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cc-by (c) Franco Fernández, Rafael et al., 2018
Si us plau utilitzeu sempre aquest identificador per citar o enllaçar aquest document: https://hdl.handle.net/2445/139398

Adenosine A2A receptor antagonists in neurodegenerative diseases:Huge potential and huge challenges

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In this opinion paper, we provide scientific-based reasons about the huge therapeutic potential of adenosine A2A receptor antagonists, and about the huge challenges to demonstrate efficacy in clinical trials, i.e., to provide data now required to approve a new medication by the regulatory bodies, such as U.S. Food and Drug Administration (FDA). Adenosine is an autacoid present in all tissue and body fluids. Adenosine, whose extracellular concentration is controlled by producing/degrading enzymes and by nucleoside transporters, acts via four (A1, A2A, A2B, and A3) specific cell surface receptors that belong to the superfamily of G-protein-coupled receptors. For decades, adenosine receptors have shown promise as targets of medications for a variety of ailments. Until recently, however, the only approved medicine was adenosine itself, i.e., the endogenous agonist, to combat arrhythmias, such as paroxysmal supraventricular tachycardia (1-3). Prospects are changing as the first medication targeting selectively the adenosine A2A receptor has been approved few years ago in Japan. The recently approved drug is an antagonist, i.e., a receptor blocker (see later). A2A receptor antagonists show promise in neuroprotection, although for Huntington's or Niemann Pick's diseases it is suggested that antagonists may be detrimental and/or there is controversy on which is the efficacious intervention, i.e., receptor activation or blockade [see Ref. (4-9) and references therein].

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FRANCO FERNÁNDEZ, Rafael, NAVARRO BRUGAL, Gemma. Adenosine A2A receptor antagonists in neurodegenerative diseases:Huge potential and huge challenges. _Frontiers In Psychiatry_. 2018. Vol. 9, núm. 68. [consulta: 31 de desembre de 2025]. ISSN: 1664-0640. [Disponible a: https://hdl.handle.net/2445/139398]

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