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What Are We Really Affecting?

September 30, 2013 by

After a week of asking questions and asking the same questions again, the mystery of what the Akt/GSK3 pathways does for us has become a little clearer.  Despite all of the questions I cannot answer related to this topic, I can say with confidence that many biological functions that rely on the activation of dopamine and G-protein coupled receptor’s signaling. I have also learned that the Akt/GSK3 pathway is important to neurological well-being and is a factor in many diseases. The article combines these pieces of information by informing us that the Atk/GSK3 pathway is controlled by a G-protein coupled receptor, and by manipulating that pathway there are changes in neural behaviors. However, it is still uncertain as to where in the pathway it is most beneficial to inhibit signaling in order to treat various diseases. With the discussion of this article it has also been established that there is still a lot to learn with the pathways of pharmaceuticals and just how selective these drugs are. This article helped us explore one pathway that is affected by dopamine receptors and how it could be affected various diseases.

I now have a better understanding of this particular pathway, but unfortunately this is only a very small piece to the puzzle to understanding the connections between pathways of neurological diseases, as well as the medications that are prescribed to help “fix” these diseases. The Akt/GSK3 pathway is only one pathway that is influential in diseases, but there is a lot of research that needs to be done to make sure pharmaceuticals are only acting on what they are supposed to.

At the end of the day, the past week has been informative and has opened my eyes to how much is unknown within our brains. I realize that a lot of that has to do with my own novice understanding, but I believe there is so much happening within the brain that progress with this type of research will take scientists a long time to quantify and actually make it useful to the public.

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