Parkinson's disease afflicts one in 100 people over age 60 and one in 25 over age 80, making it the developed world's second-most-common neurodegenerative disorder after Alzheimer's disease. Current treatments for Parkinson's are a lot better than nothing. But they mainly mask symptoms rather than slowing the underlying progression of disease.
This week, Stanford's Tom Sudhof, MD, and his colleagues published a study in Science that might eventually change this prognosis.
Let's keep it simple: Nerve cells are sometimes described as glorified electrical wires. But up close, a nerve cell looks more like a small ball with a long, bulb-studded, hollow tube (that's the "wire") coming out of one side and fuzzy clumps of hairlike projections branching from the other side.
One nerve cell's tiny, tube-associated bulbs impinge on other nerve cells' fuzzy projections. When an electrical impulse traveling down that hollow tube reaches those bulbs, they release little bubbles packed with chemicals, which land on specialized receptor molecules dotting the surface of the nearby nerve cell's fuzz. If enough molecules from enough bulbs land on enough receptors on enough of the next nerve cell's fuzz, that nerve cell may fire a brand-new electrical impulse down its long hollow tube, and so on. (Gee, did I mention that this is wa-aa-ay oversimplified?)
That last little step - the release of chemicals from the bulbs - is critical. When the joint is jumping, jillions of chemical-containing bubbles are being squirted out of nerve cells' bulbous protruberances in smoothly coordinated volleys thousands of times per minute. This process underlies all cognition, emotion, memory, and action. And, as you can imagine, it requires a complex set of production, packaging, transport and dismantling nanotechnologies our best engineers can only dream of. Failure of any component of the assemblage can spell neurodegenerative disaster. Sudhof has spent much of his career methodically reverse-engineering these molecular events at the junctions where one nerve cell meets another.
In the just-published study, Sudhof and company figured out the mechanism by which one key component, alpha-synuclein, works. Malfunction or deficits of this hitherto mysterious molecule have been strongly tied to Parkinson's disease (and Alzheimer's as well).
That's a significant first step toward truly effective therapies, and classic example of how basic research, so opaque to most of us most of the time, can pack potential payoffs for all of us.
Photo by Ethan Hein
