Journal
JOURNAL OF NEUROSCIENCE RESEARCH
Volume 91, Issue 4, Pages 585-592Publisher
WILEY
DOI: 10.1002/jnr.23185
Keywords
caffeine; adenosine A2A receptors; A2ARs; SOD1G93A mice; ALS
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Caffeine is a nonselective adenosine receptor antagonist; chronic consumption has proved protective toward neurodegenerative diseases such as Parkinson's and Alzheimer's diseases. The present study was designed to determine whether caffeine intake affected survival and/or motor performance in a transgenic model of amyotrophic lateral sclerosis (ALS). SOD1G93A mice received caffeine through drinking water from 70 days of age until death. Body weight, motor performance and survival were evaluated. Furthermore, the expression of adenosine A2A receptors (A2ARs), glial glutamate transporter (GLT1), and glial fibrillar acidic protein (GFAP) were evaluated by Western blotting. The results showed that caffeine intake significantly shortened the survival of SOD1G93A mice (log rank test, P = 0.01) and induced a nonsignificant advancing of disease onset. The expression of A2AR, GLT1, and GFAP was altered in the spinal cords of ALS mice, but caffeine did not influence their expression in either wild-type or SOD1G93 mice. These data indicate that adenosine receptors may play an important role in ALS. (c) 2013 Wiley Periodicals, Inc.
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