Mitochondria keep your brain cells alive − helping them run smoothly may protect against Parkinson’s disease

Researchers investigate role of mitochondria in Parkinson's disease, targeting key protein Drp1 for potential treatments.

In 1817, a British physician named James Parkinson published An Essay on the Shaking Palsy, describing for the first time, cases of a neurodegenerative disorder now known as Parkinson’s disease. Today, Parkinson’s disease is the second most common neurodegenerative disease in the U.S. It affects about 1 million Americans and more than 10 million people worldwide.

The signature shaking in patients with the disease is the result of dying brain cells that control movement. To date, there are no treatments available that can stop or slow down the death of those cells.

We are researchers who studyParkinson’s disease. For over a decade, our lab has been investigating the role that mitochondria – the powerhouses that fuel cells – play in Parkinson’s.

Our research has identified a key protein that could lead to new treatments for Parkinson’s disease and other brain conditions.

Unlike actual power plants, which are set in size and location, mitochondria are rather dynamic. They constantly shift in size, number and location, traveling between many different parts of the cells to meet different demands. These mitochondrial dynamics are vital to not only the function of mitochondria but also the health of cells overall.

A cell is like a factory. Multiple departments must seamlessly work together for smooth operations. Because many major processes interconnect, impaired mitochondrial dynamics could cause a domino effect across departments and vice versa. Collective malfunction in different parts of the cell eventually leads to cell death.

Emerging studies have linked imbalances in mitochondrial processes to different neurodegenerative diseases, including Parkinson’s disease. In many neurodegenerative disorders, certain disease-related factors, such as toxic proteins and environmental neurotoxins, disrupt the harmony of mitochondrial fusion and division.