Caffeine Neuroprotection Decreases A2A Adenosine Receptor Content in Aged Mice.

Caffeine Neuroprotection Decreases A2A Adenosine Receptor Content in Aged Mice. Neurochem Res. 2019 Jan 04;: Authors: Garcez ML, Damiani AP, Pacheco R, Rodrigues L, de Abreu LL, Alves MC, de Andrade VM, Boeck CR Abstract Caffeine is a bioactive compound worldwide consumed with effect into the brain. Part of its action in reducing incidence or delaying Alzheimer's and Parkinson's diseases symptoms in human is credited to the adenosine receptors properties. However, the impact of caffeine consumption during aging on survival of brain cells remains debatable. This work, we investigated the effect of low-dose of caffeine on the ectonucleotidase activities, adenosine receptors content, and paying particular attention to its pro-survival effect during aging. Male young adult and aged Swiss mice drank water or caffeine (0.3 g/L) ad libitum for 4 weeks. The results showed that long-term caffeine treatment did not unchanged ATP, ADP or AMP hydrolysis in hippocampus when compared to the mice drank water. Nevertheless, the ATP/ADP hydrolysis ratio was higher in young adult (3:1) compared to the aged (1:1) animals regardless of treatment. The content of A1 receptors did not change in any groups of mice, but the content of A2A receptors was reduced in hippocampus of mice that consumed caffeine. Moreover, the cell viability results indicated that aged mice not only had increased pyknotic neurons in the hippocampus but also had reduced damage aft...
Source: Neurochemical Research - Category: Neuroscience Authors: Tags: Neurochem Res Source Type: research