Effects of chronic caffeine intake in a mouse model of amyotrophic lateral sclerosis

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...

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Bibliographic Details
Published in:Journal of neuroscience research 2013-04, Vol.91 (4), p.585-592
Main Authors: Potenza, Rosa Luisa, Armida, Monica, Ferrante, Antonella, Pèzzola, Antonella, Matteucci, Alessandra, Puopolo, Maria, Popoli, Patrizia
Format: Article
Language:English
Subjects:
A2ARs
Adenosine A2A receptors
Administration, Oral
ALS
Amyotrophic Lateral Sclerosis - genetics
Amyotrophic Lateral Sclerosis - metabolism
Animals
Body Weight - drug effects
Body Weight - physiology
caffeine
Caffeine - administration & dosage
Disease Models, Animal
Longevity - drug effects
Mice
Mice, Transgenic
Motor Neurons - drug effects
Motor Neurons - metabolism
Motor Skills - drug effects
Receptor, Adenosine A2A - metabolism
Rotarod Performance Test
SOD1G93A mice
Spinal Cord - drug effects
Spinal Cord - metabolism
Superoxide Dismutase - genetics
Superoxide Dismutase - metabolism
Superoxide Dismutase-1
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Summary: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. © 2013 Wiley Periodicals, Inc.
ISSN:0360-4012
1097-4547
DOI:10.1002/jnr.23185