances

Enriched environments improve stroke recovery and reduce brain inflammation

WOW! You really like proving just how out-of-date you are! You don't follow research at all, do you? Are you're still employed in stroke?

Let's check how long you've been absolutely stupid and missed all the intervening research!

This enriched environment  was reported for stroke way back in 2011 by Dr. Corbett. 

• Environmental Enrichment (61 posts to December 2013)

Preconditioning with an Enriched Environment Enhances Neuroplasticity and Functional Recovery Following Cerebral Ischemia-Reperfusion Injury

THIS is the reason survivors need to be in charge, no one in the stroke medical world is putting it all together with a way to get to 100% recovery. No one seems to be up-to-date.

The latest here:

 Enriched environments improve stroke recovery and reduce brain inflammation

Chinese Medical Journals Publishing House Co., Ltd.Apr 11 2026

Stroke is one of the leading causes of death worldwide. Its recovery is often challenging as most of the stroke survivors remain chronically disabled, with motor deficits affecting a significant percentage of patients. Stroke recovery continues long after the initial injury stabilization. In the early recovery period, during the first weeks after the insult, the brain enters a prolonged phase of repair and inflammation. This chronic response can strongly influence poststroke recovery and long-term disability.

The poststroke recovery environment plays an important role in the healing process. Recent studies(Not recent at all; quit lying just to make yourself not look stupid!) suggest that environmental enrichment (EE), a recovery setting that combines greater physical activity, sensory stimulation, and social interaction, can improve recovery. However, how the stimulation affects poststroke brain inflammation and white matter pathology is not well-understood.

To address this, a team of researchers, led by Dr. Lluís Camprubí-Ferrer, from the Experimental Neuroinflammation Laboratory, Lund University, Sweden, conducted an animal-based study to understand the effect of EE on poststroke inflammation, microglial response, and myelin integrity. The study was made available online on February 25, 2026, and was published in Volume 4, Issue 1 of the journal Neuroprotection on March 01, 2026.

"EE is known for exerting beneficial effects on neuroplasticity and recovery after stroke. However, a systemic study on understanding the microglial phenotypes during the recovery period after stroke under enriched housing conditions was lacking. Our study addresses this research gap," says Dr. Camprubí-Ferrer.

The researchers induced photothrombotic (PT) stroke, a commonly used experimental model that creates a localized injury in the brain, in male mice and randomized mice into standard environment (SE) or to an EE with more space, social contact, exercise opportunities, and frequently changed objects. The mice were then monitored for sensorimotor recovery over 3 weeks. In addition, they examined the brain for signs of microglial activity and myelin damage.

The behavioral findings clearly highlighted the role of EE in PT stroke recovery. Mice housed in EE performed better on tests of paw placement, foot fault, and limb symmetry, with benefits persisting through 21 days after stroke. When the researchers combined these outcomes into an overall neurological score, the EE group showed stronger recovery.

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The tissue analysis revealed that in SE mice, larger infarcts were closely linked to stronger chronic inflammatory signals. In addition, larger lesions were associated with more myelin debris around the infarct and greater loss of myelin in white matter. In contrast, in EE mice, the usual link between infarct size and chronic inflammatory markers like galectin‐3 was largely absent. The same was true for myelin debris accumulation and white matter myelin loss. The findings suggest that enrichment weakened the tendency for larger lesions to drive stronger long-term inflammation and tissue disruption.

In white matter, higher levels of triggering receptor expressed on myeloid cells 2 (TREM2)-positive microglia were associated with better neurological recovery in EE mice. No other inflammatory or myelin marker showed such a robust relationship with behavior. This highlights TREM2-positive microglia as a potential cellular link between EE and improved functional recovery.

"Our findings suggest that interventions like EE that targets microglial marker suppression and TREM2 potentiation may contribute to post‐stroke white matter repair and improve functional outcomes," concludes Dr. Camprubí-Ferrer.

Source:

Chinese Medical Journals Publishing House Co., Ltd.

Journal reference:

Camprubí‐Ferrer, L., et al. (2026). Environmental enrichment modulates chronic poststroke inflammation and links white matter TREM2‐positive microglia in recovery in mice. Neuroprotection. DOI: 10.1002/nep3.70028. https://onlinelibrary.wiley.com/doi/10.1002/nep3.70028

Psychedelic DMT decreases stroke damage, study finds

 Didn't your competent? doctor start prescribing this years ago? Oh no, incompetence reigned because your doctor doesn't follow stroke research!

DMT (17  posts to November 2020)

Psychedelic DMT decreases stroke damage, study finds

DMT may protect the brain from stroke damage by stabilising the blood–brain barrier and reducing inflammation, new research suggests.

The naturally occurring psychoactive compound dimethyltryptamine (DMT) significantly reduced brain damage in animal models of stroke by protecting the blood–brain barrier – the membrane that controls what passes from the bloodstream into brain tissue – and by lowering inflammation.

DMT is a natural compound found in many plants and mammals, including humans. It is currently under clinical investigation as a neuroprotective agent to help restore brain function after stroke.Researchers in Budapest found that DMT treatment restored both the structure and function of damaged blood–brain barriers and improved astroglial cell activity – these are star-shaped support cells that assist nerve function.

Dr Marcell László is co-first author of the study.

László said: “We found that DMT significantly reduced infarct volume and oedema formation in a rat stroke model.”

Infarct volume refers to the amount of dead brain tissue, while oedema is swelling caused by excess fluid.

The researchers observed that DMT inhibited the production of inflammatory cytokines – proteins that trigger inflammation – in brain-endothelial and peripheral immune cells, and reduced the activation of brain microglia, the brain’s immune cells, through sigma-1 receptors.

Dr Judit Vigh, co-first author, said: “The therapeutic options currently available for stroke are very limited.

“The dual action of DMT, protecting the blood–brain barrier while reducing brain inflammation, offers a novel, complex approach that could complement existing treatments.”

Clinical trials assessing the safety, efficacy and long-term effects of DMT in human patients are now under way.

Neck Circumference a Practical Screening Tool for Metabolic Syndrome, suggests Study

 And this from years ago was not enough to establish the correlation? Your stroke medical 'professionals' ARE THAT FUCKING INCOMPETENT THEY DON'T FOLLOW RESEARCH?

Well mine always was 16.5 until after the stroke weight gain it increased to 17.5. I can't tell what it really is right now since it takes two useable hands to measure it.

Neck Circumference as a Novel Measure of Cardiometabolic Risk: The Framingham Heart Study October 2017

Neck Circumference a Practical Screening Tool for Metabolic Syndrome, suggests Study

Unravelling the Brain Resilience Following Stroke: From injury to rewiring of the brain through pathway activation, drug targets, and therapeutic interventions

 

 Since I know I blew all my cognitive resilience just surviving my stroke I'm rebuilding it with lots of social connections, mostly at bars where jazz or trivia is played. Alcohol seems to be involved, so don't listen to me, I'm not medically trained.

 A researcher asked me where my resilience came from a few years ago. I had no answer, but this probably explains it.

Your Mindset Shapes Your Life – For Better or Worse by Debbie Hampton

resilience (25 posts to September 2020) Lots in these posts which your competent? doctor should have informed you of but didn't because incompetence in not following research!

Unravelling the Brain Resilience Following Stroke: From injury to rewiring of the brain through pathway activation, drug targets, and therapeutic interventions

Author links open overlay panel, , , , , ,

https://doi.org/10.1016/j.arr.2025.102780

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Highlights

• •
  Post-stroke Glutamate excitotoxicity triggers numerous pathways, resulting in synapse loss.
• •
  Stroke leads to excessive synaptic pruning, causing loss of functional synapses and neural network efficiency.
• •
  Therapeutic targets enhancing the synaptic plasticity improve post-stroke functional impairment.

Abstract

Synaptic plasticity is a neuron's intrinsic ability to make new connections throughout life. The morphology and function of synapses are highly susceptible to any pathological condition. Ischemic stroke is a cerebrovascular event that affects various brain regions, resulting in the loss of neural networks. Stroke can alter both structural and functional plasticity of synapses, leading to long-term functional disability. Upon ischemic insult, numerous glutamate-mediated synaptic destruction pathways and glial-mediated phagocytic activity are triggered, resulting in excessive synapse loss, altering synaptic plasticity. The conventional stroke therapies to improve synaptic plasticity are still limited and ineffectual, leading to sub-optimal recovery in patients. Therefore, promoting synaptic plasticity to ameliorate sensory-motor function may be a promising strategy for long-term recovery in stroke patients. Here, we review the involvement of different molecular pathways of glutamate and glia-mediated synapse loss, current pharmacological targets, and the emerging novel approaches to improve synaptic plasticity and sensory-motor impairment post-stroke.

Introduction

As we delve into the complexities of the mammalian brain, synaptic plasticity has become an intriguing area of research in the field of neuroscience (Citri and Malenka, 2008). Synaptic plasticity is a neurophysiological phenomenon within each synapse governed by various molecular pathways, synaptic proteins, and glial cells to create a large neural network (Bitar et al., 2024, Stampanoni Bassi et al., 2019). (You don't explain anything about what in synaptic plasticity creates resilience. I can only assume you're spouting something with no knowledge.)It is the ability of pre-existing synapses to modulate the strength of their synaptic connections and the efficacy of synaptic transmission in response to any activity (Magee and Grienberger, 2020). Growing evidences indicate that synaptic plasticity plays a pivotal role in organising and reorganising the neuronal circuits in the early development of the central nervous system (CNS), thereby controlling human behaviour, memory, and emotions (Ho et al., 2011). Structural plasticity refers to the adaptive modification in the synaptic structure, such as spine number, shape, and density (Sadigh-Eteghad et al., 2018a). In contrast, functional plasticity is the brain's ability to modify and adapt the functional characteristics of neurons that include long-term potentiation (LTP) and long-term depression (LTD) (Peters et al., 2018).

Ischemic stroke is an acute cerebrovascular accident due to the blockage of blood vessels in the brain tissue (Datta et al., 2020). The current conventional therapies for ischemic stroke include intravenous thrombolytics, i.e. tissue plasminogen activator(tPA) and mechanical thrombectomy (Hurd et al., 2021). The past strategies to improve post-stroke synaptic plasticity are still limited and have not been explored much. Currently, some of the novel strategies are gaining more attention for their promising results in numerous preclinical and clinical settings to improve long-term functional impairments (Marín-Medina et al., 2024a, Su and Xu, 2020a). Synaptic loss is the key hallmark of various neurological disorders, including stroke (Wilson et al., 2023). Upon ischemic insult, multiple cellular stress pathways get triggered, including glutamate excitotoxicity, mitochondrial dysfunction, oxidative stress, blood-brain barrier (BBB) disruption, immune and complement activation, neuroinflammation, and apoptosis, which eventually causes synaptic loss (Tuo et al., 2022). Following stroke in human 32000 neurons, 230 million synapses, and 200 meters(218 yards) of myelinated fibres are lost each second which accelerates the aging by 8.7 h, and per stroke around 1.2 billion neurons, 8.3 trillion synapses, and 7140 km(4470 miles) of myelinated fibres are destroyed which accelerates the aging by 36 years (Saver, 2006). Various studies have reported that stroke can dysregulate both structural and functional synaptic plasticity, leading to post-stroke sensory-motor impairments (Yang et al., 2018, Wang et al., 2022a).

Synapse is the site of communication or the junction of neurons, enabling a well-organised flow of information throughout the brain (Caire et al., 2018). They are the highest energy-consuming sub-cellular compartment of the brain for performing all synaptic activity (Faria-Pereira and Morais, 2022, Fedorovich and Waseem, 2018). Mitochondria are mainly present on the synaptic terminal to meet the excessive energy demand for synaptic transmission through Adenosine triphosphate (ATP) production and Ca²⁺ buffering (Sheng and Cai, 2012, Duarte et al., 2023, Lee et al., 2018, Devine and Kittler, 2018). During ischemic injury, glutamate excitotoxicity alters mitochondrial functioning and trafficking by increasing the production of cofilin rods, thus, ATP supply to the synapses is interrupted. In addition, numerous other glutamate-mediated molecular pathways get triggered, resulting in altered synaptic plasticity and synapse loss (Shu et al., 2019a). Moreover, glial cells like microglia and astrocytes are well-known synaptic sculptors that play an important role in synaptic pruning and maintaining brain homeostasis (Huo et al., 2024, Bosworth and Allen, 2017). Synaptic pruning is part of the CNS development process, including the targeted elimination of non-functional synapses to maintain their appropriate number and improve neural network efficiency (Cornell et al., 2022). Nevertheless, microglia and astrocytes act as double-edged swords upon stroke, engulfing the viable synapses by recognising the “eat me” signals through their surface receptors, resulting in synaptic loss (Neher et al., 2013). Various proinflammatory cytokines are released during the glia-mediated synaptic loss, leading to disruption of the BBB, further aggravating brain injury and synaptic plasticity (Alsbrook et al., 2023).

This present review comprehensively describes the molecular basis of glutamate and glia-mediated synaptic loss in ischemic stroke, current pharmacological targets (Table 1), and the emerging novel approaches for enhancing synaptic plasticity to overcome sensory-motor disability post-stroke. A diversified literature search was conducted in the PubMed, Google Scholar, ScienceDirect, and ResearchGate databases over the last 25 years. Relevant studies were found by using keywords like (synaptic plasticity, stroke, synaptic pruning, stem cell, neurostimulation, optogenetics). Exclusion criteria involve studies irrelevant to the topic and those published in languages other than English.

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