 First of all, I'd like to say a great thank you to the both the Brain Foundation Committee and their donors for this grant. It means a great deal to us to get this project off the ground. This project is looking at aneurysmal subarachnoid hemorrhage, which is really a devastating condition. For people that have aneurysmal subarachnoid hemorrhage, it's probably about a 50% mortality rate before you actually get to hospital. The incidence of it is relatively low in comparison to other neurological diseases, but the impact is generally on a younger population. Because of this, the cost to the community is probably on a par with the schemic stroke in terms of both resources and the emotional costs to families and friends of the person that's affected. There is an initial brain injury caused by aneurysmal subarachnoid hemorrhage, and that's caused by erupture and aneurysm, which is a weakening of the vessel wall. We can't do a great deal about the initial brain injury. It's difficult to predict who's at risk of aneurysmal subarachnoid hemorrhages. It's thought that there's maybe up to 5% of the population walking around with aneurysms in their head. We don't really know which ones are going to rupture. But what we do focus a lot on in neurosurgical departments is how to prevent the secondary injury that occurs after you have the initial insult. One of the most feared things that happens after the hemorrhage is something called vasospasm, where you get spasm of the vessels in the brain caused by irritation of the blood. In the natural history of subarachnoid hemorrhage, probably about a third of patients experience vasospasm, and our approach to vasospasm has unfortunately not moved on a great deal in the past 30 years. In 1989 there was a big trial called the British Pneumotipine trial, which treated people with a drug called Pneumotipine for 21 days after their subarachnoid hemorrhage. That's the protocol that we still use today. It hasn't moved on a great deal. For this project, I'm planning to look at the immune system in subarachnoid hemorrhage, and particularly a group of proteins in the blood called the complement system. The complement is a sort of bombastic cascade of proteins that activates each other. It's activated by bacteria, and it's activated by foreign substances, and it's activated by things like bleeding. It amplifies down this cascade. In autopsy samples, in cases of vasospasm, we see complement deposition on the walls of these blood vessels. Disregulated complement system has already been associated with a number of diseases, and a number of neurological diseases. Our question is, is dysregulation of the complement system involved in the pathogenesis of the vasospasm? If so, can we identify some therapeutic targets for this? We plan to collect some blood and cerebral spinal fluid from the patients that present to our hospital. We also plan to keep a bank of data and a bank of these samples for researchers to use in the future. Hopefully we can further the understanding of the molecular mechanisms that lead to vasospasm five to nine days down the line after the initial hemorrhage. Thanks again to the Brain Foundation.