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    Home > Active Ingredient News > Study of Nervous System > CELL: Reactivation of CaMKII can protect optic nerve cells to prevent vision loss from glaucoma

    CELL: Reactivation of CaMKII can protect optic nerve cells to prevent vision loss from glaucoma

    • Last Update: 2021-07-27
    • Source: Internet
    • Author: User
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    Glaucoma is a group of eye diseases with characteristic optic nerve damage and visual field defects
    .


    The World Health Organization has listed it as the second most common blind eye disease worldwide


    Retinal Ganglion Cells (RGC) are the only output neurons that transmit visual information from the retina to the brain


    Recently, a study published in CELL found that a gene therapy can protect the optic nerve cells and protect the eyesight of a mouse model of glaucoma
    .


    These findings provide a way forward for the development of neuroprotective therapies for glaucoma


    Discovered that a gene therapy can protect the optic nerve cells and protect the eyesight of a mouse model of glaucoma


    The CaMKII (calcium/calmodulin-dependent protein kinase II) pathway regulates key cell processes and functions throughout the body, including the retinal ganglion cells in the eye
    .

    The research team found that whenever retinal ganglion cells are exposed to toxins or trauma caused by optic nerve crush, the CaMKII pathway signal is impaired, indicating that there is a correlation between CaMKII activity and retinal ganglion cell survival
    .

    Whenever retinal ganglion cells are exposed to toxins or trauma caused by optic nerve crush, the CaMKII pathway signal is damaged, which indicates that there is a correlation between CaMKII activity and retinal ganglion cell survival
    .


    When looking for interventions, they found that activating the CaMKII pathway through gene therapy proved to have a protective effect on retinal ganglion cells
    .


    Gene therapy of mice before toxic damage (causing rapid damage to cells) and after optic nerve crush (causing slower damage) increased CaMKII activity and strongly protected retinal ganglion cells


    They found that activating the CaMKII pathway through gene therapy proved to have a protective effect on retinal ganglion cells


    77% of retinal ganglion cells survived 12 months after poisoning, compared with 8% in control mice


    According to the cell activity measured by the electroretinogram and the activity pattern of the visual cortex, the increased survival rate of retinal ganglion cells translates into a greater possibility of preserving visual function
    .


    Compared with untreated mice, treated mice are more likely to respond defensively (by hiding, freezing, or wagging their tails) when displaying overhead stimuli designed to simulate threats


    "If we make retinal ganglion cells more resistant and tolerant to the damage that causes glaucoma cell death, they may be able to survive longer and maintain their function," Chen concluded


     

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