Open Access

Retraction Note to: A new inducible transgenic mouse model for C9orf72-associated GGGGCC repeat expansion supports a gain-of-function mechanism in C9orf72-associated ALS and FTD

  • Renate K. Hukema1, 7Email author,
  • Fréderike W. Riemslagh1, 2,
  • Shamiram Melhem2,
  • Herma C. van der Linde1,
  • Lies-Anne W. F. M. Severijnen1,
  • Dieter Edbauer3,
  • Alex Maas4,
  • Nicolas Charlet-Berguerand5,
  • Rob Willemsen1 and
  • John C. van Swieten2, 6
Contributed equally
Acta Neuropathologica CommunicationsNeuroscience of Disease20164:129

https://doi.org/10.1186/s40478-016-0401-9

Received: 22 November 2016

Accepted: 1 December 2016

Published: 9 December 2016

The original article was published in Acta Neuropathologica Communications 2014 2:166

Retraction note

The authors are retracting this article [1]. Careful re-examination of the transgenic mice used in this study has indicated that they contain a transgenic sequence containing a 90CGG repeat, associated with fragile X-associated tremor/ataxia syndrome (FXTAS). Apparently, a mixture of two constructs containing the G4C2 repeat and the CGG repeat sequence was injected in oocytes to generate transgenic mice. The presence of the CGG repeat can explain the neuropathology described in the mice used for this study. We are therefore unable to present this transgenic mouse as model for C9orf72 related amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).

Notes

Declarations

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Authors’ Affiliations

(1)
Department of Clinical Genetics, Erasmus Medical Center
(2)
Department of Neurology, Erasmus Medical Center
(3)
German Center for Neurodegenerative Diseases
(4)
Department of Cell Biology, Erasmus Medical Center
(5)
Department of Neurobiology and Genetics, IGBMC, INSERM U964, CNRS UMR7104, University of Strasbourg
(6)
Department of Neurology, Neuroscience Campus Amsterdam
(7)

References

  1. Hukema RK et al (2014) A new inducible transgenic mouse model for C9orf72-associated GGGGCC repeat expansion supports a gain-of-function mechanism in C9orf72-associated ALS and FTD. Acta Neuropathol Commun 2:166. doi:https://doi.org/10.1186/s40478-014-0166-y View ArticlePubMedPubMed CentralGoogle Scholar

Copyright

© The Author(s). 2016

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