Adenosine A2A receptor gene disruption protects in an α-synuclein model of Parkinson's disease.
basic_science · Level V
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- Record sourced from PubMed, PMID 22367999.
- Also identified by DOI 10.1002/ana.22630 and PMC identifier 3292742.
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Abstract
To investigate the putative interaction between chronic exposure to adenosine receptor antagonist caffeine and genetic influences on Parkinson's disease (PD), we determined whether deletion of the adenosine A(2A) receptor in knockout (KO) mice protects against dopaminergic neuron degeneration induced by a mutant human α-synuclein (hm(2)-αSYN) transgene containing both A53T and A30P. The A(2A) KO completely prevented loss of dopamine and dopaminergic neurons caused by the mutant α-synuclein transgene without altering levels of its expression. The adenosine A(2A) receptor appears required for neurotoxicity in a mutant α-synuclein model of PD. Together with prior studies the present findings indirectly support the neuroprotective potential of caffeine and more specific A(2A) antagonists.
Medical subject headings
- Gene Deletion
- Parkinson Disease
- Receptor, Adenosine A2A
- alpha-Synuclein