We’re kicking off with a short video clip and update on Professor Anthony Schapira’s talk - ‘What have we learnt about the causes of Parkinson’s?’
Watch Professor Schapira discussing the causes of Parkinson’s here - http://bit.ly/1b10aMK
Find out more:
We know that Parkinson's symptoms are caused by the death of dopamine producing cells in a part of the midbrain known as the substantia nigra. We do not know precisely why the cells die or what causes the process to start in the first place. These questions play on the mind of some newly diagnosed people with Parkinson's but they are also central to the search for ways to prevent and/or cure the condition. Professor Tony Schapira summarised the current state of research into these two questions.
For many years it was thought that environmental factors were to blame and various candidates, including exposure to pesticides, solvents or some recreational drugs were identified that were associated with a mildly increased risk of Parkinson's. Conversely, some other environmental factors, including drinking coffee and smoking cigarettes were found to correlate with a reduced risk. Later, several genetic factors were identified that contributed to an increased risk of Parkinson's. The most recent understanding is that both play a part, and that environmental factors may modify the genes in a way that causes Parkinson's.
The study of the human genome remains a very fruitful area for research and it is encouraging that the NHS has initiated the human genome project with the aim of fully sequencing thousands of patients and associating this information with data about lifestyle and health.
It is also important to understand the reasons why Parkinson's causes death of cells and why this progresses through the affected brain. Professor Schapira identified three mechanisms which may contribute to the death of dopamine producing cells. Mitochondria are the power sources in cells. There is a process to recycle. Mitochondria at the end of their useful lives and if this malfunctions the cell can die.
Another theory involves alpha synuclein which is a very common substance in the body. In people with Parkinson's alpha synuclein can become misfolded which causes it to clump together in a way that can damage the cell. This tendency can spread from one cell to another, which may explain the progression of Parkinson's through the brain. Stem cell transplantation research suffered a setback a few years ago when alpha synuclein misfolding was seen to spread into the transplanted stem cells.
The third mechanism concerns lysosomes, which provide a sophisticated rubbish sorting and recycling function in brain cells. Disrupted function of lysosomes is seen in Parkinson's and some other neurological conditions.
In summary despite a great deal of research into these topics we do not understand enough about the causes of, or the progression of, Parkinson's to allow us to slow, stop or reverse the condition. There are several promising lines of enquiry that have reached advanced laboratory trials. Further research is required to identify the most promising of these with a view to trials in patients.
Alan Cameron, Research Supporter