Essentially, when you have a patient who has developed these fluctuations, I think the use of enzyme inhibitors will be quite desirable. Simply because we know that if you can block the catechol-O-methyltransferase enzyme that is responsible of degradation of levodopa in the liver, you can extend the levodopa bioavailability by about 20, 25%, which is a considerable number and in many patients is already sufficient to provide more stability even if they are only on three, maximum four, doses a day...
Essentially, when you have a patient who has developed these fluctuations, I think the use of enzyme inhibitors will be quite desirable. Simply because we know that if you can block the catechol-O-methyltransferase enzyme that is responsible of degradation of levodopa in the liver, you can extend the levodopa bioavailability by about 20, 25%, which is a considerable number and in many patients is already sufficient to provide more stability even if they are only on three, maximum four, doses a day. Equally, if you use other enzyme inhibitors, particularly MAO-B for instance, you can provide an additional benefit by extending dopamine availability in the brain. So, really I think particularly the young generations of neurologists and doctors should try to think a bit outside the box and think that it is not just managing Parkinson’s about increasing the number of tablets of levodopa until people take it one every two or three hours, which makes the condition of the patient not necessarily better but certainly has a negative impact on the quality of life because you have to remember every two hours to take a tablet. Rather, keeping the treatment schedule simple may actually provide a clinical benefit and at the same time increase adherence and keep the quality of life of the people with Parkinson’s a lot better for a longer period.