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.

Tuesday, March 3, 2026

Psychedelics and the Extracellular Matrix: Rewiring Neuroplasticity and Metaplasticity for Next-Generation Psychiatric Therapies

 Oh, your incompetent? doctor didn't put together protocols on psychedelics years ago? And your incompetent board of directors hasn't fired them yet?

What about all these drugs for stroke recovery? Doesn't your doctor read the literature AND create protocols from that research? NO? SO TOTALLY INCOMPETENT THEN?

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)

    • Psychedelics and the Extracellular Matrix: Rewiring Neuroplasticity and Metaplasticity for Next-Generation Psychiatric Therapies


    1 ∙ 2 ∙ 3 ∙ 1 hui_ying@jlu.edu.cn ∙ 2,4 xiaohui.wang@ciac.ac.cn
    Affiliations & Notes
    Article Info
    Publication History:
    Received August 11, 2025; Revised January 24, 2026; Accepted February 19, 2026; Published online February 27, 2026
    DOI:  

    Abstract

     Classic psychedelics such as psilocybin, lysergic acid diethylamide (LSD), and N,N-dimethyltryptamine (DMT) have emerged as potent modulators of neuroplasticity and metaplasticity in the adult brain, offering novel therapeutic strategies for neuropsychiatric disorders. Recent findings reveal that beyond their transient psychotropic effects, these compounds activate serotonin 5-HT2A receptors and downstream signaling cascades—including CaMKII, ERK, mTOR, and brain-derived neurotrophic factor (BDNF) pathways—thereby inducing synaptogenesis, dendritic spine remodeling, and transcription of immediate early genes. Critically, the brain's extracellular matrix (ECM), particularly perineuronal nets (PNNs), has been identified as a central regulator of synaptic stability and a key target of psychedelic action. Psychedelics transiently disrupt ECM integrity by loosening PNNs and reorganizing pericellular scaffolds, a process that reopens developmentally restricted critical periods of plasticity and restores circuit-level flexibility. These ECM-mediated metaplastic effects appear essential to the sustained therapeutic outcomes observed in clinical studies of psychedelic-assisted therapy for depression, post-traumatic stress disorder (PTSD), addiction, and potentially neurodegenerative diseases. This manuscript synthesizes current cellular, molecular, and translational evidence highlighting the ECM as a dynamic and permissive substrate through which classic psychedelics exert long-lasting structural and functional brain changes, underscoring its potential as a target for precision interventions in neuropsychiatric care.

    Abstract

    Classic psychedelics such as psilocybin, lysergic acid diethylamide (LSD), and N,N-dimethyltryptamine (DMT) have emerged as potent modulators of neuroplasticity and metaplasticity in the adult brain, offering novel therapeutic strategies for neuropsychiatric disorders. Recent findings reveal that beyond their transient psychotropic effects, these compounds activate serotonin 5-HT2A receptors and downstream signaling cascades—including CaMKII, ERK, mTOR, and brain-derived neurotrophic factor (BDNF) pathways—thereby inducing synaptogenesis, dendritic spine remodeling, and transcription of immediate early genes. Critically, the brain's extracellular matrix (ECM), particularly perineuronal nets (PNNs), has been identified as a central regulator of synaptic stability and a key target of psychedelic action. Psychedelics transiently disrupt ECM integrity by loosening PNNs and reorganizing pericellular scaffolds, a process that reopens developmentally restricted critical periods of plasticity and restores circuit-level flexibility. These ECM-mediated metaplastic effects appear essential to the sustained therapeutic outcomes observed in clinical studies of psychedelic-assisted therapy for depression, post-traumatic stress disorder (PTSD), addiction, and potentially neurodegenerative diseases. This manuscript synthesizes current cellular, molecular, and translational evidence highlighting the ECM as a dynamic and permissive substrate through which classic psychedelics exert long-lasting structural and functional brain changes, underscoring its potential as a target for precision interventions in neuropsychiatric care.
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