echemi logo
Product
  • Product
  • Supplier
  • Inquiry
    Home > Biochemistry News > Biotechnology News > A new mechanism to prevent toxic DNA damage opens up a treatment avenue for Huntington's disease

    A new mechanism to prevent toxic DNA damage opens up a treatment avenue for Huntington's disease

    • Last Update: 2021-09-13
    • Source: Internet
    • Author: User
    Search more information of high quality chemicals, good prices and reliable suppliers, visit www.echemi.com

    The researchers said that this breakthrough study, published in Cell Reports, may bring much-needed treatments to this rare genetic disease that is currently incurable


    Huntington's disease is a progressive and destructive neurodegenerative disease with an incidence of about 1 in 10,000 in the UK


    This disease is caused by the accumulation of toxic repeat expansion of three DNA fragments called nucleotides (C, A, and G) in the Huntingtin protein (HTT) gene, commonly referred to as repeat expansion disorder


    In this study, the researchers investigated the role of FAN1


    Using human cells and technologies that can read DNA repeat amplification, researchers found that FAN1 can prevent the accumulation of DNA mismatch repair factors, thereby preventing repeat amplification, thereby reducing the toxicity of patient-derived cells


    Dr.


    Drugs that can mimic or enhance the inhibitory effect of FAN1 on mismatch repair will change the course of the disease


    Professor Sarah Tabrizi, senior author of the study and director of the Huntington’s Center for University College London, the Institute of Neurology, University College London, and the Queen’s Square Dementia Institute, University of London, said: “Our next step is to determine whether this interaction is What an important physiological model and examination if it is easy to handle


    The co-senior author of the study, Dr.


    Professor Steve Jackson Program and Adrestia Interim CEO, said: "My colleagues and I are very happy to work with Professor Tabrizi, Dr.


    This research was funded by the CHDI Foundation and the British Dementia Research Institute


    Journal Reference :

    1. Robert Goold, Joseph Hamilton, Thomas Menneteau, Michael Flower, Emma L.



    This article is an English version of an article which is originally in the Chinese language on echemi.com and is provided for information purposes only. This website makes no representation or warranty of any kind, either expressed or implied, as to the accuracy, completeness ownership or reliability of the article or any translations thereof. If you have any concerns or complaints relating to the article, please send an email, providing a detailed description of the concern or complaint, to service@echemi.com. A staff member will contact you within 5 working days. Once verified, infringing content will be removed immediately.

    Contact Us

    The source of this page with content of products and services is from Internet, which doesn't represent ECHEMI's opinion. If you have any queries, please write to service@echemi.com. It will be replied within 5 days.

    Moreover, if you find any instances of plagiarism from the page, please send email to service@echemi.com with relevant evidence.