Degenerative brain disease, such as Parkinson's and Alzheimer's, cause anguish to millions by robbing them of essential functions such as memory and movement. Research by Dr Maria Grazia Spillantini and colleagues at the Centre for Brain Repair of the University of Cambridge is helping to pinpoint how some of these debilitating diseases occur.
Degenerative brain disease, such as Parkinson's and Alzheimer's, cause anguish to millions by robbing them of essential functions such as memory and movement. Research by Dr Maria Grazia Spillantini and colleagues at the Centre for Brain Repair of the University of Cambridge is helping to pinpoint how some of these debilitating diseases occur.
Degenerative brain disease, such as Parkinson's and Alzheimer's, cause anguish to millions by robbing them of essential functions such as memory and movement. Research by Dr Maria Grazia Spillantini and colleagues at the Centre for Brain Repair of the University of Cambridge is helping to pinpoint how some of these debilitating diseases occur.
Dr Spillantini is the William Scholl University Lecturer in Neurology and a fellow of Clare Hall.
Dr Spillantini has been working to identify the proteins which seem to play an important role in the onset of neurodegenerative diseases. In 1994, in collaboration with Dr Michel Goedert and Mr Ross Jakes at the Medical Research Council Laboratory of Molecular Biology in Cambridge, she cloned and characterised a protein in the brain called alpha-synuclein. When Spillantini stained post-mortem tissue using antibodies to the protein, she found that the dark "Lewy bodies", which are typical of Parkinson's and related diseases, "lit up". In other words they were packed with this particular protein.
Subsequently, Dr Spillantini and colleagues were able to produce test-tube fillaments of the protein indistinguishable from those occurring in Lewy bodies. An important link had been found.
She has also investigated a protein called tau, which is associated with dementias such as Alzheimer's. She discovered that the deposits produced in the brain of patients with some forms of dementia reflect a change in the ratio of the type of tau isoforms being produced, and that this in turn depends on a mutation of the tau gene.
The remarkable conclusion of this research is that common proteins, always widespread in the brain, may in some circumstances wreak havoc. The question now is what triggers the switch. This will be the future focus of the research. Dr Spillantini comments, "If we can find some way to intervene to slow or prevent the aggregation of these proteins, we might offer some hope to the millions who will develop these devastating illnesses."
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