Display options
Cite
Bruno C, Sieverding K, Freischmidt A, et al. Haploinsufficiency of TANK-binding kinase 1 prepones age-associated neuroinflammatory changes without causing motor neuron degeneration in aged mice. Brain Commun. 2020;2(2):fcaa133doi: 10.1093/braincomms/fcaa133.
Bruno, C., Sieverding, K., Freischmidt, A., Satoh, T., Walther, P., Mayer, B., Ludolph, A. C., Akira, S., Yilmazer-Hanke, D., Danzer, K. M., Lobsiger, C. S., Brenner, D., & Weishaupt, J. H. (2020). Haploinsufficiency of TANK-binding kinase 1 prepones age-associated neuroinflammatory changes without causing motor neuron degeneration in aged mice. Brain communications, 2(2), fcaa133. https://doi.org/10.1093/braincomms/fcaa133
Bruno, Clara, et al. "Haploinsufficiency of TANK-binding kinase 1 prepones age-associated neuroinflammatory changes without causing motor neuron degeneration in aged mice." Brain communications vol. 2,2 (2020): fcaa133. doi: https://doi.org/10.1093/braincomms/fcaa133
Bruno C, Sieverding K, Freischmidt A, Satoh T, Walther P, Mayer B, Ludolph AC, Akira S, Yilmazer-Hanke D, Danzer KM, Lobsiger CS, Brenner D, Weishaupt JH. Haploinsufficiency of TANK-binding kinase 1 prepones age-associated neuroinflammatory changes without causing motor neuron degeneration in aged mice. Brain Commun. 2020 Aug 21;2(2):fcaa133. doi: 10.1093/braincomms/fcaa133. eCollection 2020. PMID: 33005894; PMCID: PMC7519725.
Copy Download .nbib Format: NLM
Share it on

Brain Commun. 2020 Aug 21;2(2):fcaa133. doi: 10.1093/braincomms/fcaa133. eCollection 2020.

Haploinsufficiency of TANK-binding kinase 1 prepones age-associated neuroinflammatory changes without causing motor neuron degeneration in aged mice.

Brain communications

Clara Bruno, Kirsten Sieverding, Axel Freischmidt, Takashi Satoh, Paul Walther, B Mayer, Albert C Ludolph, Shizuo Akira, Deniz Yilmazer-Hanke, Karin M Danzer, Christian S Lobsiger, David Brenner, Jochen H Weishaupt

Affiliations

  1. Department of Neurology, University of Ulm, 89081 Ulm, Germany.
  2. Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan.
  3. Central Facility for Electron Microscopy, University of Ulm, 89081 Ulm, Germany.
  4. Institute of Epidemiology and Medical Biometry, Ulm University, Ulm, Germany.
  5. Department of Neurology, Clinical Neuroanatomy, Neurology, University of Ulm, 89081 Ulm, Germany.
  6. Institut du Cerveau et de la Moelle Épinière, Institut National de la Santé et de la Recherche Médicale, Centre National de la Recherche Scientifique, Sorbonne Université, 75013 Paris, France.
  7. Division of Neurodegenerative Disorders, Department of Neurology, Medical Faculty Mannheim, Mannheim Center for Translational Neurosciences, Heidelberg University, 61867 Mannheim, Germany.

PMID: 33005894 PMCID: PMC7519725 DOI: 10.1093/braincomms/fcaa133

Abstract

Loss-of-function mutations in TANK-binding kinase 1 cause genetic amyotrophic lateral sclerosis and frontotemporal dementia. Consistent with incomplete penetrance in humans, haploinsufficiency of TANK-binding kinase 1 did not cause motor symptoms in mice up to 7 months of age in a previous study. Ageing is the strongest risk factor for neurodegenerative diseases. Hypothesizing that age-dependent processes together with haploinsufficiency of TANK-binding kinase 1 could create a double hit situation that may trigger neurodegeneration, we examined mice with hemizygous deletion of

© The Author(s) (2020). Published by Oxford University Press on behalf of the Guarantors of Brain.

Keywords: ALS; TBK1; ageing; inflammation; neurogenetics

References

  1. Nat Commun. 2015 Jan 12;6:6047 - PubMed
  2. J Immunother Cancer. 2017 Feb 21;5:18 - PubMed
  3. Nat Neurosci. 2015 May;18(5):631-6 - PubMed
  4. J Clin Invest. 1999 Jan;103(1):5-9 - PubMed
  5. J Neurosci Res. 2011 May;89(5):718-28 - PubMed
  6. PLoS One. 2012;7(4):e34640 - PubMed
  7. J Neurosci. 2017 Apr 26;37(17):4493-4507 - PubMed
  8. J Exp Med. 2010 Sep 27;207(10):2053-63 - PubMed
  9. Nat Neurosci. 2017 Aug;20(8):1162-1171 - PubMed
  10. Neuropathol Appl Neurobiol. 2013 Feb;39(1):19-34 - PubMed
  11. Nat Med. 2013 Mar;19(3):313-21 - PubMed
  12. Elife. 2019 Jul 16;8: - PubMed
  13. Trends Mol Med. 2016 Jun;22(6):511-527 - PubMed
  14. J Neurosci. 2014 Sep 3;34(36):11929-47 - PubMed
  15. Hum Mol Genet. 2017 Oct 1;26(R2):R105-R113 - PubMed
  16. Front Aging Neurosci. 2018 Aug 06;10:236 - PubMed
  17. Front Immunol. 2019 Apr 05;10:711 - PubMed
  18. Autophagy. 2010 May;6(4):495-505 - PubMed
  19. EMBO J. 2000 Sep 15;19(18):4976-85 - PubMed
  20. Int J Mol Sci. 2017 Apr 05;18(4): - PubMed
  21. Nat Immunol. 2012 Nov;13(11):1101-9 - PubMed
  22. Immunity. 2017 Sep 19;47(3):566-581.e9 - PubMed
  23. Neuron. 2020 Jun 3;106(5):789-805.e5 - PubMed
  24. Nat Neurosci. 2008 Apr;11(4):420-2 - PubMed
  25. Acta Neuropathol Commun. 2015 May 23;3:31 - PubMed
  26. Immunity. 2012 Aug 24;37(2):223-34 - PubMed
  27. Science. 2011 Jul 8;333(6039):228-33 - PubMed
  28. J Leukoc Biol. 2010 Dec;88(6):1171-80 - PubMed
  29. Sci Signal. 2011 Aug 09;4(187):pe39 - PubMed
  30. J Exp Med. 2019 Feb 4;216(2):267-278 - PubMed
  31. Nat Commun. 2015 Jan 21;6:6074 - PubMed
  32. Mol Cell. 2011 Feb 18;41(4):458-70 - PubMed
  33. Autophagy. 2019 Oct;15(10):1719-1737 - PubMed
  34. Ann N Y Acad Sci. 2000 Jun;908:244-54 - PubMed
  35. Aging Dis. 2019 Apr 1;10(2):367-382 - PubMed
  36. J Biol Chem. 2001 May 11;276(19):16223-31 - PubMed
  37. Acta Neuropathol. 2015 Jul;130(1):77-92 - PubMed
  38. J Exp Med. 2004 Jun 21;199(12):1641-50 - PubMed

Publication Types