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  • Oeckl, Patrick (author)

Different neuroinflammatory profile in amyotrophic lateral sclerosis and frontotemporal dementia is linked to the clinical phase

  • Article/chapterEnglish2019

Publisher, publication year, extent ...

  • 2018-09-17
  • BMJ Publishing Group Ltd,2019
  • printrdacarrier

Numbers

  • LIBRIS-ID:oai:DiVA.org:umu-157233
  • https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-157233URI
  • https://doi.org/10.1136/jnnp-2018-318868DOI

Supplementary language notes

  • Language:English
  • Summary in:English

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  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

Notes

  • Objective: To investigate the role of neuroinflammation in asymptomatic and symptomatic amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) mutation carriers.Methods: The neuroinflammatory markers chitotriosidase 1 (CHIT1), YKL-40 and glial fibrillary acidic protein (GFAP) were measured in cerebrospinal fluid (CSF) and blood samples from asymptomatic and symptomatic ALS/FTD mutation carriers, sporadic cases and controls by ELISA.Results: CSF levels of CHIT1, YKL-40 and GFAP were unaffected in asymptomatic mutation carriers (n=16). CHIT1 and YKL-40 were increased in gALS (p<0.001, n=65) whereas GFAP was not affected. Patients with ALS carrying a CHIT1 polymorphism had lower CHIT1 concentrations in CSF (-80%) whereas this polymorphism had no influence on disease severity. In gFTD (n=23), increased YKL-40 and GFAP were observed (p<0.05), whereas CHIT1 was nearly not affected. The same profile as in gALS and gFTD was observed in sALS (n=64/70) and sFTD (n=20/26). CSF and blood concentrations correlated moderately (CHIT1, r=0.51) to weak (YKL-40, r=0.30, GFAP, r=0.39). Blood concentrations of these three markers were not significantly altered in any of the groups except CHIT1 in gALS of the Ulm cohort (p<0.05).Conclusion: Our data indicate that neuroinflammation is linked to the symptomatic phase of ALS/FTD and shows a similar pattern in sporadic and genetic cases. ALS and FTD are characterised by a different neuroinflammatory profile, which might be one driver of the diverse presentations of the ALS/FTD syndrome.

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  • Weydt, Patrick (author)
  • Steinacker, Petra (author)
  • Anderl-Straub, Sarah (author)
  • Nordin, FridaUmeå universitet,Klinisk neurovetenskap(Swepub:umu)franon02 (author)
  • Volk, Alexander E. (author)
  • Diehl-Schmid, Janine (author)
  • Andersen, Peter M.,1962-Umeå universitet,Klinisk neurovetenskap,Department of Neurology, Ulm University hospital, Ulm, Germany(Swepub:umu)pean0001 (author)
  • Kornhuber, Johannes (author)
  • Danek, Adrian (author)
  • Fassbender, Klaus (author)
  • Fliessbach, Klaus (author)
  • Jahn, Holger (author)
  • Lauer, Martin (author)
  • Mueller, Kathrin (author)
  • Knehr, Antje (author)
  • Prudlo, Johannes (author)
  • Schneider, Anja (author)
  • Thal, Dietmar R. (author)
  • Yilmazer-Hanke, Deniz (author)
  • Weishaupt, Jochen H. (author)
  • Ludolph, Albert C. (author)
  • Otto, Markus (author)
  • Umeå universitetKlinisk neurovetenskap (creator_code:org_t)

Related titles

  • In:Journal of Neurology, Neurosurgery and Psychiatry: BMJ Publishing Group Ltd90:1, s. 4-100022-30501468-330X

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