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Blood-brain barrier dysfunction in multiple system atrophy: A human postmortem study.

Ramil Gabdulkhaev1, Hiroshi Shimizu1, Masato Kanazawa2

  • 1Department of Pathology, Brain Research Institute, Niigata University, Niigata, Japan.

Neuropathology : Official Journal of the Japanese Society of Neuropathology
|December 12, 2024
PubMed
Summary

Multiple system atrophy (MSA) involves phosphorylated alpha-synuclein (p-αsyn) affecting oligodendrocyte precursor cells (OPCs). This study found impaired blood-brain barrier (BBB) function in MSA brains, with protein leakage linked to p-αsyn in OPCs.

Keywords:
blood–brain barrierclaudin‐5multiple system atrophyoligodendrocyte precursor cellsphosphorylated α‐synuclein

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Area of Science:

  • Neuroscience
  • Neuropathology

Background:

  • Multiple system atrophy (MSA) is a rare neurodegenerative disease.
  • Pathological hallmark is phosphorylated alpha-synuclein (p-αsyn) in glial cytoplasmic inclusions (GCIs).
  • Oligodendrocyte precursor cells (OPCs) are affected in MSA and are crucial for remyelination and blood-brain barrier (BBB) integrity.

Purpose of the Study:

  • To investigate the hypothesis that BBB is impaired in MSA due to aberrant interactions between affected OPCs and cerebral vasculature.
  • To examine neuropathological changes in the primary motor area of postmortem MSA brains.

Main Methods:

  • Neuropathological examination of postmortem brains from MSA patients and controls.
  • Double immunofluorescence to quantify claudin-5 expression in capillary endothelial cells.
  • Assessment of fibrinogen and IgG extravasation.
  • 3D visualization using chemical tissue clearing and light sheet microscopy.
  • Detection of p-αsyn-positive GCIs in perivascular OPCs.

Main Results:

  • Significantly lower claudin-5 expression in MSA capillary endothelial cells compared to controls.
  • Increased fibrinogen extravasation into the brain parenchyma in MSA patients.
  • Leakage of IgG detected specifically in MSA brain parenchyma.
  • Accumulation of p-αsyn-positive GCIs found along the cerebral vasculature within OPCs.

Conclusions:

  • Blood-brain barrier (BBB) dysfunction and fibrinogen extravasation are consistent findings in MSA.
  • These BBB alterations are likely triggered by the deposition of p-αsyn in perivascular OPCs.
  • Aberrant interactions between affected OPCs and cerebral vasculature contribute to BBB impairment in MSA.