The study showed that proteolysis was suppressed during oxidative stress, but increased during recovery. Stroke is the world's third leading cause of death after heart disease and cancer. It generally occurs in elderly people and is almost always induced by ischemia, a lack of blood flow in the brain. The stroke victim experiences a flaccid paralysis, followed by spasticity. This delayed effect may be the result of delayed cell death in the brain.
Proteolysis is suppressed during periods of oxidative stress.
During recovery from oxidative stress, proteolysis increases. When tBHP, a drug known to cause oxidative stress, was applied to cells hydroxyl radical production increased dramatically when compared with production in untreated cells. Treatment with antioxidants decreased Tau proteolysis. These effects were only seen during recovery and not during oxidative stress. The experiments established a model for the effects of stroke.