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FRIDAY, Jan. 4 (HealthDay News) -- The nerve cell death that helps drive Parkinson's disease may be triggered by a harmful modification in a particular nerve cell protein, new research reveals.
The modification in question -- an apparently toxic mix of the protein alpha-synuclein and the critical neurotransmitter dopamine -- can be found in all Parkinson's patients, researchers say.
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The change short-circuits a process that allows aging nerve cells to stay healthy by purging themselves of damaged molecules, researchers explain in the Jan. 2 online issue of The Journal of Clinical Investigation.
"The general idea is that, in Parkinson's, the neurons accumulate lots of garbage," explained study author Dr. Ana Maria Cuervo, an associate professor in the department of anatomy and structural biology at Yeshiva University's Albert Einstein College of Medicine, in New York City.
"Normally," she said, "this garbage is removed before it builds up, and is dumped into garbage containers called lysosomes, which make sure things can move about the neurons fast and freely."
Such a filtering process for disposing of damaged molecules is known as "autophagy," a term that literally means "self-eating."
"But sometimes, this mechanism fails," Cuervo noted. "And now we have found the reason why. It is because of the formation of this particular modified protein, which acts kind of like chewing gum in the middle of the nerve cell."
"It's not a normal protein," she stressed. "It's very sticky, and any other proteins passing by get stuck to it, so you get all these abnormal things, these stones in the middle of the cell's highways, that are not being removed, and eventually the [brain] cells can't move things around as they should, and they die."
In an earlier effort, the same research team had found that mutant forms of alpha-synuclein -- as opposed to modified forms -- also block the desired breakdown of damaged nerve cell molecules. Such mutant proteins are present in the 5 percent to 10 percent of Parkinson's patients struck with a relatively rare, familial form of the disease.
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