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    Home > Biochemistry News > Biotechnology News > Go to mystify Parkinson's disease

    Go to mystify Parkinson's disease

    • Last Update: 2022-09-15
    • Source: Internet
    • Author: User
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    A team led by researchers at Brigham and Women's Hospital and Harvard Medical School has taken a step toward solving a core puzzle of Parkinson's disease: What is the normal function of this protein? This misfolding of the protein leads to the characteristic aggregation


    In an interview with Gazette, the study's senior author, Vikram Khurana, discussed recent advances and new, personalized approaches to treating Parkinson's disease, as well as the implications of recent discoveries made by neurology lecturer Erinc Hallacli and postdoc Sumaiya Nazeen


    Are we making progress on new treatments for Parkinson's?

    Khurana: We've made tremendous progress, but we also face great challenges


    α-conucleoprotein is a protein whose misfolding is characteristic of Parkinson's


    Khurana: When you knock out α-conucleus proteins out of mice, the mice have little problem, but when you look in more detail at the neurophysiology of mice and the neurons made from these mice, you see that there is a flaw in the way these neurons transmit signals


    How does misfolded α-conucleoprotein cause disease?

    Khurana: Typically, these proteins are high in content and have the characteristics first described by prions, which trigger the misfolding of these normal proteins when they misfold


    You mentioned that α-conucleated protein is useful in transporting vesicles


    Khurana: α-conucleated protein is also abundant in cells far from vesicle membranes


    RNA-binding proteins regulate mRNA, which is the messenger molecule in our cells responsible for transcribing DNA into proteins


    Is it possible that the conuclear protein destroys the p-body and slows down the degradation of the mRNA?

    Khurana: That's what we found


    Why is it important to know this?

    Khurana: Putting Parkinson's disease aside for the time being, gene regulation is very important, and we think of small chameleon proteins like α — conucleus proteins — which we call essential disorders — that are ideal sensors to transmit biological information at the far end of the cell, leading to a response


    First, we found that patients with p-protein mutations had a higher


    Neurodegenerative diseases seem to be particularly difficult to overcome in science – why?

    Khurana: Every problem looks tricky before it's solved, and sometimes progress comes very suddenly


    First, let's take chronic diseases as an example


    Of course, even in a patient's brain, it is conceivable that different brain regions require different treatments
    .
    For example, Parkinson's patients usually come to our clinic when they develop movement disorders, but in the second half of the disease, non-motor symptoms, such as dementia and psychosis, become more prominent and debilitating
    .
    At the time of introduction, we may need to be in the mode of prevention of dementia, but in the mode of treatment of sports diseases, these therapies may be completely different
    .
    In time, perhaps we will need a combination of strategies
    .

    Then there is heterogeneity
    .
    When we first diagnosed Parkinson's disease, not only did patients progress at different rates, but different patients also induced Parkinson's disease in different
    ways.
    In the final stages, the disease may look very similar, but the pathways to get there may be different
    .
    These different paths may require different policies
    .

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