Enjoy your cuppa java!
A lot of them!
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Neuropharmacology. 2014 Jul 11. pii: S0028-3908(14)00267-6. doi: 10.1016/j.neuropharm.2014.06.029. [Epub ahead of print]
Chronic Caffeine Treatment Protects Against Experimental Autoimmune Encephalomyelitis in Mice: Therapeutic Window and Receptor Subtype Mechanism.
Wang T1, Xi NN1, Chen Y1, Shang XF1, Hu Q1, Chen JF2, Zheng RY3.
Abstract
Chronic treatment with caffeine, the most widely consumed psychoactive drug and a non-selective antagonist of adenosine receptors, can protection against myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). In this study, we investigated the mechanism underlying caffeine-mediated neuroprotection against EAE by determining the effective therapeutic time-window of caffeine and the involvement of adenosine A2A and A1 receptor. We found that administration of caffeine during the effector phase (10→20 days post-immunization, d.p.i., corresponding to appearance of neurological deficits) but not the induction phase (0→10 d.p.i., before the appearance of ascending flaccid paralysis) significantly ameliorated EAE-induced neurobehavioral deficits, reduced the infiltration of inflammatory cells into the spinal cord and reduced the demyelination of spinal cord. Furthermore, genetic deletion of the A2AR exacerbated MOG-induced brain damage and caffeine administering to A2AR knockout mice reversed this EAE pathology by acting at non-A2AR target. The protective effect of chronic caffeine treatment was associated with up-regulation of brain A1R (but not A2AR). The identification of the effective therapeutic window of caffeine at the effector phase and clarification of non-A2AR target (likely A1R) in caffeine action in EAE models advance the therapeutic prospective that chronic caffeine consumption may attenuate brain damage in MS.
Only registered and activated users can see links., Click Here To Register...
Neuropharmacology. 2014 Jul 11. pii: S0028-3908(14)00267-6. doi: 10.1016/j.neuropharm.2014.06.029. [Epub ahead of print]
Chronic Caffeine Treatment Protects Against Experimental Autoimmune Encephalomyelitis in Mice: Therapeutic Window and Receptor Subtype Mechanism.
Wang T1, Xi NN1, Chen Y1, Shang XF1, Hu Q1, Chen JF2, Zheng RY3.
Abstract
Chronic treatment with caffeine, the most widely consumed psychoactive drug and a non-selective antagonist of adenosine receptors, can protection against myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). In this study, we investigated the mechanism underlying caffeine-mediated neuroprotection against EAE by determining the effective therapeutic time-window of caffeine and the involvement of adenosine A2A and A1 receptor. We found that administration of caffeine during the effector phase (10→20 days post-immunization, d.p.i., corresponding to appearance of neurological deficits) but not the induction phase (0→10 d.p.i., before the appearance of ascending flaccid paralysis) significantly ameliorated EAE-induced neurobehavioral deficits, reduced the infiltration of inflammatory cells into the spinal cord and reduced the demyelination of spinal cord. Furthermore, genetic deletion of the A2AR exacerbated MOG-induced brain damage and caffeine administering to A2AR knockout mice reversed this EAE pathology by acting at non-A2AR target. The protective effect of chronic caffeine treatment was associated with up-regulation of brain A1R (but not A2AR). The identification of the effective therapeutic window of caffeine at the effector phase and clarification of non-A2AR target (likely A1R) in caffeine action in EAE models advance the therapeutic prospective that chronic caffeine consumption may attenuate brain damage in MS.
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