Sunday, March 12, 2017
I thoroughly enjoyed reading these weeks articles and found them refreshing to read because they presented a new disease, schizophrenia, to study and different methods in which to study the disease. I preferred the Ayhan et. Al paper studying the neurodevelopmental origin of schizophrenia. When did the effects of the gene, Disrupted-In Schizophrenia-1 (DISC1), mutating develop abnormalities in the brain to become schizophrenia or other mood disorders. Through my first read through this article, it was a bit difficult understanding how exactly their method of expressing mutant hDISC1 in mice was done. Maybe I got lost in all the details, but if the presenters could possibly review how this was done I would have a better understanding, specifically going over Figure 1A. What I found the most interesting about the Ayhan et. Al paper was that they used both male and female mice to conduct the study and they were able to extract data that was more prominent in one sex compared to another. Female mice go through their 4-day Estrous cycle so I wonder if that had an effect in female mice showing increased depressive like symptoms. Thinking about this in its clinical application to humans, knowing that the effects of mutant DISC1 depends on when the protein is expressed, would we be able to do DNA tests before let’s say a baby is born to be able to prevent the protein from being expressed. I feel as though I am approaching “Designer Baby” space of genetics, but if we know what gene largely expresses schizophrenic phenotypes would we be able to prevent that expression in any way. As for the Burrows et al paper, I really found it interesting that they were studying the effects of environment in the expression of the schizophrenic phenotype. This paper countered argued the first paper by saying it does not only come down to nature (genetics) but also nurture (environment). My only quarrel with the paper was that it did not seem to include both sexes of mice since they did not find a significance difference. Furthermore taking this paper into use clinically for humans, would an early intervention in providing a healthy, stimulating environment for those pre-disposed to express the mutant DISC1 gene help prevent that expression or rather delay it?