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Scientists identify factor protecting brain from Parkinson's

A factor which keeps our brain cells alive and so protects us from neurodegenerative conditions such as Parkinson's disease has been identified by an international team of researchers, raising the hope of new therapies for this debilitating disease. The study, which was partl...

A factor which keeps our brain cells alive and so protects us from neurodegenerative conditions such as Parkinson's disease has been identified by an international team of researchers, raising the hope of new therapies for this debilitating disease. The study, which was partly funded by the EU, is published in the latest edition of the journal PLoS Biology. People with Parkinson's disease experience a range of symptoms, including tremor, stiffness and slowness of movement. Patients also find it harder to carry out daily tasks such as dressing, walking, eating and writing. The disease is caused by a loss of brain cells in a part of the brain called the substantia nigra. These cells normally produce the messenger molecule dopamine, and it is the reduction in dopamine levels caused by the death of these cells which causes the symptoms of Parkinson's. Understanding what causes the cells of the substantia nigra to die off is an important area of research. During development and throughout our lives, so-called neurotrophic factors keep our brain cells alive, and a drop in the level of these factors, or problems with the molecules on cells which identify them, is thought to contribute to the development of neurodegenerative diseases. In this study, the researchers looked at a neurotrophic factor called GDNF (glial cell line-derived neurotrophic factor) and its receptor, Ret. They succeeded in producing mice whose Ret receptors were switched off in the substantia nigra, meaning the GDNF molecule is unable to attach itself to the cell. 'This meant that for the first time, it was possible to investigate the effect of a missing GDNF signals on the development and long-term behaviour of the nigro-striatal system,' explained Rüdiger Klein of the Max Planck Institute for Neurobiology, who led the research. The scientists found that the nigro-striatal system developed normally without Ret. However, as the mice got older, the effects of their defective Ret receptors began to show; the nerve cells of the substantia nigra died early, and the older the mice got, the more nerve cells they lost. 'Our nerve cells help us to understand which factors the nerve cells need to survive,' said Professor Klein. The researchers hope their work will feed into the development of new treatments, such as stem cell therapy to replace the lost neurons.