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.

Saturday, May 3, 2025

Microglial Mechanisms and Therapeutic Potential in Brain Injury Post-Intracerebral Hemorrhage

 Will your incompetent doctor do nothing with this? Well, do you have an incompetent doctor, or not? No knowledge of ALL this earlier research would be my definition of incompetence!

  • Microglial activation (3 posts to September 2021)
  • microglial (3 posts to August 2018)
  • microglial inflammation (1 post to April 2025)
  • microglial polarization (1 post to September 2022)
  • Microglial Mechanisms and Therapeutic Potential in Brain Injury Post-Intracerebral Hemorrhage

    Authors Gong Y, Li H, Cui H, Gong Y

    Received 1 October 2024

    Accepted for publication 13 February 2025

    Published 26 February 2025 Volume 2025:18 Pages 2955—2973

    DOI https://doi.org/10.2147/JIR.S498809

    Checked for plagiarism Yes

    Review by Single anonymous peer review

    Peer reviewer comments 2

    Editor who approved publication: Professor Ning Quan



    Yuhua Gong,1,2 Hui Li,1 Huanglin Cui,1 Yuping Gong2

    1School of Smart Health, Chongqing Polytechnic University of Electronic Technology, Chongqing, 401331, People’s Republic of China; 2Ultrasound Department of the Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, People’s Republic of China

    Correspondence: Yuhua Gong; Yuping Gong, Department of Ultrasound, the Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, People’s Republic of China, Email gongyuhua@cqcet.edu.cn; gyp826@hospital.cqmu.edu.cn

    Abstract: Intracerebral hemorrhage (ICH) is a particularly common public health problem with a high mortality and disability rate and no effective treatments to enhance clinical prognosis. The increased aging population, improved vascular prevention, and augmented use of antithrombotic agents have collectively contributed to the rise in ICH incidence over the past few decades. The exploration and understanding of mechanisms and intervention strategies has great practical significance for expanding treatments and improving prognosis of ICH. Microglia, as resident macrophages of central nervous system, are responsible for the first immune defense post-ICH. After ICH, M1 microglia is firstly activated by primary injury and thrombin; subsequently, reactive microglia can further amplify the immune response and exert secondary injury(Correctly called the 

    neuronal cascade of death! Signifying an immediate need to prevent that! 

    Neuroprotection is a milquetoast term saying nothing!)

      (eg, oxidative stress, neuronal damage, and brain edema). The pro-inflammatory phenotype transmits to M2 microglia within 7 days post-ICH, which plays a key role in erythrophagocytosis and limiting the inflammatory secondary injury. Microglial M2 polarization has significant implications for improving prognosis, this process can be mediated through crosstalk with other cells, metabolic changes, and microbiota interaction. Clarifying the effect, timing, and potential downstream effects of multiple mechanisms that synergistically trigger anti-inflammatory responses may be necessary for clinical translation. Analyses of such intricate interaction between microglia cells and brain injury/repair mechanisms will contribute to our understanding of the critical microglial responses to microenvironment and facilitating the discovery of appropriate intervention strategies. Here, we present a comprehensive overview of the latest evidences on microglial dynamics following ICH, their role in driving primary/secondary injury mechanisms as well as neurorepair/plasticity, and possible treatment strategies targeting microglia.

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