A study of mice has furnished researchers with new evidence that the onset of symptoms associated with Parkinson's disease may be triggered by the loss of two types of brain cells, not just one as previously thought.
Working with colleagues from the University of Georgia, Emory scientists showed a link between the loss of both norepinephrine and dopamine neurons and the delayed onset of symptoms associated with Parkinson's disease.
AdvertisementIt had been thought to date that the loss of only dopamine neurons triggered symptoms.
Parkinson's disease affects motor coordination and is characterized by symptoms such as tremors of hands, arms, legs, jaw and face; rigidity or stiffness of limbs and trunk; bradykinesia, or slowness of movement; and postural instability. The disease most often occurs in those over 50.
"People don't start showing symptoms of Parkinson's disease until about 80 percent of their dopamine neurons are gone, which is when you cross some sort of threshold. Our study looked at what happens while the dopamine neurons are dying and people still appear fine," says Dr. David Weinshenker, Assistant Professor of Human Genetics in Emory University School of Medicine.
"The lack of symptoms until the death of most of the dopamine neurons suggested the existence of a system that can temporarily compensate for the loss of the dopamine," he added.
The researcher further said that post-mortem Parkinson's disease brains showed the loss of both dopamine and norepinephrine neurons.
"We know that norepinephrine is important for regulating the activity of dopamine neurons, so we suspected that the dopamine neurons and the norepinephrine neurons function in concert. As the dopamine neurons start dying, the norepinephrine neurons compensate by signalling the surviving dopamine cells to dramatically increase their activity and the output of dopamine," said Dr. Weinshenker.
"Eventually, the norepineprhine neurons die, the surviving dopamine neurons lose their ability to release extra dopamine, and symptoms start to appear," he added.
In the course of study, the researchers brought about 80 per cent loss of dopamine cells in healthy, one-year-old mice with the help of drugs, but did not observe any motor impairment in the animals.
The symptoms of Parkinson's disease-resting tremor, hunched posture and deficits in co-ordinated movement-were, however, noticed during when the researcher tested mice unable to synthesize norepinephrine and those that had trouble in releasing dopamine properly.
The study indicates that having a normal complement of dopamine neurons is not enough for normal motor function, but norepinephrine also needs to be present to ensure proper dopamine release.
"Although there are no cures for Parkinson's disease, some moderately effective treatments are available, but most target the dopamine neurons only and are effective for only a limited amount of time. In light of this study, it's quite possible that simultaneously treating both the dopamine and norepinephrine loss could further ameliorate the symptoms of Parkinson's disease," says Dr. Weinshenker.
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