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New therapeutic target for Parkinson’s disease discovered

Restoring contacts between mitochondria and lysosomes improves neuronal function

Northwestern Medicine scientists have uncovered a new mechanism by which mutations in a gene parkin contribute to familial forms of Parkinson’s disease. The discovery opens a new avenue for Parkinson’s therapeutics, scientists report in a new study.

The Northwestern scientists discovered that mutations in parkin result in a breakdown of contacts between two key workers in the cell — lysosomes and mitochondria.

Mitochondria are the main producers of energy in cells, and lysosomes recycle cellular debris that accumulates during normal function of our cells. These organelles are especially important in our brains because neurons are highly dependent on energy production by mitochondria, and because of their activity, neurons produce an abundance of cellular debris that must be cleared by lysosomes.

In a prior study, published in Nature, Dr. Dimitri Krainc, chair of neurology and director of Simpson Querrey Center for Neurogenetics at Northwestern University Feinberg School of Medicine, and his group discovered that lysosomes and mitochondria form contacts with each other. After the initial discovery, Northwestern scientists tried to understand the function of these contacts in Parkinson’s disease.

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