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  • Ogaki, Kotaro (author)

Multiple system atrophy and apolipoprotein E

  • Article/chapterEnglish2018

Publisher, publication year, extent ...

  • 2018-02-14
  • Wiley,2018
  • printrdacarrier

Numbers

  • LIBRIS-ID:oai:DiVA.org:su-155970
  • https://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-155970URI
  • https://doi.org/10.1002/mds.27297DOI

Supplementary language notes

  • Language:English
  • Summary in:English

Part of subdatabase

Classification

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

Notes

  • Background: Dysregulation of the specialized lipid metabolism involved in myelin synthesis and maintenance by oligodendrocytes has been associated with the unique neuropathology of MSA. We hypothesized that apolipoprotein E, which is associated with neurodegeneration, may also play a role in the pathogenesis of MSA. Objective: This study evaluated genetic associations of Apolipoprotein E alleles with risk of MSA and -synuclein pathology, and also examined whether apolipoprotein E isoforms differentially affect -synuclein uptake in a oligodendrocyte cell.Methods: One hundred sixty-eight pathologically confirmed MSA patients, 89 clinically diagnosed MSA patients, and 1,277 control subjects were genotyped for Apolipoprotein E. Human oligodendrocyte cell lines were incubated with -synuclein and recombinant human apolipoprotein E, with internalized -synuclein imaged by confocal microscopy and cells analyzed by flow cytometry.Results: No significant association with risk of MSA or was observed for either Apolipoprotein E 2 or 4. -Synuclein burden was also not associated with Apolipoprotein E alleles in the pathologically confirmed patients. Interestingly, in our cell assays, apolipoprotein E 4 significantly reduced -synuclein uptake in the oligodendrocytic cell line.Conclusions: Despite differential effects of apolipoprotein E isoforms on -synuclein uptake in a human oligodendrocytic cell, we did not observe a significant association at the Apolipoprotein E locus with risk of MSA or -synuclein pathology.

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Added entries (persons, corporate bodies, meetings, titles ...)

  • Martens, Yuka A. (author)
  • Heckman, Michael G. (author)
  • Koga, Shunsuke (author)
  • Labbe, Catherine (author)
  • Lorenzo-Betancor, Oswaldo (author)
  • Wernick, Anna I. (author)
  • Walton, Ronald L. (author)
  • Soto, Alexandra I. (author)
  • Vargas, Emily R. (author)
  • Nielsen, Henrietta M.Stockholms universitet,Institutionen för neurokemi,Mayo Clinic, USA(Swepub:su)hniel (author)
  • Fujioka, Shinsuke (author)
  • Kanekiyo, Takahisa (author)
  • Uitti, Ryan J. (author)
  • van Gerpen, Jay A. (author)
  • Cheshire, William P. (author)
  • Wszolek, Zbigniew K. (author)
  • Low, Phillip A. (author)
  • Singer, Wolfgang (author)
  • Dickson, Dennis W. (author)
  • Bu, Guojun (author)
  • Ross, Owen A. (author)
  • Stockholms universitetInstitutionen för neurokemi (creator_code:org_t)

Related titles

  • In:Movement Disorders: Wiley33:4, s. 647-6500885-31851531-8257

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