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Analyzing the Parkinson's Disease Mouse Model Induced by Adeno-associated Viral Vectors Encoding Human α-Synuclein
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Analyzing the Parkinson's Disease Mouse Model Induced by Adeno-associated Viral Vectors Encoding Human α-Synuclein

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Adenosine A2A receptor gene disruption protects in an α-synuclein model of Parkinson's disease

Anil Kachroo1, Michael A Schwarzschild

  • 1MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, Massachusetts General Hospital, Boston, USA. akachroo@partners.org

Annals of Neurology
|February 28, 2012
PubMed

Insights

Mice lacking the adenosine A(2A) receptor were protected from neurodegeneration caused by mutant alpha-synuclein. This suggests the adenosine A(2A) receptor is required for Parkinson's disease neurotoxicity.

Area of Science:

  • Neuroscience
  • Genetics
  • Pharmacology

Background:

  • Parkinson's disease (PD) is a neurodegenerative disorder.
  • Caffeine, an adenosine receptor antagonist, may have neuroprotective effects in PD.
  • The role of the adenosine A(2A) receptor in PD pathogenesis is not fully understood.

Purpose of the Study:

  • To investigate the interaction between chronic caffeine exposure and genetic factors in PD.
  • To determine if deleting the adenosine A(2A) receptor protects against neurodegeneration in a PD mouse model.

Main Methods:

  • Utilized knockout (KO) mice lacking the adenosine A(2A) receptor.
  • Introduced a mutant human alpha-synuclein (hm(2)-αSYN) transgene (A53T and A30P mutations) to induce neurodegeneration.
  • Assessed dopaminergic neuron survival and dopamine levels.

Main Results:

  • Complete prevention of dopamine and dopaminergic neuron loss in A(2A) KO mice.
  • No alteration in mutant alpha-synuclein transgene expression levels.
  • The adenosine A(2A) receptor is essential for neurotoxicity in this PD model.

Conclusions:

  • The adenosine A(2A) receptor is required for neurotoxicity in a mutant alpha-synuclein-induced PD model.
  • These findings indirectly support the neuroprotective potential of caffeine and A(2A) antagonists in PD.

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