Kellendonk and Moore

The focus of this week's papers was the Neural mechanisms behind Schizophrenia. I was not too particularly fond of either of these papers firstly because of the wide sporadic range of the experiments. Also, schizophrenia is large, multi-symptom disorder, which does not have a well suited model. Each paper expressed this, and continued to work with the model anyway. Moore's paper tried to use their MAM E-17 model, and then for specific experiments, did not compare themselves to the previous MAM E-15 model on some occasions.

Kellendonk's work was focused on D2 receptors in the Striatum. I was often confused when trying to differentiate between their definitions of working memory and cognitive functions. They tested a variety of sections of the brain and hypothesized a circuit that, when interrupted, causes schizophrenia like symptoms. The over expression of D2 receptors and overactive dopamine release seems to contribute to interrupting this circuit. It seems interesting, but what the circuit does in the brain is unknown, or not well communicated in the paper. It seemed to me that the Kellendonk team found a center piece of a very large puzzle but no connecting pieces around it. They look into cognitive function but it seemed like they didn't find any conclusive relationship between the circuit disruption. Also, the lesion model used did not seem like a realistic substitute for schizophrenia.

The Moore paper took a different approach in studying different aspects of the disorder. They basically concluded that development during puberty in neuron density affects the outcome of the disorder as adults. Their method took a large physiological approach as they referenced size of specific brain regions after application of their MAM -17, and tried to create a useful model of schizophrenic symptoms via methylation during development.

I would like to see that previous papers modeling Schizophrenia so that I may better understand the physiology because much of what was in these papers was a bit daunting to understand. The overreaching problem seems to be the lack of understanding of Schizophrenia. Creating a model is interesting, but I think it should be focused on one specific symptom based off of one specific variable, and go from there.