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Poststroke Induction of α-Synuclein Mediates Ischemic Brain Damage.

TaeHee Kim1, Suresh L Mehta2, Balarama Kaimal2

  • 1Department of Neurological Surgery, Neuroscience Training Program.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|July 1, 2016
PubMed
Summary

Alpha-synuclein (α-Syn) plays a key role in stroke-induced brain damage. Reducing α-Syn expression or blocking its phosphorylation improves neurological recovery and reduces infarct size after stroke, suggesting it as a therapeutic target.

Keywords:
brainneuroprotectionstrokeα-synuclein

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pathology

Background:

  • Alpha-synuclein (α-Syn) is implicated in Parkinson's disease and other synucleinopathies.
  • The role of α-Syn in acute neurodegenerative disorders like stroke remains unclear.
  • Stroke involves complex pathophysiological mechanisms that may involve α-Syn.

Purpose of the Study:

  • To investigate the role of α-Syn in poststroke brain damage.
  • To determine if preventing α-Syn expression is neuroprotective after stroke.
  • To explore α-Syn as a potential therapeutic target for stroke.

Main Methods:

  • Induction of transient focal ischemia in adult rodent models.
  • Assessment of α-Syn protein expression and localization.
  • α-Syn knockdown and knockout studies.
  • Evaluation of infarct volume and neurological recovery.
  • Analysis of molecular markers of mitochondrial fragmentation, oxidative stress, apoptosis, and autophagy.
  • Investigation of serine-129 phosphorylated α-Syn (pα-Syn) and its kinase, PLK2.

Main Results:

  • Transient focal ischemia upregulated α-Syn expression and nuclear translocation.
  • α-Syn knockdown or knockout significantly reduced infarct size and improved neurological recovery.
  • α-Syn knockdown attenuated postischemic markers of mitochondrial dysfunction, oxidative stress, apoptosis, and autophagy.
  • Ischemia increased serine-129 phosphorylation (pα-Syn) and nuclear translocation of α-Syn.
  • Mice lacking PLK2 (kinase for S129 phosphorylation) showed improved outcomes after ischemia.

Conclusions:

  • α-Syn contributes to neuronal damage and functional deficits after stroke.
  • Reducing α-Syn expression or blocking its S129 phosphorylation is neuroprotective.
  • α-Syn represents a promising therapeutic target for minimizing brain damage following stroke.