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Study suggests loss of 2 types of neurons -- not just 1 -- triggers Parkinson's symptoms
August 14, 2007New evidence indicates that the loss of two types of brain cells--not just one as previously thought--may trigger the onset of symptoms associated with Parkinson's disease.
The evidence, based on mouse models, shows a link between the loss of both norepinephrine and dopamine neurons and the delayed onset of symptoms associated with Parkinson's disease. It was originally thought that the loss of only dopamine neurons triggered symptoms. Dopamine is a neurotransmitter critical for coordinating movement.
Results of the study by Emory scientists, along with the University of Georgia, will appear in the Proceedings of the National Academy of Sciences, Early Edition online during the week of Aug. 13-17 and in the Aug. 21 print edition.
The research was conducted by Karen Rommelfanger, graduate student in the laboratory of David Weinshenker, PhD, assistant professor of human genetics in Emory University School of Medicine and Gary Miller, PhD, associate professor in Emory's Rollins School of Public Health. The team also included Gaylen Edwards and Kimberly Freeman at the University of Georgia.
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. Weinshenker. "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."
"The dogma in the field is that Parkinson's disease involves a selective loss of dopamine neurons. The truth is, if you look at postmortem Parkinson's disease brains, you will see that both dopamine and norepinephrine neurons are gone," Dr. Weinshenker explains. "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 signaling the surviving dopamine cells to dramatically increase their activity and the output of dopamine. Eventually, the norepineprhine neurons die, the surviving dopamine neurons lose their ability to release extra dopamine, and symptoms start to appear."
To test their hypothesis, the researchers gave healthy, one-year-old mice the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetra-hydropyridine (MPTP) at a dose that kills about 80 percent of the dopamine cells, but observed no motor impairments in the mice. Surprisingly, when they tested mice unable to synthesize norepinephrine and that have trouble releasing dopamine properly, they observed symptoms of Parkinson's disease including resting tremor, hunched posture and deficits in coordinated movement. These results indicate that having a normal complement of dopamine neurons is not enough for normal motor function; 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.
Emory University
The research was conducted by Karen Rommelfanger, graduate student in the laboratory of David Weinshenker, PhD, assistant professor of human genetics in Emory University School of Medicine and Gary Miller, PhD, associate professor in Emory's Rollins School of Public Health. The team also included Gaylen Edwards and Kimberly Freeman at the University of Georgia.
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. Weinshenker. "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."
"The dogma in the field is that Parkinson's disease involves a selective loss of dopamine neurons. The truth is, if you look at postmortem Parkinson's disease brains, you will see that both dopamine and norepinephrine neurons are gone," Dr. Weinshenker explains. "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 signaling the surviving dopamine cells to dramatically increase their activity and the output of dopamine. Eventually, the norepineprhine neurons die, the surviving dopamine neurons lose their ability to release extra dopamine, and symptoms start to appear."
To test their hypothesis, the researchers gave healthy, one-year-old mice the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetra-hydropyridine (MPTP) at a dose that kills about 80 percent of the dopamine cells, but observed no motor impairments in the mice. Surprisingly, when they tested mice unable to synthesize norepinephrine and that have trouble releasing dopamine properly, they observed symptoms of Parkinson's disease including resting tremor, hunched posture and deficits in coordinated movement. These results indicate that having a normal complement of dopamine neurons is not enough for normal motor function; 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.
Emory University
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Normal individuals who scored high on a measure of impulsive/antisocial traits display a hypersensitive brain reward system, according to a brain imaging study by researchers at Vanderbilt University.
Psychopaths' brains wired to seek rewards, no matter the consequences
The brains of psychopaths appear to be wired to keep seeking a reward at any cost, new research from Vanderbilt University finds. The research uncovers the role of the brain's reward system in psychopathy and opens a new area of study for understanding what drives these individuals.
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Ritalin boosts learning by increasing brain plasticity
Doctors treat millions of children with Ritalin every year to improve their ability to focus on tasks, but scientists now report that Ritalin also directly enhances the speed of learning.
Safety data favor norepinephrine over dopamine for shock
Physicians treating patients with shock should consider norepinephrine instead of dopamine as a tool for stabilizing blood pressure, according to an editorial in the March 4, 2010, issue of the New England Journal of Medicine (NEJM).
Critical brain chemical shown to play role in severe depression
The next advance in treating major depression may relate to a group of brain chemicals that are involved in virtually all our brain activity, according to a study published today in Biological Psychiatry.
Communication breakdown: what happens to nerve cells in Parkinson's disease
A new study from The Montreal Neurological Institute and Hospital - The Neuro - at McGill University is the first to discover a molecular link between Parkinson's disease and defects in the ability of nerve cells to communicate.
Brain dopamine receptor density correlates with social status
People have typically viewed the benefits that accrue with social status primarily from the perspective of external rewards. A new paper in the February 1st issue of Biological Psychiatry, published by Elsevier suggests that there are internal rewards as well.
US Parkinson's rates highest in whites, Hispanics, and Midwest, Northeast
The largest epidemiological study of Parkinson's disease in the United States has found that the disease is more common in the Midwest and the Northeast and is twice as likely to strike whites and Hispanics as blacks and Asians.
Brain abnormalities in Parkinson's patients develop before symptoms occur
Scientists who have identified brain networks damaged in Parkinson's disease have new evidence that these systems become abnormal a few years before symptoms appear.
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Dopamine Handbook by Leslie Iversen (Author), Susan Iversen (Author), Stephen Dunnett (Author), Anders Bjorklund (Author) The discovery of dopamine in 1957-1958 was one of the seminal events in the development of modern neuroscience, and has been extremely important for the development of modern therapies of neurological and psychiatric disorders. Dopamine has a fundamental role in almost all aspects of behavior: from motor control to mood regulation, cognition and addiction and reward, and dopamine research has been unique within the neurosciences in the way it has bridged basic science and clinical practice. Over the decades research into the role of dopamine in health and disease has been in the forefront of modern neuroscience. The Dopamine Handbook is the first single-volume publication to capture current progress and excitement in this dynamic research field. |
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DopaBean - 60 - Capsule by Solaray Description: Mucuna pruriens 15% L DOPA Size: 60ct 333mg Directions: As a dietary supplement, take one capsule in the morning and one capsule in the afternoon with a meal or a glass of water. Serving Size: 1 Capsule 60 Servings per container Ingredients: Amount per serving: |
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Dopamine [VHS] Starring: John Livingston, Sabrina Lloyd, Bruno Campos, Rueben Grundy, Kathleen Antonia Directed By: Mark Decena Also With: Timothy Breitbach (Writer), Mark Decena (Writer), Andrew Jon Thomson (Producer), Brian Benson (Producer), Chris Miller (Producer), Christopher James Hall (Producer), Debbie Brubaker (Producer) Indie flick Dopamine wants to know: Is love a transcendent, spiritual experience, or simply the result of hormones like dopamine (a chemical in the brain that inspires pleasure)? Rand (John Livingston, Where's Marlowe?), a San Francisco computer programmer developing a virtual pet, is convinced it's all neurochemistry--until he meets Sarah (Sabrina Lloyd of the TV show Sliders), a teacher at a pre-school where the pet is being tested. During their nervous, awkward dates, he struggles to maintain his cynical, hormone-driven perspective as his feelings seem increasingly real. The dialogue and ideas in Dopamine are clever, if not exactly convincing; unfortunately, the pace and performances are stiff and morose--the romance feels more predetermined by the filmmakers' schematic plan... |
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