Parkinson’s disease is a progressive neurological condition manifesting as tremors, stiffness, trouble balancing and a lack of movement coordination. The mutation in the PARKIN gene is one of the known causes of Parkinson’s disease. However, further insights into the gene’s influence on brain cells are not completely understood.
Northwestern University researchers in the USA have now inched further in closing this knowledge gap. In a recent study, published in the Science journal, they found that mutated gene flares up an energy crisis in brain cells. This happens because the mutation snaps the communication link between two cell components – lysosomes and mitochondria. Mitochondria generate the energy required for cell functions, while lysosomes ensure cells remain clean by clearing all wastes.
This study ushers in the development of new therapies for Parkinson’s disease. Dr Dimitri Krainc, senior author of the study and chair of neurology and director of Simpson Querrey Center for Neurogenetics at Northwestern University Feinberg School of Medicine, says, “The future course of this study involves the development of therapeutic strategies for improving the contacts between mitochondria-lysosome.”
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Survival of neurons
The PARKIN gene plays a crucial role in the survival of the neurons in a brain region called substantia nigra (a part of the middle brain). PARKIN carries the information to produce a protein, parkin, which controls several cell functions. The parkin protein helps clear accumulated toxic proteins, checks mitochondria function, clears damaged ones, and protects neurons from oxidative stress.
However, the PARKIN gene’s effect on mitochondria and its energy production was not known previously, which the current study has revealed.
Gene mutations
Mitochondria and lysosomes are crucial for the proper functioning of cells. In their previous study, Dr Krainc and his team had found that mitochondria and lysosomes form chemical contacts. However, the role of this connection in Parkinson’s disease was unknown.
In this current study, Dr Krainc’s team discovered that the PARKIN gene disrupted the exchange of chemicals between mitochondria and lysosomes of neuronal cells in the substantia nigra of the brain.
Progression of Parkinson’s
Dr Krainc says, “[As per our present study] parkin protein regulates the activity of one of the binding proteins that connect mitochondria with lysosomes.” He explains that they found the mutated PARKIN gene could not activate this binding protein. As a result, there were weak connections and reduced numbers of mitochondria-lysosome connections. Due to this, the lysosome could not supply the necessary amino acids to the mitochondria to produce the energy.
This hampered the functioning of mitochondria. Consequently, the neurons in the substantia nigra did not get sufficient energy to perform their function. They hence began to degenerate, leading to the progression of Parkinson’s.
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