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.
No comments:
Post a Comment