Research

The branch has committed to support research. In the last five years from 2010 to 2015, we have raised nearly £45,000 specifically for research plus over £16,000 for Head Office.

One of these projects was at Oxford led by Professor Wood which focused on new ways to make dopamine-producing cells for studying Parkinson’s. Professor Wood is involved with a number of Parkinson’s related research projects such as the recent successful project to “sneak drugs into the brain“. Recent research by the team at Oxford made the news recently by demonstrating the conversion of skin cells into nerve cells.

People with Parkinson’s don’t have enough of the chemical dopamine because some nerve cells in their brain have died. Levodopa is the main drug used to treat the symptoms of Parkinson’s. It works by helping the remaining nerve cells to make more dopamine, which helps them transmit messages that are important for the co-ordination of movement.

Although levodopa generally works well at first, it can cause serious side-effects. Between 20 and 45% of people who take levodopa for more than five years will develop uncontrollable movements known as dyskinesia.

Some people are more likely to get dyskinesia, and some people develop dyskinesia much earlier than others. Younger age, more troublesome Parkinson’s symptoms and higher doses of levodopa may all increase the risk of dyskinesia. But these factors don’t completely explain why some people are more likely to be affected.

People with dyskinesia may be offered deep brain stimulation (DBS). DBS involves surgery to implant wires which target a specific part of the brain. A small electrical current sent through these wires can help relieve Parkinson’s symptoms such as tremor and stiffness. People who have DBS can often have their levodopa dose lowered, which can reduce dyskinesia. But DBS works better for some people than it does for others.

The key to people’s different experiences with dyskinesia and DBS may lie in their genes. And genes that are involved in the strength of connections between nerve cells may be particularly important. Professor Wood and his team have already shown that a small difference in one of these genes – brain derived neurotrophic factor (BDNF) – is linked with how soon people develop dyskinesia.

What the researchers are doing

The aim of this study is to find more genes linked with dyskinesia risk and how well DBS works. To do this, the researchers will look for subtle differences in specific genes. They will focus on genes that may be involved in the connections between nerve cells. They will also look at any promising genes that emerge from a recent detailed study of genetic risk factors for Parkinson’s.

The team needs to look at a large number of people’s genes to pinpoint ones that might only have a small effect. To achieve this, they will use tissue from the Queen Square brain bank and blood samples from people living with Parkinson’s. Importantly, the researchers have detailed information about the people behind the genes, including if and when they developed dyskinesia. And in the case of people who had DBS, how well it worked. This will allow them to look for links between subtle differences in specific genes and people’s experiences with dyskinesia and DBS.

How will the research help people with Parkinson’s?

The results of this study may eventually help doctors to tailor people’s treatments depending on their genes. If someone is at low risk of developing dyskinesia, they could start levodopa treatment earlier. And DBS surgery could be offered to people who are most likely to benefit.

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