About one million Americans suffer from Parkinson’s disease, a neurological disorder that dramatically and often gradually affects the brain’s strong dopamine-producing region, the substantia nigra. Although there is no cure, medications are often designed to replace or enhance dopamine, which can help reduce the movement impairments that come with debilitating diseases.
More recent research has turned to investigating specific cellular mechanisms involved in disease progression, such as genetic mutations that prevent the clearing of debris in the brain, or targeting other protein clumps.
A breakdown in intracellular communication between lysosomes and mitochondria is not only key to the progression of inherited Parkinson’s disease, but may also be targeted by new treatments for the debilitating disease, new findings from Northwestern Medicine have found.
“The results of this study suggest that dysregulation of mitochondria-lysosome contacts contributes to the pathophysiology of Parkinson’s disease,” said Dimitri Krainc, corresponding author of the study. “We think restoring this mitochondria-lysosome contact represents an important new therapeutic opportunity for Parkinson’s disease.”
Both organelles play critical roles in overall health. Mitochondria are the main producers of energy, while lysosomes recycle debris that accumulates regularly through normal cellular function. Their role is even more important in the brain, where neurons depend on mitochondria for fuel, and because of their workload, they generate large amounts of debris that require lysosomes to clean up and recycle.
Researchers have now discovered that in some forms of Parkinson’s disease, the way lysosomes “feed” amino acids to mitochondria is disrupted.It is associated with mutations in the parkin gene second most common Known causes of the condition.
This dysfunction can have a snowball effect, cutting off the energy supply to neurons and causing them to degenerate.
While it’s still early days, the researchers hope that more research into the function of this key pathway will lead to targeted treatments to restore communication between organelles and, ultimately, a new way to slow disease progression and symptoms.
The study was published in the journal scientific progress.
source: Northwestern Medicine
