New data offer hints to why Parkinson's disease so selectively harms brain cells that produce the chemical dopamine, say researchers at Washington University School of Medicine in St. Louis.
Dopamine is involved in brain cell communications including the signals that control movement. As Parkinson's kills the dopamine-producing cells, patients begin to develop tremors, problems moving and other symptoms.
The new research shows that a drug known to damage dopamine-producing nerve cells and mimic Parkinson's disease does so by rapidly damaging cellular energy generators called mitochondria. This damage impairs the ability of mitochondria to circulate around the cell as they normally would. As a result, axons, the extended arms nerve cells use to send messages, wither; a few days later, the body or main portion of the cell also dies.
"Much of the research into Parkinson's disease treatments is focused on saving the bodies of these cells, but our results suggest that keeping axons healthy also is essential,"says Karen O'Malley, PhD, of Washington University School of Medicine in St. Louis. "When axons die back, dopamine is no longer delivered to the neurons that need it. The cell body also has fewer connections to other cells, and it needs those connections to survive."
The results were published May 11 in The Journal of Neuroscience.
Many processes and facilities for cellular maintenance are in the body of the nerve cell, and their products sometimes have to travel a significant distance to reach the axon's end.
"If you think, for example, about one of your peripheral nerves, the cell body is located in the spinal column, but some of the axons extend as far as your big toe," says O'Malley, professor of neurobiology. "That's like the cell body sits in an office in St. Louis and the end of the axon is in Chicago."
O'Malley compares the axon's system for transporting supplies to a railroad. Mitocho
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Washington University School of Medicine