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Tuxworth RI, Taylor MJ, Martin Anduaga A, et al. Attenuating the DNA damage response to double-strand breaks restores function in models of CNS neurodegeneration. Brain Commun. 2019;1(1):fcz005doi: 10.1093/braincomms/fcz005.
Tuxworth, R. I., Taylor, M. J., Martin Anduaga, A., Hussien-Ali, A., Chatzimatthaiou, S., Longland, J., Thompson, A. M., Almutiri, S., Alifragis, P., Kyriacou, C. P., Kysela, B., & Ahmed, Z. (2019). Attenuating the DNA damage response to double-strand breaks restores function in models of CNS neurodegeneration. Brain communications, 1(1), fcz005. https://doi.org/10.1093/braincomms/fcz005
Tuxworth, Richard I, et al. "Attenuating the DNA damage response to double-strand breaks restores function in models of CNS neurodegeneration." Brain communications vol. 1,1 (2019): fcz005. doi: https://doi.org/10.1093/braincomms/fcz005
Tuxworth RI, Taylor MJ, Martin Anduaga A, Hussien-Ali A, Chatzimatthaiou S, Longland J, Thompson AM, Almutiri S, Alifragis P, Kyriacou CP, Kysela B, Ahmed Z. Attenuating the DNA damage response to double-strand breaks restores function in models of CNS neurodegeneration. Brain Commun. 2019 Jul 02;1(1):fcz005. doi: 10.1093/braincomms/fcz005. eCollection 2019. PMID: 32954257; PMCID: PMC7425387.
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Brain Commun. 2019 Jul 02;1(1):fcz005. doi: 10.1093/braincomms/fcz005. eCollection 2019.

Attenuating the DNA damage response to double-strand breaks restores function in models of CNS neurodegeneration.

Brain communications

Richard I Tuxworth, Matthew J Taylor, Ane Martin Anduaga, Alaa Hussien-Ali, Sotiroula Chatzimatthaiou, Joanne Longland, Adam M Thompson, Sharif Almutiri, Pavlos Alifragis, Charalambos P Kyriacou, Boris Kysela, Zubair Ahmed

Affiliations

  1. Institute of Cancer and Genomic Sciences, University of Birmingham, Birmingham B15 2TT, UK.
  2. Department of Genetics & Genome Biology, University of Leicester, Leicester LE1 7RH, UK.
  3. Centre for Biomedical Science, Centre of Gene and Cell Therapy, School of Biological Sciences, Royal Holloway University of London, Surrey TW20 0EX, UK.
  4. Neuroscience and Ophthalmology, College of Medical and Dental Sciences, Institute of Inflammation and Ageing, University of Birmingham, Birmingham B15 2TT, UK.
  5. Applied Medical Science College, Shaqra University, Addawadmi, Riyadh, Saudi Arabia.
  6. Aston Medical School, Aston Medical Research Institute, Aston University, Aston Triangle, Birmingham B4 7ET, UK.

PMID: 32954257 PMCID: PMC7425387 DOI: 10.1093/braincomms/fcz005

Abstract

DNA double-strand breaks are a feature of many acute and long-term neurological disorders, including neurodegeneration, following neurotrauma and after stroke. Persistent activation of the DNA damage response in response to double-strand breaks contributes to neural dysfunction and pathology as it can force post-mitotic neurons to re-enter the cell cycle leading to senescence or apoptosis. Mature, non-dividing neurons may tolerate low levels of DNA damage, in which case muting the DNA damage response might be neuroprotective. Here, we show that attenuating the DNA damage response by targeting the meiotic recombination 11, Rad50, Nijmegen breakage syndrome 1 complex, which is involved in double-strand break recognition, is neuroprotective in three neurodegeneration models in

© The Author(s) (2019). Published by Oxford University Press on behalf of the Guarantors of Brain.

Keywords: CNS trauma; DNA damage; neurodegeneration; neuroprotection; spinal cord injury

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