• New genetic clues on multiple sclerosis

    From ScienceDaily@1:317/3 to All on Fri Jan 28 21:30:36 2022
    New genetic clues on multiple sclerosis risk

    Date:
    January 28, 2022
    Source:
    Karolinska Institutet
    Summary:
    An international team of researchers has discovered that a cell
    type in the central nervous system known as oligodendrocytes might
    have a different role in the development of multiple sclerosis
    (MS) than previously thought. The findings could open for new
    therapeutical approaches to MS.



    FULL STORY ==========================================================================
    An international team of researchers led by Karolinska Institutet in
    Sweden have discovered that a cell type in the central nervous system
    known as oligodendrocytes might have a different role in the development
    of multiple sclerosis (MS) than previously thought. The findings,
    published in the journal Neuron, could open for new therapeutical
    approaches to MS.


    ==========================================================================
    MS is driven by immune cells attacking oligodendrocytes and the myelin
    they produce, which is an insulating layer ensheathing nerve cells. These attacks disrupt information flow in the brain and spinal cord and causes
    nerve damage that triggers symptoms associated with MS such as tremors
    and loss of gait.

    Understanding which mechanisms influence the risk of MS is central
    to finding effective therapies. Previous genetic studies have found
    regions in the human genome that contain mutations (single nucleotide polymorphisms) associated with increased risk of MS.Many of these regions
    are localized near genes that are active in immune cells.

    Open configuration of the genome In this study, the researchers show in
    mice and human brain samples that oligodendrocytes and their progenitors
    have an open configuration of the genome near immune genes and at
    MS-risk associated regions. This suggests that the MS risk mutations
    may have a role in the activation of nearby genes in oligodendrocytes
    and their progenitors, meaning they could play a more important part
    than previously thought in the development of MS.

    "Our findings suggest that the risk for multiple sclerosis might manifest
    by misfunction not only of immune cells, but also of oligodendrocytes
    and their precursor cells," says Gonc,alo Castelo-Branco, professor
    at the Department of Medical Biochemistry and Biophysics, Karolinska Institutet, who conducted the study with co-first authors Mandy Meijer,
    a PhD student, and Eneritz Agirre, a researcher. "These findings indicate
    that these cells can also be targeted for therapeutical approaches for
    MS, to prevent misfunction that might be caused by these mutations."
    The study was funded by the European Union Horizon 2020, European
    Committee for Treatment and Research in Multiple Sclerosis, Swedish
    Research Council, the Swedish Brain Foundation, the Swedish Cancer
    Society, Knut and Alice Wallenberg Foundation, the Swedish Society
    for Medical Research, the Ming Wai Lau Centre for Reparative Medicine,
    "La Caixa" Foundation, NIH, the National Institute on Aging, the Olav
    Thon Foundation and Karolinska Institutet.

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    ========================================================================== Journal Reference:
    1. Mandy Meijer, Eneritz Agirre, Mukund Kabbe, Cassandra A. van
    Tuijn, Abeer
    Heskol, Chao Zheng, Ana Mendanha Falca~o, Marek Bartosovic,
    Leslie Kirby, Daniela Calini, Michael R. Johnson, M. Ryan
    Corces, Thomas J. Montine, Xingqi Chen, Howard Y. Chang, Dheeraj
    Malhotra, and Gonc,alo Castelo- Branco. Epigenomic priming of
    immune genes implicates oligodendroglia in multiple sclerosis
    susceptibility. Neuron, 2022 DOI: 10.1016/ j.neuron.2021.12.034 ==========================================================================

    Link to news story: https://www.sciencedaily.com/releases/2022/01/220128141316.htm

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