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 Canadian Researchers See Mitochondrial Interference As Key To Parkinson’s Disease

Canadian researchers believe they may have found another clue to how Parkinson’s disease ravages the human body after discovering that two genes linked to the disease appear to disrupt a cell’s ability to repair itself.

In a healthy human cell, the mitochondria—the tiny organelles known colloquially as a cell’s “power plant”—survive by removing damaged proteins from the cell.

But researchers at the Montreal Neurological Institute and Hospital in Canada now think that two genes linked to hereditary Parkinson’s disease, called PINK1 and parkin, allow damaged proteins to “pinch off” from the mitochondria, keeping the organelle from functioning and, eventually, leading the cell to break down.

“The deterioration of mechanisms designed to maintain the integrity and function of mitochondria throughout the lifetime of a cell has been suggested to underlie the progression of several neurodegenerative diseases, including Parkinson’s disease,” the researchers said in announcing their findings. “When mitochondria … malfunction they can contribute to Parkinson’s disease. If they are to survive and function, mitochondria need to degrade oxidized and damaged proteins.”

The researchers announced their findings in the latest issue of The EMBO Journal.

“Our conclusion is that the loss of this PINK1 and parkin-dependent trafficking system impairs the ability of mitochondria to selectively degrade oxidized and damaged proteins and leads, over time, to the mitochondrial dysfunction noted in hereditary Parkinson’s disease,” says Institute Professor Heidi McBride.

The findings aren’t just a sign of hope for the millions of Parkinson’s sufferers: Mitochondrial breakdown is thought to be a factor in a variety of awful diseases from cardiac problems to Alzheimer’s disease.

Some scientist even believe that mitochondrial breakdown is what leads people to age in the first place.

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