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Multiple system atrophy and apolipoprotein E.

Kotaro Ogaki1, Yuka A Martens1, Michael G Heckman2

  • 1Department of Neuroscience, Mayo Clinic, Jacksonville, Florida, USA.

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|February 15, 2018
PubMed
Summary
This summary is machine-generated.

Apolipoprotein E (APOE) isoforms did not show a significant association with Multiple System Atrophy (MSA) risk or alpha-synuclein pathology. However, APOE ε4 reduced alpha-synuclein uptake in oligodendrocytes in cell assays.

Keywords:
apolipoprotein Egeneticsmultiple system atrophyoligodendrocyteprotection

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Area of Science:

  • Neuroscience
  • Genetics
  • Lipid Metabolism

Background:

  • Oligodendrocyte lipid metabolism dysregulation is linked to Multiple System Atrophy (MSA) neuropathology.
  • Apolipoprotein E (APOE), known for its role in neurodegeneration, was investigated for its potential involvement in MSA pathogenesis.

Purpose of the Study:

  • To assess genetic links between Apolipoprotein E (APOE) alleles and the risk of developing MSA.
  • To investigate the association of APOE alleles with alpha-synuclein pathology in MSA patients.
  • To determine if APOE isoforms differentially influence alpha-synuclein uptake in oligodendrocytes.

Main Methods:

  • Genotyping of Apolipoprotein E (APOE) alleles in 168 pathologically confirmed MSA patients, 89 clinically diagnosed MSA patients, and 1,277 controls.
  • Incubation of human oligodendrocyte cell lines with alpha-synuclein and recombinant human APOE.
  • Confocal microscopy and flow cytometry to analyze alpha-synuclein internalization by oligodendrocytes.

Main Results:

  • No significant association was found between Apolipoprotein E (APOE) ɛ2 or ɛ4 alleles and the risk of MSA.
  • Alpha-synuclein burden in pathologically confirmed MSA patients was not associated with APOE alleles.
  • APOE ɛ4 significantly decreased alpha-synuclein uptake in the studied oligodendrocyte cell line.

Conclusions:

  • While APOE isoforms exhibit differential effects on alpha-synuclein uptake in oligodendrocytes, no significant genetic association was observed between the APOE locus and MSA risk or alpha-synuclein pathology.
  • The study did not find a direct genetic link between APOE and MSA risk or pathology, despite in vitro findings.
  • Further research may be needed to elucidate the complex role of APOE in MSA pathogenesis.