The C9orf72 hexanucleotide repeat expansion in FTD and ALS
Author:
Publisher
Springer Science and Business Media LLC
Subject
Cellular and Molecular Neuroscience,Clinical Neurology
Link
http://www.nature.com/articles/nrneurol.2012.58.pdf
Reference9 articles.
1. DeJesus-Hernandez, M. et al. Expanded GGGGCC hexanucleotide repeat in non-coding region of C9ORF72 causes chromosome 9p-linked FTD and ALS. Neuron 72, 245–256 (2011).
2. Renton, A. E. et al. A nexanucleotide repeat expansion in C9ORF72 is the cause of chromosome 9p21-linked ALS–FTD. Neuron 71, 257–268 (2011).
3. Simon-Sanchez, J. et al. The clinical and pathological phenotype of C9orf72 hexanucleotide repeat expansions. Brain http://dx.doi.org/10.1093/brain/awr353 .
4. Snowden, J. S. et al. Distinct clinical and pathological characteristics of frontotemporal dementia associated with C9ORF72 mutations. Brain http://dx.doi.org/10.1093/brain/awr355 .
5. Mackenzie, I. R. et al. Heterogeneity of ubiquitin pathology in frontotemporal lobar degeneration: classification and relation to clinical phenotype. Acta Neuropathol. 112, 539–549 (2006).
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