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Effects of chronic caffeine intake in a mouse model of amyotrophic lateral sclerosis
Author(s) -
Potenza Rosa Luisa,
Armida Monica,
Ferrante Antonella,
Pèzzola Antonella,
Matteucci Alessandra,
Puopolo Maria,
Popoli Patrizia
Publication year - 2013
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.23185
Subject(s) - amyotrophic lateral sclerosis , caffeine , sod1 , adenosine , glutamate receptor , adenosine receptor , receptor , medicine , endocrinology , adenosine a1 receptor , genetically modified mouse , astrocyte , glial fibrillary acidic protein , pharmacology , biology , transgene , disease , central nervous system , immunohistochemistry , biochemistry , agonist , gene
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). SOD1 G93A 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 A 2A receptors (A 2A Rs), 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 SOD1 G93A mice (log rank test, P = 0.01) and induced a nonsignificant advancing of disease onset. The expression of A 2A R, GLT1, and GFAP was altered in the spinal cords of ALS mice, but caffeine did not influence their expression in either wild‐type or SOD1 G93 mice. These data indicate that adenosine receptors may play an important role in ALS. © 2013 Wiley Periodicals, Inc.