Sunday, March 12, 2017

Week 6

The first paper I read was Kellendonk et al.'s, which I found very interesting and thorough. While I've never studied schizophrenia, I found this paper giving enough in-depth background to understand their studies. While reading, I felt that the paper was so thorough that it actually became a bit repetitive. By the end, there was an accumulation of support for D2 activation and its major role in the striatum. In addition, this was connected with an increase in D1 activation in the prefrontal cortex, which led to a decrease in working memory functioning. However, and this may be due to my lack of neuroanatomy and understanding of circuits, I'm unclear on how the alteration in D1 activity led to the behavioral symptoms of cognitive deficits. In addition, it would be interesting to see how D1 antagonists could be used clinically to alleviate cognitive behaviors associated with schizophrenia and not yet addressed by current medication (I did notice they mentioned D1 antagonists in the discussion, but were inconclusive in their ultimate effectiveness). I think one of the most interesting clinical points that the authors brought up was that if turning off the D2 receptor enhancement did not affect the cognitive deficits, how could we treat schizophrenic patients if their brains have already adapted in line with this schizophrenic model? This idea is pretty grim for schizophrenic treatment, and I think more research should be done into how these alterations come about and what can be done to prevent permanent morphologies. 

Moore et al.'s paper was, in my opinion, the outlier of all of the papers we read. As I often criticize the realities of animal models, I believe this paper was extremely useful in providing the outline to how to create a proper animal model and thorough ways in which to test it. This paper, while starkingly different, provided an appropriate compliment to Kellendonk et al.'s, who claimed that genetic manipulation, while useful, is extremely limited in scope. Additionally, if the E17 is actually representative of a clinical model, this could be instrumental in providing biomarkers in order to prevent morphological changes before it's "too late". I think the E17 model proves, at least by my standards, representative of schizophrenia, and because of its focus on development from the root cause, it seems to be more reliable and informative. 

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