Large expansions of a non-coding GGGGCC-repeat in the first intron of the 
C9orf72 gene are a common cause of both amyotrophic lateral sclerosis (ALS) and 
frontotemporal dementia (FTD). G-rich sequences have a propensity for forming 
highly stable quadruplex structures in both RNA and DNA termed G-quadruplexes. 
G-quadruplexes have been shown to be involved in a range of processes including 
telomere stability and RNA transcription, splicing, translation and transport. 
Here we show using NMR and CD spectroscopy that the C9orf72 hexanucleotide 
expansion can form a stable G-quadruplex, which has profound implications for 
disease mechanism in ALS and FTD.