Targeting adenosine A2A receptors in Parkinson's disease.

By M. Schwarzschild, Luigi Francesco Agnati, Kjell Fuxe, Jiang-fan Chen, M. Morelli. 2006

439 citations recorded by the source corpus.

The adenosine A2A receptor has emerged as an attractive non-dopaminergic target in the pursuit of improved therapy for Parkinson's disease (PD), based in part on its unique CNS distribution. It is highly enriched in striatopallidal neurons and can form functional heteromeric complexes with other G-protein-coupled receptors, including dopamine D2, metabotropic glutamate mGlu5 and adenosine A1 receptors. Blockade of the adenosine A2A receptor in striatopallidal neurons reduces postsynaptic effects of dopamine depletion, and in turn lessens the motor deficits of PD. A2A antagonists might partially improve not only the symptoms of PD but also its course, by slowing the underlying neurodegeneration and reducing the maladaptive neuroplasticity that complicates standard 'dopamine replacement' treatments. Thus, we review here a prime example of translational neuroscience, through which antagonism of A2A receptors has now entered the arena of clinical trials with realistic prospects for advancing PD therapeutics.

Subfields: Molecular Biology, Physiology, Polymers and Plastics

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In Molecular Biology

1. Lim Heo
2. Michael Feig
3. Collin F Arbour
4. Yang Zhang
5. Robin Pearce
6. Justin A. Lemkul
7. David Baker

Citations in the corpus

• Multi-State Modeling of G-protein Coupled Receptors at Experimental Accuracy (2021, background): “They are involved in various biological roles such as behavior regulation and regulation of immune system activity.(1,2,10,11) They are subdivided into several classes according to sequence homology and functional similarity: class A (rhodopsin), B1 (secretin), B2 (adhesion), C (glutamate), F (frizz”
• Frontiers in Synaptic Neuroscience Synaptic Neuroscience (neutral): “Here, adenosine A2 receptors, which are coupled to the similar second messenger cascades as D1 receptors (Premont et al., 1977; Schwarzschild et al., 2006) had to be activated for t-LTP induction.”
• Epidemiology and etiology of Parkinson’s disease: a review of the evidence (2011, background): “nist and experimental evidence suggests that it may exert a neuroprotective effect [475, 476].”