My poster is split into seven different sections. The first, introduction, defines an ischemic stroke as "the result of something inhibiting blood flow to the brain, which prevents oxygen and glucose from reaching brain cells." This causes mass cell death in the brain, and while scientists have found ways to put an end to a stroke, there are no current medications specially designed to assist with post-stroke recovery. 

TET proteins are a family of proteins found in the brain that are known to assist in brain function and recovery in the wake of trauma to the brain. The objective of this research is to better understand how TET1 assists in the recovery process and, down the line, how scientists can utilize it in potential treatments.

To do this, we bred different mice to express different levels and/or mutations of TET1, and then while my lab mates tested the mice’s mental capability and weight loss, I cut and stained brains to analyze the severity of stroke damage. Examples of these scans are in the top right corner.

The conclusion section explains the data that stands out from the rest: notably that M TETI V/+ mice, on average, suffered the smallest rates of tissue damage compared to other groups, but also had the most weight loss across time; M TETI V/V suffered the greatest average tissue death of all the groups; and M TETI +/- mice are the only cohort whose neuro score improved with time.

This is not enough data to make a conclusive statement on the role of TET1 in post-stroke brain recovery. In terms of future directions, the lab plans to perform more brain surgery to have a wider data pool, and also begin using immunofluorescence assays to identify the exact number of dead cells and see where TET1 gathers in the wake of a stroke.