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Week 6

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            The papers this week discussed genetic and environmental influences on schizophrenia. The first paper, Ayhan and collaborators looked at the effects of mutant hDISC1 on pre and postnatal mice. What confuses me about the first paper is the testing groups, especially since in the discussion, they mentioned that future research can be done on other age ranges. If schizophrenia typically develops between adolescence and adulthood, why wouldn’t experimenters choose postnatal, sexual maturation, and adulthood? If they discovered the differences in expression of the mutant via differences in neurobehavioral effects in these age groups instead, I think that there would be better implications for treatments. Since schizophrenia is treated through its symptoms, understanding where those symptoms stem from and why they manifest later could be really interesting. I don’t necessarily think that there is clinical significance in looking at prenatal mice in regards to this gene mutation unless researchers discover that what causes this gene to mutate is something that occurs prenatally. Perhaps the goal was to potentially look at differences in people who are born with schizophrenia and those who develop it? Maybe the timing of when this gene is expressed has something to do with that?
            My confusion continued into the second paper. According to the introduction, it has already been shown that environmental enrichment can ameliorate schizophrenia-like behaviors. But, this paper wanted to clarify whether environmental enrichment influences the behavior of mGlu5 KO mice. It’s an interesting study, but how is it applicable to humans? For this to have clinical significance, we first need to know if a person is deficient in these receptors. Does this deficiency appear when symptoms appear or is it from birth? I’d be curious to see if researchers induced schizophrenia-like behaviors using a mutant gene, like the first paper, but then looked at how mGlu5 levels change throughout the lifespan. 

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