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Sökning: onr:"swepub:oai:DiVA.org:umu-98911" > Serum microRNAs in ...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003855naa a2200529 4500
001oai:DiVA.org:umu-98911
003SwePub
008150128s2014 | |||||||||||000 ||eng|
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-989112 URI
0247 a https://doi.org/10.1093/brain/awu2492 DOI
040 a (SwePub)umu
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Freischmidt, Axel4 aut
2451 0a Serum microRNAs in patients with genetic amyotrophic lateral sclerosis and pre-manifest mutation carriers
264 c 2014-09-05
264 1b Oxford University Press (OUP),c 2014
338 a print2 rdacarrier
520 a Knowledge about the nature of pathomolecular alterations preceding onset of symptoms in amyotrophic lateral sclerosis is largely lacking. It could not only pave the way for the discovery of valuable therapeutic targets but might also govern future concepts of pre-manifest disease modifying treatments. MicroRNAs are central regulators of transcriptome plasticity and participate in pathogenic cascades and/or mirror cellular adaptation to insults. We obtained comprehensive expression profiles of microRNAs in the serum of patients with familial amyotrophic lateral sclerosis, asymptomatic mutation carriers and healthy control subjects. We observed a strikingly homogenous microRNA profile in patients with familial amyotrophic lateral sclerosis that was largely independent from the underlying disease gene. Moreover, we identified 24 significantly downregulated microRNAs in pre-manifest amyotrophic lateral sclerosis mutation carriers up to two decades or more before the estimated time window of disease onset; 91.7% of the downregulated microRNAs in mutation carriers overlapped with the patients with familial amyotrophic lateral sclerosis. Bioinformatic analysis revealed a consensus sequence motif present in the vast majority of downregulated microRNAs identified in this study. Our data thus suggest specific common denominators regarding molecular pathogenesis of different amyotrophic lateral sclerosis genes. We describe the earliest pathomolecular alterations in amyotrophic lateral sclerosis mutation carriers known to date, which provide a basis for the discovery of novel therapeutic targets and strongly argue for studies evaluating presymptomatic disease-modifying treatment in amyotrophic lateral sclerosis.
653 a amyotrophic lateral sclerosis
653 a microRNA
653 a mutation carriers
653 a SOD1
653 a C9ORF72
7001 a Mueller, Kathrin4 aut
7001 a Zondler, Lisa4 aut
7001 a Weydt, Patrick4 aut
7001 a Volk, Alexander E.4 aut
7001 a Bozic, Anze Losdorfer4 aut
7001 a Walter, Michael4 aut
7001 a Bonin, Michael4 aut
7001 a Mayer, Benjamin4 aut
7001 a von Arnim, Christine A. F.4 aut
7001 a Otto, Markus4 aut
7001 a Dieterich, Christoph4 aut
7001 a Holzmann, Karlheinz4 aut
7001 a Andersen, Peteru Umeå universitet,Klinisk neurovetenskap,Department of Neurology, Ulm University, Ulm, Germany;Virtual Helmholtz Institute RNA dysmetabolism in Amyotrophic Lateral Sclerosis and Fronto-temporal Dementia, Germany4 aut0 (Swepub:umu)pean0001
7001 a Ludolph, Albert C.4 aut
7001 a Danzer, Karin M.4 aut
7001 a Weishaupt, Jochen H.4 aut
7102 a Umeå universitetb Klinisk neurovetenskap4 org
7730 t Braind : Oxford University Press (OUP)g 137:11, s. 2938-2950q 137:11<2938-2950x 0006-8950x 1460-2156
8564 u https://academic.oup.com/brain/article-pdf/137/11/2938/11142136/awu249.pdf
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-98911
8564 8u https://doi.org/10.1093/brain/awu249

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