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, December 27, 2025

Quinic Acid (QA) Ameliorate Alzheimer's Disease Pathology by Enhancing Endogenous Neurogenesis through Regulating Wnt/β-Catenin Pathway

 Didn't your competent doctor get a protocol going on thisthis year?  Oh no, you DON'T have a functioning stroke doctor, do you? Another reason for coffee. I bet your incompetent? doctor still hasn't installed a 24 hour coffee station.

  • quinic acid (1 post to March 2025)

    • Quinic Acid (QA) Ameliorate Alzheimer's Disease Pathology by Enhancing Endogenous Neurogenesis through Regulating Wnt/β-Catenin Pathway


    First published: 23 December 2025
     
    https://doi.org/10.1002/alz70855_099238
     

    Abstract

    Background

    The Wnt/β-catenin signaling pathway play a vital role in regulating neurogenesis, neuroprotection, synaptic plasticity, and the regulation of amyloid-β in Alzheimer's disease. Activation of this pathway promotes the proliferation of neural progenitor cells and supports their differentiation into neurons. In Alzheimer's disease, the Wnt/β-catenin pathway is often dysregulated, leading to decreased neurogenesis and contributing to cognitive decline. Activation of this pathway offers promising therapeutic strategy for Alzheimer's disease by supporting neuronal regeneration, enhancing cognitive function and reducing neurodegeneration

    Method

    The present study is aimed to investigate the altered neurogenesis in Alzheimer's disease. The AD model were established using Phytohaemagglutinin (PHA) both in vitro and in vivo. Here, we tested Quinic acid (QA), a natural compound, for its potential in halting the disease progression and regulating the Wnt//β-catenin pathway. The growth promoting and neuroprotective activity of QA was confirmed through BrdU proliferation and ROS assay. Behavioral studies and EEG wave spectrum were observed in vivo model of AD for evaluating the altered cognition and memory pattern. The effect of QA compound was further investigated at molecular level using immunoassays for protein and qPCR for gene expression both in vitro and in vivo to confirm their role in activation the Wnt/β-catenin signaling pathway and delaying the disease progression.

    Result

    Our findings showed that QA exhibit promising results against AD pathology. It not only involved in the proliferation of neural progenitor cells (NPCs) and upregulated the neuronal differentiation of cells, but also decreased AD pathology by down regulating the BACE1 and elevated level of ADAM10 which are AD markers. QA can alleviate cognitive deficits by promoting neurogenesis, through regulating the Wnt/β-catenin signal pathway confirmed by upregulation of β-catenin and downregulation of GSK3- β markers. These findings suggest that neuroprotective activity of QA compound was Wnt/ β-catenin meditated which is one of critically involved mediator for neurogenesis and neuronal survivor.

    Conclusion

    In conclusion, these finding suggest that neuronal survivor and neuroprotection serve as better therapeutic approach against the AD and Wnt β/-catenin pathway can be used as modulator to achieve target by delaying the progression of AD.

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