Parkinson’s discovery opens door to new targeted therapies

Around a million Americans are living with Parkinson’s disease, the neurological condition that greatly, and most often progressively, affects the dopamine-producing powerhouse area of the brain, the substantia nigra. While there is no cure, medication is generally aimed at substituting or boosting dopamine, which can help lessen the movement-impairment that comes with the debilitating disease.

Studies recently have pivoted towards investigating specific cellular mechanisms involved in the disease’s progression, such as genetic mutations that prevent debris cleanup in the brain, or targeting other protein clumps.

The latest discovery out of Northwestern Medicine has found that the intracellular communication breakdown between lysosomes and mitochondria is not just key to the progression of genetic Parkinson’s but could be also be a target for new therapies to treat the debilitating disease.

“Findings from this study suggest that dysregulation of mitochondria-lysosome contacts contributes to the Parkinson’s disease pathophysiology,” said Dimitri Krainc, the study’s corresponding author. “We propose that restoring such mitochondria-lysosome contacts represents an important new therapeutic opportunity for Parkinson’s disease.”

Both organelles play a vital role in overall health; mitochondria are the primary producers of energy, while lysosomes recycle debris that routinely builds up through normal cell function. Their roles are even more important in the brain, in which neurons rely on the fuel from mitochondria, and because of their workload they produce a lot of debris that needs to be cleaned up and recycled by lysosomes.

The researchers have now discovered that the way lysosomes ‘feed’ mitochondria amino acids is interrupted in certain forms of Parkinson’s disease. It’s associated with the parkin gene mutation, the second most common known cause of the condition.

This dysfunction has a snowball effect, cutting off energy supplies to neurons, resulting in their degeneration.

While still early days, the researches hope more work on this crucial pathway function will lead to targeted treatment to restore communication between the organelles and ultimately result in a new way to slow disease progression and symptoms.

The study was published in the journal Science Advances.

Source: Northwestern Medicine

Around a million Americans are living with Parkinson’s disease, the neurological condition that greatly, and most often progressively, affects the dopamine-producing powerhouse area of the brain, the substantia nigra. While there is no cure, medication is generally aimed at substituting or boosting dopamine, which can help lessen the movement-impairment that comes with the debilitating disease.

Studies recently have pivoted towards investigating specific cellular mechanisms involved in the disease’s progression, such as genetic mutations that prevent debris cleanup in the brain, or targeting other protein clumps.

The latest discovery out of Northwestern Medicine has found that the intracellular communication breakdown between lysosomes and mitochondria is not just key to the progression of genetic Parkinson’s but could be also be a target for new therapies to treat the debilitating disease.

“Findings from this study suggest that dysregulation of mitochondria-lysosome contacts contributes to the Parkinson’s disease pathophysiology,” said Dimitri Krainc, the study’s corresponding author. “We propose that restoring such mitochondria-lysosome contacts represents an important new therapeutic opportunity for Parkinson’s disease.”

Both organelles play a vital role in overall health; mitochondria are the primary producers of energy, while lysosomes recycle debris that routinely builds up through normal cell function. Their roles are even more important in the brain, in which neurons rely on the fuel from mitochondria, and because of their workload they produce a lot of debris that needs to be cleaned up and recycled by lysosomes.

The researchers have now discovered that the way lysosomes ‘feed’ mitochondria amino acids is interrupted in certain forms of Parkinson’s disease. It’s associated with the parkin gene mutation, the second most common known cause of the condition.

This dysfunction has a snowball effect, cutting off energy supplies to neurons, resulting in their degeneration.

While still early days, the researches hope more work on this crucial pathway function will lead to targeted treatment to restore communication between the organelles and ultimately result in a new way to slow disease progression and symptoms.

The study was published in the journal Science Advances.

Source: Northwestern Medicine