Ischemic stroke is a devastating disease currently affecting over seven million people in the US alone. Patients experience a wide range of deficits following a stroke, including physical disability, mood changes, and dementia. Despite a number of promising preclinical studies indicating the efficacy of novel therapeutics, there has been no successful bench-to-bedside treatment since 1996. There are several biological and experimental reasons for this translational roadblock. The timepoints examined and the functional outcomes measured in animal models must have translational relevance. To this end, I holistically studied chronic post-stroke behavior. Using a battery of behavioral tests, I assessed cognitive function, activities of daily living, motor function, and anxiety-like behavior for twelve weeks after stroke. I developed an original, high-throughput behavioral data analysis pipeline to identify previously unknown changes in behavior after stroke. Using a machine learning algorithm, I successfully predicted procedure group based on behavioral differences. The changes I found can be used in future studies testing potential treatments to improve outcomes. Another challenge in developing effective stroke treatments is the window of time within which a therapy must be administered to be beneficial. Currently approved treatments have a maximum therapeutic window of about 16 hours, but there is a myriad of reasons why a patient may miss that window. I completed preliminary studies to assess the receptor IL-17RA as a potential target for therapy in the chronic phase of stroke. The primary ligand for IL-17RA, IL-17A, is known to have a detrimental effect on infarct size in the acute phase of stroke, but it has not been thoroughly studied in the chronic phase. As IL-17A has been implicated in short-term memory, it may play a critical role in the development of post-stroke dementia. I found that when IL-17RA is deleted in a cell-specific manner prior to stroke, there was no impact on infarct volume. As such, the influence of IL-17RA on functional outcomes can be assessed by applying the battery of behavioral tests I developed to these cell-specific knockout models. Together, these studies begin to bridge the gap between preclinical promise and translational success in stroke research.