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Multiple system atrophy: alpha-synuclein and neuronal degeneration.

Mari Yoshida1

  • 1Department of Neuropathology, Institute for Medical Science of Aging, Aichi Medical University, Aichi, Japan. myoshida@aichi-med-u.ac.jp

Neuropathology : Official Journal of the Japanese Society of Neuropathology
|November 21, 2007
PubMed
Summary

Multiple system atrophy (MSA) involves alpha-synuclein accumulation in glial and neuronal cells. Japanese MSA cases show more OPCA than SND, unlike Western patterns, suggesting racial differences in this neurodegenerative disease.

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Area of Science:

  • Neuroscience
  • Pathology
  • Genetics

Background:

  • Multiple system atrophy (MSA) is a rare, sporadic neurodegenerative disease.
  • It presents clinically as olivopontocerebellar atrophy (OPCA), striatonigral degeneration (SND), or Shy-Drager syndrome (SDS).
  • The defining pathological feature is alpha-synuclein aggregation in glial cytoplasmic inclusions (GCIs).

Purpose of the Study:

  • To investigate the pathological spectrum of MSA.
  • To characterize the initial features of alpha-synuclein accumulation in MSA.
  • To explore potential racial differences in MSA phenotypes.

Main Methods:

  • Retrospective analysis of pathological features in 102 MSA cases.
  • Evaluation of alpha-synuclein distribution, including GCIs, neuronal cytoplasmic inclusions (NCIs), and neuronal nuclear inclusions (NNIs).
  • Comparison of pathological subtypes (OPCA-predominant, SND-predominant, equivalent) and their frequency across different populations.

Main Results:

  • 39% of cases showed combined SND and OPCA pathology, 33% OPCA-predominant, and 22% SND-predominant.
  • Japanese MSA cases exhibited a higher frequency of OPCA-type compared to SND-type, contrasting with Western populations.
  • Early-stage MSA showed alpha-synuclein accumulation in neuronal nuclei and cytoplasm, not just GCIs.

Conclusions:

  • MSA pathology exhibits a spectrum, with varying frequencies of OPCA and SND subtypes potentially influenced by race.
  • Alpha-synuclein aggregation occurs in both glial and neuronal cells, including non-fibrillar forms in neurons.
  • A complex interplay involving the oligo-myelin-axon-neuron unit likely drives MSA pathogenesis.