Parkinson's disease is the second most common neurodegenerative disorder in the United States, surpassed only by Alzheimer's disease. Approximately 1 million Americans have Parkinson's disease, and more than 50,000 new cases are diagnosed each year. The symptoms of Parkinson's disease include tremors or trembling, general slowness of movement, stiffness or rigidity of muscles, and difficulty maintaining balance and gait.
Parkinson's disease results from the loss of nerve cells, or neurons, that produce an important brain chemical called dopamine. Neurobiologists previously believed that the tremors and muscular rigidity of this disease were caused by decreases in the activity of neurons in the motor cortex.
Dopamine is a neurotransmitter, a chemical that neurons release to their neighbors to signal them to fire nerve impulses. Dopamine is known to control movement, balance, emotion, and the sense of pleasure.
Normally, when a signal needs to travel through the brain, neurons release dopamine to transport the signal across the gap, or synapse, between neurons. A kind of protein pump, called a transporter, recycles dopamine back to the signaling neurons to prepare for the next burst of signal.
In studies 10 years ago, Marc Caron, Ph.D., James B. Duke professor of cell biology at Duke and a co-investigator in the current study, used the techniques of genetic engineering to produce a strain of mice that lacked this protein transporter. Treatment of these mice with a chemical that completely stops the production of dopamine resulted in mice that quickly ran out of their supply of the neurotransmitter. The treated mice became rigid and immobile, displaying symptoms similar to those experienced by patients with Parkinson's disease.
In the current study, the researchers measured the electrical activity si
'"/>
Contact: Marla Vacek Broadfoot
marla.broadfoot@duke.edu
919-660-1306
Duke University Medical Center
18-Oct-2006