Final Summary Post

Now at the end of my 2017 summer research, I have developed a mature computer model of a cell illustrating the possible reaction pathways affected by hypertension and Alzheimer’s Disease. Although this model is not at a stage to begin transferring the model into code format it has significantly progressed since the beginning of this summer. To recap, I spent this summer using the program Cell Designer to build a computer model of the reaction pathways within a cell that is affected by hypertension and Alzheimer’s Disease. The goal of this model is to provide researchers with information to link hypertension with the development of Alzheimer’s Disease.

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Inflammation Pathways

My model had no inflammation pathways which I wanted to add as part of the developing features of Alzheimer’s Disease. Therefore, I added three to four reaction pathways that ultimately resulted in the inflammation of the cell. These pathways include the AGE/RAGE pathway which is activated when the AGE  protein and the RAGE protein come together to form a complex. This complex then results in the creation of reactive oxidative species (ROS). The activation of ROS then activates the NFkB pathways which ultimately results in the inflammation of the cell. Unfortunately, the model is currently not accessible to me therefore I can not further explain the reaction pathways in greater detail.

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First Pathway

The first reaction pathway that I added to my model was the JAK/STAT pathway. I was hesitant to add my own pathways to the model for the fear of accidentally deleting previous work or adding an incorrect pathway. However, after overcoming that initial fear I began to model the JAK/STAT pathway. This pathway began with the phosphorylation of the JAK2 protein by activation of the Angiotensin II receptor and Angiotensin II coming together to form a complex. The phosphorylated JAK2 protein then went to on activate the phosphorylation of STAT1 and STAT3 protein which formed a heterodimer, which is a complex of two separate proteins. This heterodimer is then transported to the nucleus. Next, the STAT3 protein and the cJun protein form a complex that activates the transcription, and then translation of the protein thrombin which ultimately assists the body in the coagulation of blood.

Accumulating Literature

My research this summer was based on computational neuroscience which is a combination of using computer based programs like Cell Designer in order to model the chemical reactions within a cell. The first step of this research is to build a working model of the cell-based reactions. To build the model, I would  need to read literature based on my topic  – Alzheimer’s Disease and hypertension and accordingly model the pathways depicted on Cell Designer. Visually modeling these reactions and illustrating how a cell can develop features that lead to Alzheimer’s Disease would then provide the foundation to create mathematical algorithms to predict specific outcomes on alteration of the model.

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The Role of Hypertension in Alzheimer’s Disease Progression

Hello! My name is Sonali Shirali and I am a rising sophomore and a neuroscience major at the College of William and Mary. This summer I am conducting research on the role of hypertension and how it correlates with the rise and progression of Alzheimer’s Disease. Specifically, I will be looking into the pathway of the hormone Angiotensin II and how it might affect increasing blood pressure levels and influence Alzheimer’s Disease.