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Dimitri Krainc
Heathcare

The Surprising Connection Between Cell Powerhouses and Parkinson’s

Let me take you on a journey inside the brain, where two vital parts of our cells—mitochondria and lysosomes—have a much bigger role than we might realize. Imagine the mitochondria as little powerhouses, generating the energy our cells need to function, and lysosomes as recyclers, breaking down and clearing out waste. When these two organelles interact normally, everything works as it should. But what if this interaction goes wrong? That’s the heart of groundbreaking research led by Dimitri Krainc, MD, PhD, and his team at Northwestern Medicine.

Recently, they uncovered how this interaction goes awry in Parkinson’s disease, a condition that affects millions of people worldwide. Their study, published in Nature Communications, is the first to reveal that in the neurons of people with Parkinson’s, mitochondria and lysosomes are in prolonged, abnormal contact. This miscommunication disrupts the proper distribution of mitochondria, leading to the breakdown of neuron function.

Dr. Krainc, who chairs the Department of Neurology at Northwestern and leads the Simpson Querrey Center for Neurogenetics, explains it simply: “These contact sites between mitochondria and lysosomes form dynamically in neurons and become misregulated in Parkinson’s disease, leading to a series of harmful events.” It’s like a ripple effect, where one small problem sets off a chain of bigger issues in the brain’s neurons.

Parkinson’s, one of the most common neurodegenerative diseases, targets neurons in a region of the brain responsible for motor control, causing the gradual loss of movement. With no cure or disease-modifying treatments yet, scientists are focusing on understanding the root causes to find new therapies.

Krainc’s research zooms in on a key player in this story—a mutated enzyme called β-glucocerebrosidase (GBA), which is one of the biggest risk factors for Parkinson’s. Soojin Kim, a dedicated PhD student at Northwestern and lead author of the study, used advanced super-resolution microscopy to watch these mitochondria and lysosomes interact in the neurons of Parkinson’s patients. What she found was eye-opening: neurons with GBA mutations showed much longer mitochondria-lysosome contacts than healthy neurons.

“This misregulation could be a critical step in how the disease develops,” says Dr. Krainc. The implications are huge. By understanding how these contact sites work—and how they fail—we may unlock new ways to treat or even prevent Parkinson’s.

Digging deeper, the team discovered that this malfunctioning contact leads to fewer mitochondria in the neuron’s axons, the long part of the cell responsible for sending signals. Fewer mitochondria means less energy for the cell, contributing to its decline. But there’s hope: the researchers found that by increasing the levels of a specific protein called TBC1D15, they could partially reverse the harmful effects.

These findings don’t just apply to Parkinson’s. According to Krainc, “Inter-organelle contacts could play a role in many neurodegenerative diseases.” This research opens the door to exploring how mitochondria and lysosomes—two seemingly ordinary cellular components—may hold the key to understanding and treating some of the most challenging diseases of our time.

Backed by funding from the National Institutes of Health and other prestigious awards, this research marks a major step forward in the fight against Parkinson’s. As Dr. Krainc and his team continue to explore the intricate workings of our neurons, there’s hope that one day, these discoveries will lead to new treatments and brighter futures for those affected by neurodegenerative diseases.

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