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This scientific commentary refers to ‘Serum microRNAs in patients with genetic amyotrophic lateral sclerosis and pre-manifest mutation carriers’ by Freischmidt et al. (doi: 10.1093/brain/awu249). Defective RNA processing has occupied centre stage in the pathogenesis of amyotrophic lateral sclerosis (ALS) since the identification of TARDBP (also known as TDP-43) inclusions in 95% of cases and pathogenic mutations in RNA processing genes such as TARDBP , FUS and MATR3 (Sreedharan et al. , 2008; Vance et al. , 2009; Johnson et al. , 2014). FUS and TARDBP are known to regulate mRNA transcription, splicing, stability and transport (Tollervey et al. , 2011; Rogelj et al. , 2012) but they are also part of the large Drosha complex that regulates microRNA (miRNA) biogenesis (Gregory et al. , 2004). Dysregulation of miRNA expression has been shown in many cancers and more recently in Alzheimer’s disease and is predicted to play a mechanistic role and/or be an indirect biomarker of disease.In this issue of Brain , Freischmidt et al. (2014) report that levels of a specific subset of miRNAs are reduced in the serum of patients …

brain

A serum microRNA signature for amyotrophic lateral sclersosis reveals convergent RNA processing defects and identifies presymptomatic mutation carriers