 If I was to ask you, what is the leading cause of neurological disability worldwide? What would your answer be? Stroke? Dementia? Well, what if I was to tell you that the correct answer is migraine? Because it is. Migraine is a third most prevalent disease on the planet, affecting over 1 billion people, including me, and including many of you here in the audience tonight. And as all of us who have ever felt or looked something like this will agree, it's much more than just a headache. Migraine attacks cause severe pain, gastric disturbances, light sensitivity, and inflammation. And in chronic cases, migraine attacks can occur over 15 times per month, leading to a significant level of disability. Unfortunately, we aren't able to cure migraine, but drugs do exist to manage the symptoms when a migraine attack occurs. However, these drugs don't necessarily work in every patient, and even if they do, they come with a wide range of side effects, some of which may be just as de-abilitating as the migraine itself. As such, new drugs need to be developed. The goal of my research is to pave the way for new migraine therapeutics. We know of a protein in the brain called pituitary delite cyclase-activating peptide, which makes my head hurt to say, so I'll just call it PACAP. PACAP binds to the PAC-1 receptor in the brain, leading to the onset of a migraine. Thus, it is thought that if we can stop this interaction from occurring via a drug, this may prove to be a new way of treating migraine. As this interaction isn't fully understood, I aim to uncover the way in which PACAP binds to the PAC-1 receptor so as to aid future drug development efforts. The binding between PACAP and PAC-1 is like fitting two puzzle pieces together. When they bind, the PAC-1 receptor is activated and sends a signal leading to the onset of a migraine. Now, I can take part of the PAC-1 receptor and mutate it, and if that part of the receptor is important for binding, mutating it will effectively change the shape of that puzzle piece, meaning PACAP can't bind as well. This results in a change in the signal that the PAC-1 receptor produces, which I can measure. Alternatively, if that part of the receptor is unimportant for binding, mutating it won't have any effect on the way in which PACAP and PAC-1 bind. If I mutate different sites on the receptor one by one, I can see if the signal produced by the PAC-1 receptor changes, and this allows me to build a picture of the exact way in which PACAP and PAC-1 bind. With my research, future studies can create a drug which binds to the PAC-1 receptor in the same way as PACAP, but instead of activating it, blocks it, telling that migraine to PAC its PACs. Thank you.