One of the easiest ways to target treatments for Parkinson’s Disease is to try and replace the dopamine that’s missing in the brain. Interestingly, if we try and give patients dopamine as a chemical it doesn’t actually cross the blood-brain barrier – it’s impervious. The molecule is too big.
So what we realised back in the 1960s was that if we made the precursor of dopamine known as L-dopa or levodopa – that did get into the brain. And we combined that with a drug that could stop it being broken down in the gut, and so allowing more of it to get to the brain. In the brain, levodopa is converted by the remaining cells that are there, from levodopa into dopamine. It’s stored inside those remaining cells and then released in a sort of timely fashion to try and control the symptoms. Unfortunately, the half-life is such that most patients will need to take the tablet at least three times a day.