The study showed that mutations in the LRRK2 gene interfere with the activity of specific micro RNAs - small stretches of RNAs (ribonucleic acids) that control the expression of two proteins, E2F1 and DP. The study used the fruit fly as a model.
Professor Bingwei Lu, who led the research said 'MicroRNA, whose role in the body has only recently begun to be figured out, has been implicated in cancer, cardiac dysfunction and faulty immune response. But this is the first time it has been identified as a key player in a neurodegenerative disease'.
The scientists also discovered that reducing protein levels of E2F1 and DP in LRRK2 mutant flies prevented nerve cells from dying.
Professor Lu said that ‘This alone has immediate therapeutic implications. Many pharmaceutical companies are already making compounds that act on these two proteins’.
Current drug treatments only work temporarily, as they do not prevent the nerve cells from dying. E2F1 and DP represent targets that could potentially stop nerve cell death, providing more long term benefits for Parkinson's patients.
Parkinson's disease is characterised by tremors and uncoordinated muscle movements, which is due to the loss of nerve cells in the brain that release dopamine and help control body movements. Symptoms present once approximately 80 per cent of these nerve cells have died.
Commenting on the findings, Dr Kieran Breen, director of Parkinson’s UK said that 'Working out how subtle genetic changes affect nerve cells is one of the biggest challenges for Parkinson's. This discovery sheds new light on the fundamental causes of Parkinson’s and will bring us closer to a cure'.
'This breakthrough represents a significant step forward towards developing treatments that will actually stop the process of nerve cell death — something no current treatments can do'.
The study was conducted at Stanford University in the US and is published in Nature.