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Acta Neuropathologica Communications logoLink to Acta Neuropathologica Communications
. 2016 Dec 9;4:129. doi: 10.1186/s40478-016-0401-9

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 Hukema 1,7,✉,#, Fréderike W Riemslagh 1,2,#, Shamiram Melhem 2, Herma C van der Linde 1, Lies-Anne W F M Severijnen 1, Dieter Edbauer 3, Alex Maas 4, Nicolas Charlet-Berguerand 5, Rob Willemsen 1,#, John C van Swieten 2,6,#
PMCID: PMC5148842  PMID: 27938413

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).

Footnotes

The online version of the original article can be found under doi:10.1186/s40478-014-0166-y.

References

  • 1.Hukema RK, et al. 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. 2014;2:166. doi: 10.1186/s40478-014-0166-y. [DOI] [PMC free article] [PubMed] [Google Scholar] [Retracted]

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