Parkinson’s Disease


21 Oct 2013

  • Brain Disease, Parkinson’s Disease

Parkinson’s disease (PD) is the second most common form of age-related brain dysfunction and will become even more important as a larger proportion of our global population becomes aged. At present there are no treatments to stop the development or progression of PD. Current treatments aim to replace the chemical lost after the death of one particular group of brain cells. This works very well for some of the movement problems in parkinsonism (a family of related diseases that includes but is not limited to PD), but is not useful for a number of other serious problems that arise. It is important that we learn more about what happens before the death of these brain cells (neurons), in order to design drug treatments that might stop or slow the disease process before cell death occurs. The chemical lost is dopamine (DA), and simply replacing DA does not seem to improve many symptoms of PD like memory loss, depression, sleep disturbance, and hallucinations.


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Recently we have discovered that changes (mutations) in the building blocks of some proteins (the molecular machines that make cells work) are “linked” to PD. Linkage in this sense, means that the mutation in the protein is very likely to make a person develop PD, and that this is passed from parent to child, resulting in families highly susceptible to PD. Mutations in genes coding for several proteins are now known causes of PD, and we study most of them in parallel in our research group to understand the common problems that these mutations produce. A better understanding of what these proteins do in the normal brain, and what happens when the go wrong in PD, will help us design drugs to treat, and hopefully prevent genetic forms of PD. The information we get from these experiments may help us treat other types of parkinsonism, as well as informing us more generally about brain function in other neurodegenerative disorders, such as Alzheimer’s and Huntington’s disease.

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