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Neuronal Oxidative Stress Promotes α-Synuclein Aggregation In Vivo.

Seok Joon Won1,2, Rebecca Fong1,2, Nicholas Butler1,2

  • 1Department of Neurology, University of California at San Francisco, San Francisco, CA 94158, USA.

Antioxidants (Basel, Switzerland)
|December 23, 2022
PubMed
Summary

Chronic neuronal oxidative stress accelerates alpha-synuclein aggregation in the brain, a key factor in Parkinson's disease development. This study demonstrates a synergistic effect between genetic factors and oxidative stress in promoting disease pathology.

Keywords:
Parkinson’s diseaseaggregatecysteinemotor functionoxidative stressproximity ligation assayα-synuclein

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Area of Science:

  • Neuroscience
  • Pathology
  • Genetics

Background:

  • Parkinson's disease (PD) risk is influenced by genetic and environmental factors.
  • Genetic factors often affect alpha-synuclein (α-syn) aggregation/degradation, while environmental factors induce oxidative stress.
  • In vitro studies link oxidative stress to accelerated α-syn aggregation, but in vivo evidence over time is limited.

Purpose of the Study:

  • To investigate the in vivo impact of chronic neuronal oxidative stress on α-syn aggregate formation.
  • To assess the interaction between genetic α-syn overexpression and impaired cysteine uptake-induced oxidative stress.
  • To evaluate the functional consequences of these interactions on motor function.

Main Methods:

  • Utilized three transgenic mouse strains: hSyn (α-syn overexpression), EAAT3-/- (neuronal oxidative stress), and double-transgenic hSyn/EAAT3-/-.
  • Quantified α-syn aggregates using immunohistochemistry for phosphoserine 129 α-synuclein and proximity ligation assays.
  • Assessed motor function via pole and rotarod tests.

Main Results:

  • Double-transgenic hSyn/EAAT3-/- mice showed significantly higher α-syn aggregate density than hSyn littermates across all brain regions.
  • EAAT3-/- mice exhibited negligible aggregate formation, indicating a synergistic interaction.
  • Impaired motor function correlated with increased α-syn aggregation in double-transgenic mice.

Conclusions:

  • Chronic, low-grade neuronal oxidative stress promotes α-synuclein aggregate formation in vivo.
  • This oxidative stress-induced aggregation may be a key mechanism linking environmental factors to PD pathology.
  • Findings highlight the critical role of oxidative stress in the progression of Parkinson's disease.