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Multiple system atrophy: experimental models and reality.

Cassia Overk1, Edward Rockenstein1, Elvira Valera1

  • 1Department of Neurosciences, University of California, San Diego, La Jolla, CA, 92093-0624, USA.

Acta Neuropathologica
|October 24, 2017
PubMed
Summary
This summary is machine-generated.

Multiple system atrophy (MSA) is a fatal neurodegenerative disease. Research explores alpha-synuclein (α-syn) accumulation in brain cells to improve disease models and find treatments.

Keywords:
In vivo modelsMultiple system atrophySynucleinopathies

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Area of Science:

  • Neuroscience
  • Pathology
  • Genetics

Background:

  • Multiple system atrophy (MSA) is a fatal synucleinopathy affecting the aging population.
  • Characterized by parkinsonism, dysautonomia, and ataxia.
  • Unlike other synucleinopathies, α-synuclein (α-syn) primarily accumulates in oligodendroglial cells in MSA.

Purpose of the Study:

  • To investigate the mechanisms of α-synuclein (α-syn) deposition in oligodendrocytes and neurons in MSA.
  • To evaluate existing in vivo models of MSA.
  • To guide the development of improved MSA models and therapeutic strategies.

Main Methods:

  • Review of existing in vivo models, including transgenic mice and viral vector-based models.
  • Analysis of studies investigating α-synuclein (α-syn) transfer versus overexpression in oligodendroglial cells.
  • Comparison of model recapitulation of MSA neuropathological and functional aspects.

Main Results:

  • Current in vivo models partially replicate MSA's neuropathological and functional features.
  • The precise mechanisms of α-synuclein (α-syn) accumulation in oligodendrocytes and neurons remain unclear.
  • No single model fully replicates the entire spectrum of MSA.

Conclusions:

  • Improved understanding of α-synuclein (α-syn) accumulation mechanisms is crucial for developing better MSA models.
  • Development of models that fully recapitulate MSA pathology is needed.
  • Translatable biomarkers for early-stage MSA are essential for devising effective disease-modifying therapeutics.