Interestingly, I have started to tackle these papers more from the angle of the model/design/paradigm than the actual research question, a surprising shift from my usual perspective that really has only changed while participating in this class. While reading the Burrows paper, I began questioning the translatability of the model because of the environmental enrichment factor. Sure, this way of treating test animals is starkly different from the norm of a basic cage with food and water, but what is the real function? Humans don’t exist in any “paradigm” BUT an enriched environment, except in extreme circumstances. However, after thinking about it, I resolved that that’s not the point – the point is the comparison between the two experimental groups and the difference between the gene-environment interactions. I do feel that the authors should acknowledge the flaw of that model to account for possible differences in human gene-environment interactions, though, as it’s harder to make the distinction of what environmental factors could make a difference in the schizophrenic genotype/endophenotype.
The Ayhan paper was so dense and so fascinating – I’ve always wanted to read more about DISC1. This paper’s model is the most refreshingly convincing model of probably any paper we’ve read so far in this class, and the resulting endophenotypes are promising that treatments based on DISC1 models could be extremely successful. I was also glad to see representation of female mice in the experiment, as we know that there are sex differences in schizophrenia with humans.