Interestingly, transcriptional profiling of C9orf72-deficient spinal cords revealed age-related upregulation of inflammatory pathways, which overlapped with C9-associated FTD patient tissue more than sporadic FTD tissue, suggesting that altered or enhanced neuroinflammation may also exist in C9orf72-carrier brain tissue [21, 112]. This evidence concerns the gene C9 and frontotemporal dementia.