Summer Summary

This summer was tremendously productive for me. I coded my lab’s modeling process into MATLAB, which can analyze data in more sophisticated ways than our old program. This allowed me to tweak some methods in order to find a more accurate way of looking at treatment effects. I then created a tutorial for future lab members that introduces MATLAB and coding principles as well as provides detailed instructions on how to mathematize a model using biochemical systems theory. I created a poster that neatly summarizes my findings regarding insulin signaling in Parkinson’s disease. Finally, I wrote up my findings and submitted my paper to a journal. I even began to work on my next project! For my honors thesis, I plan on studying insulin signaling in neurodegeneration. Over the next year, I’ll create models of insulin signaling in Alzheimer’s disease and Huntington’s disease as well as Parkinson’s. The last week of summer work I was able to get a start on forming a qualitative model of insulin signaling and Alzheimer’s.

Writing an Article

As a summary for my summer research, I wrote an article to submit to a research journal. The writing process did not take as long as I expected because I was so familiar with the information. I did have to spend quite a few days deciding which data to include. I couldn’t publish a graph of every single species change, so I had to decide which graph summarized each individual process the best. The most difficult part was reading through all the requirements of the particular journal I chose and making sure my paper, figures, and references were all in the correct format. The first journal I selected got back to me within 24 hours and said that the subject was not relevant to their target audience, but I reworked the formatting and submitted it to a different, less specific journal. This time, it took about 10 days for an editor to get back to me. This second journal accepted the article for peer review, and now I am waiting to hear back from them again with a final word on whether it’s been accepted as well as any corrections from the peer reviewer. I am so excited to share my research with a wider audience!

Treat the Cause, Not the Symptoms

So far I’ve spent the summer going through seemingly endless iterations of coding, looking at graphs, adjusting some numbers, looking at slightly different graphs… and so on. Finally this week I got my baseline and disease state models working correctly, and began to research treatment strategies! It was a relief to be able to look at something besides MATLAB code for a little while. So far I have added some known Parkinson’s treatments as well as an experimental Huntington’s disease treatment, an immunosuppressant, some anti-inflammatory drugs, an antidepressant, and an insulin sensitizer, all of which target destructive mechanisms in my model.

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Insulin and the Parkinsonian Brain

According to the American Diabetes Association, about 9.3% of the American population has diabetes, with the number rising every year. It is among the top 10 causes of death in the US. Diabetes has a high impact on our society; it’s not surprising that insulin is a household term. Type-2 diabetes is caused by a diet high in fat and sugar and is the result of the body developing a resistance to insulin signaling. Insulin resistance not only creates the abnormal blood glucose levels associated with diabetes, but also impairs central nervous system signaling. Insulin signaling in the dopaminergic (DA) neurons that degenerate in Parkinson’s disease can be inhibited by chronic inflammation and reactive oxygen species (ROS), both of which are elevated in Parkinson’s disease. Conversely, insulin signaling increases dopamine reuptake from the synapse, prevents mitochondrial dysfunction and related ROS production, reduces tau protein accumulation in Lewy bodies, which are characteristic of Parkinson’s, and helps prevent apoptosis by inhibiting the caspase cascade.

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A Computational Biochemical Model of Insulin Resistance in Parkinson’s Disease

Hello! I’m Ellie Braatz, a rising senior Neuroscience major and Chemistry minor working in Dr. Randolph Coleman’s lab. This summer I plan on developing a computational model of insulin resistance in Parkinson’s disease. Parkinson’s disease is a neurodegenerative disorder caused by a loss of dopamine-producing neurons in the substantia nigra area of the brain. Symptoms of Parkinson’s disease include motor and behavioral problems such as tremors, rigidity, and an increased risk of dementia, depression, and anxiety. Insulin resistance, caused by a diet high in fats and sugars, is a precursor to type-II diabetes. With an aging population that exhibits an increasing tendency toward obesity, these two conditions are likely to converge more frequently in the near future.

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