The purpose of this study was to evaluate tight junction protein changes during different time points of cuprizone treatment in the corpus callosum and cortex of mice. Cuprizone is a copper chelator that causes demyelination and is used as an animal model of multiple sclerosis. Demyelination is the result of the breakdown of the myelin sheath that insulates neurons and can cause nerve impulses to slow down or even fail. It is important to study demyelination because it causes neurological problems associated with multiple sclerosis and current treatments are lacking. Studies in our lab have shown an early breakdown of the blood brain barrier during cuprizone treatment. Tight junction proteins are molecules that maintain the integrity of the blood brain barrier that protects cells in the brain. TJ proteins have barrier functions that hold cells together and facilitate signaling in the central and peripheral nervous system. Mice were given 0.3% cuprizone as a diet for two different time periods, three days and one week. The brains were extracted and sliced, and the tight junction proteins were immunolabeled and imaged using a confocal microscope. Cuprizone fed and control mice staining patterns were quantified and compared in the corpus callosum and cortex at three days and one-week of treatment.