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Parkinson's Disease (PD) is a disease that affects approximately 1.5 million Americans. PD occurs when the part of the brain that produces dopamine (a neurological chemical that transmits signals between certain brain cells) dies, therefore, causing a shortage of dopamine. Dopamine signaling between certain brain cells permits normal and smooth motor control and when there is a shortage the symptoms of PD begin to appear. PD is a chronic progressive nervous disease that appears later in life and is characterized by symptoms such as:
In order to study the effects of possible successful treatments for PD, an animal model is required. Two strategies have been shown to produce PD in the common marmoset. The first involved producing bilateral 6-hydroxydopamine (6-OHDA)-lesions in a particular part of the brain called the "Nigra-Striatal Pathway." The 6-OHDA is a drug that is toxic only to brain cells that produce and release dopamine. Following the injection of 6-OHDA, common marmosets displayed behaviors characteristic of human PD patients, because dopamine signaling between brain cells has been destroyed. With such a PD model, drugs can be administered and monitored for potential treatments to counteract PD.
The 6-OHDA model is one that is used to study the long-term effects of drug treatments for PD. If an exploratory drug, however, is in need for preliminary testing the 1-methyl-4phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated marmoset is utilized. MPTP produces similar PD symptoms to 6-OHDA because it also destroys dopamine producing cells. After administering MPTP to common marmosets they display PD symptoms such as muscle tremors and decreased movements. They, however, show a substantial behavioral recovery shortly after the administration of MPTP, thus allowing studies of short-term drug treatments.
One drug with potential for a treatment PD is L-dopa, a brain chemical from which dopamine is derived. It appears that L-dopa effectively reverses PD symptoms, although it does have unpleasant side-effects. L-dopa causes nausea, vomiting, and difficulty performing voluntary actions. Many researchers are, therefore, trying to combat these side-effects by administering L-dopa with other drugs. Unfortunately L-dopa does not retain its effects for reversing PD for long. Researchers, therefore, are trying to find a chemical equivalent of L-dopa using the MPTP-treated model because it is the most appropriate PD model available. By continuing research on the marmoset models researchers hope to decrease the millions of Americans suffering from PD.
Hughes, N. R., Mitchelll, I. J., & Brotchie, J. M. (1996). The Bilateral 6-Hydroxydopamine-Lesioned Marmoset Model of Parkinson's Disease. The Basal Ganglia V, 505-510.
Pearce, R. K., Jackson, M., Britton, D. R., Shiosaki, K., Jenner, P., Marsden, C. D. (1998). Actions of the D1 Agonists A-77636 and A-86929 on Locomotion and Dyskinesia in MPTP-treated L-dopa-primed Common Marmosets. Psychopharmacology, 142, 51-60.
Chicago Time Tribune archive articles: http://chicagotribune.com/tools/search/archives/form
National Institute of Neurological Disorders and Stroke: http://www.ninds.nih.gov
New York Times archive articles: http://www.nytimes.com/archives
Parkinson's Disease Foundation: http://www.parkinsons-foundation.org
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Text by Rebecca Dallwig. Layout by Matt Hoffman.Development of this web page was supported by a grant from the Wisconsin Advanced Telecommunications Foundation, the University of Wisconsin (Extension & Systems), and grants number RR00167 and number RR15311, National Primate Centers Program, National Center for Research Resources, National Institutes of Health.
Page last modified: January 22, 2001
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