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Event Abstract Back to Event Blockade of Adenosine Receptors by Caffeine Provides Neuroprotection in a Lentiviral Mouse Model of Machado-Joseph Disease Nelio Goncalves1, 2, 3*, Ana T. Simoes2, 3, Rodrigo A. Cunha2, 4 and Luis Pereira-de-Almeida2, 3 1 University of Coimbra, PhD Programme in Experimental Biology and Biomedicine, Center for Neuroscience and Cell Biology, Portugal 2 University of Coimbra, Center for Neuroscience and Cell Biology, Portugal 3 University of Coimbra, Faculty of Pharmacy, Portugal 4 University of Coimbra, Institute of Biochemistry, Faculty of Medicine, Portugal Machado Joseph Disease (MJD) or spinocerebellar ataxia type 3, a devastating brain disease, is one of the nine dominantly-inherited polyglutamine neurodegenerative disorders presently known, and it is considered to result from a toxic gain of function of mutant ataxin-3, a polyubiquitin-binding protein. The mechanisms accounting for neuronal degeneration are still largely unknown and there is currently no treatment available. One candidate strategy to manage MJD neurodegeneration might be the antagonism of adenosine A2A receptors (A2ARs). In fact, A2AR blockade has been shown to afford robust neuroprotection in different neurodegenerative disorders based on the key role of A2ARs to control glutamatergic transmission, apoptotic neuronal death, astrocytic function and neuroinflammation. This prompts the hypothesis that the manipulation of A2AR function might also be beneficial in MJD.A non-selective antagonism of the A2AR function promoted by the chronic consumption of caffeine (applied through the drinking water – 1g/L) was carried out in a lentiviral mouse model of MJD (Alves et al, 2008). Preliminary data suggest that caffeine led to an increase in the number of mutant ataxin-3 intranuclear inclusions in the striatum, a reduction in the loss of immunoreactivity for the dopaminergic marker DARPP-32, a decrease in the number of pycnotic nuclei and a reduction of the MJD-associated astrogliosis over time, when compared to the control group that only drank water. Further studies are necessary to confirm if blockade of A2ARs is indeed able to control striatal pathology associated with MJD. Conference: 11th Meeting of the Portuguese Society for Neuroscience, Braga, Portugal, 4 Jun - 6 Jun, 2009. Presentation Type: Poster Presentation Topic: Neurodegenerative Disorders Citation: Goncalves N, Simoes AT, Cunha RA and Pereira-de-Almeida L (2009). Blockade of Adenosine Receptors by Caffeine Provides Neuroprotection in a Lentiviral Mouse Model of Machado-Joseph Disease. Front. Neurosci. Conference Abstract: 11th Meeting of the Portuguese Society for Neuroscience. doi: 10.3389/conf.neuro.01.2009.11.105 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 10 Aug 2009; Published Online: 10 Aug 2009. * Correspondence: Nelio Goncalves, University of Coimbra, PhD Programme in Experimental Biology and Biomedicine, Center for Neuroscience and Cell Biology, Coimbra, Portugal, neliomotag@gmail.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Nelio Goncalves Ana T Simoes Rodrigo A Cunha Luis Pereira-de-Almeida Google Nelio Goncalves Ana T Simoes Rodrigo A Cunha Luis Pereira-de-Almeida Google Scholar Nelio Goncalves Ana T Simoes Rodrigo A Cunha Luis Pereira-de-Almeida PubMed Nelio Goncalves Ana T Simoes Rodrigo A Cunha Luis Pereira-de-Almeida Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.
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