Parkinson's disease: new data

A radically new role of the Parkin protein in brain health

LifeSciencesToday based on Trinity College Dublin: Gene Implicated in Parkinson's Disease Repairs and Replaces Nerve Cells

The function of a protein known as Parkin is to repair or destroy damaged nerve cells, depending on the degree of their damage, scientists have learned. Patients with Parkinson's disease often carry a mutant form of the Parkin gene, which can explain the accumulation of damaged neurons with impaired functions in their brain.

Parkin protein-expressing cells (red) during apoptosis. (Photo: Trinity College Dublin)

Scientists from Trinity College Dublin have made an important breakthrough in our understanding of the functions of Parkin, a protein that regulates the repair and replacement of nerve cells in the brain. This scientific breakthrough offers a new perspective on how and why neuronal death occurs in Parkinson's disease. A research team led by Seamus Martin, Professor of Medical Genetics, recently published their discovery in the peer-reviewed journal Cell Reports (Carroll et al., Parkin Sensitizes towards Apoptosis Induced by Mitochondrial Depolarization through Promoting Degradation of Mcl-1).

Although the association of mutations in the Parkin gene with early onset Parkinson's disease has been known to scientists for many years, it was very difficult to understand exactly what Parkin does in cells. Professor Martin and his colleagues found that in response to certain types of cell damage, Parkin can initiate the self-destruction of affected neurons, initiating one of the controlled processes of "cell suicide" – apoptosis.

Using the most advanced research methods, Professor Martin's laboratory, funded by the Science Foundation Ireland, has established that the Parkin protein is activated by damage to mitochondria, which leads to one of two results – either self-destruction or restoration of the neuron. Which of these options is chosen depends on the degree of damage to the mitochondria.

A drawing from an article in Cell Reports.

These new data suggest that one of the problems with Parkinson's disease may be the disruption of the process of removing diseased neurons with defective mitochondria. Instead, there is an accumulation of damaged neurons that are unable to perform their functions.

Commenting on the results of his research, Professor Martin notes: "This unexpected discovery turns our ideas about Parkin functions upside down. Until now, we considered Parkin an internal brake on the death of nerve cells, helping to delay their death. However, our new data suggest the opposite: in fact, Parkin helps to weed out damaged and diseased nerve cells, which probably facilitates their replacement. This suggests that Parkinson's disease may be the result of the accumulation of defective neurons due to the failure of this cellular process."

"We are very grateful for the support of the Scientific Foundation of Ireland, which funded this research. Our work is an excellent example of how fundamental research leads to fundamental breakthroughs in our understanding of the development of diseases. Without such knowledge, it would be very difficult to develop new treatments," adds Professor Martin.

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