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- New studies in human genetics have revealed information about genetic connections to memory and motor behavior. Researchers are interested in investigating the role of genetics in motor learning, in conjunction with related studies taking place in the Human Motor Control Section of the National Institute of Neurological Diseases and Stroke (NINDS). Participants in motor learning studies conducted at NINDS will be asked to provide blood samples for further evaluation.
- To create a repository of blood samples from patients and healthy subjects who are participating in NINDS motor learning studies.
- Individuals between 18 and 100 years of age who are or will be participating in motor learning research studies at the National Institutes of Health.
- Blood draws for genetic testing will usually be done on the same day as the motor learning study. Participants will provide one blood sample for research.
- No treatment will be provided under this study.
The objective of this study is to create a bio-repository of blood samples from patients and healthy subjects who are participating in NINDS motor learning studies. Blood will be analyzed for BDNF and samples stored for future genetic studies. . A variety of genes that may affect motor learning are being increasingly identified, and variations among these genes, referred to as polymorphisms, may help explain individual differences.
We will enroll up to five hundred healthy volunteers and five hundred volunteers with movement difficulties who are between the ages of 18 and 100 and who are already participating, or will be participating, in other protocols dealing with motor learning research studies at the National Institutes of Health (NIH).
This is an observational and repository protocol that involves a single blood sample for genetic analysis. This will allow the genetic characterization of subjects participating in motor learning protocols to be analyzed and tested for the role of genetics in motor learning results.
We will compare genetic variations with the different behavioral, electrophysiologic, imaging, or other outcomes acquired in the associated motor learning studies. Thus, we will determine whether specific polymorphisms are associated with different measures of motor learning.
Time Perspective: Prospective
National Institutes of Health Clinical Center, 9000 Rockville Pike
National Institutes of Health Clinical Center (CC)
Published on BioPortfolio: 2014-08-27T03:14:32-0400
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A condition caused by the neurotoxin MPTP which causes selective destruction of nigrostriatal dopaminergic neurons. Clinical features include irreversible parkinsonian signs including rigidity and bradykinesia (PARKINSON DISEASE, SECONDARY). MPTP toxicity is also used as an animal model for the study of PARKINSON DISEASE. (Adams et al., Principles of Neurology, 6th ed, p1072; Neurology 1986 Feb;36(2):250-8)
A group of disorders which feature impaired motor control characterized by bradykinesia, MUSCLE RIGIDITY; TREMOR; and postural instability. Parkinsonian diseases are generally divided into primary parkinsonism (see PARKINSON DISEASE), secondary parkinsonism (see PARKINSON DISEASE, SECONDARY) and inherited forms. These conditions are associated with dysfunction of dopaminergic or closely related motor integration neuronal pathways in the BASAL GANGLIA.
Parkinsonism following encephalitis, historically seen as a sequella of encephalitis lethargica (Von Economo Encephalitis). The early age of onset, the rapid progression of symptoms followed by stabilization, and the presence of a variety of other neurological disorders (e.g., sociopathic behavior; TICS; MUSCLE SPASMS; oculogyric crises; hyperphagia; and bizarre movements) distinguish this condition from primary PARKINSON DISEASE. Pathologic features include neuronal loss and gliosis concentrated in the MESENCEPHALON; SUBTHALAMUS; and HYPOTHALAMUS. (From Adams et al., Principles of Neurology, 6th ed, p754)
Conditions which feature clinical manifestations resembling primary Parkinson disease that are caused by a known or suspected condition. Examples include parkinsonism caused by vascular injury, drugs, trauma, toxin exposure, neoplasms, infections and degenerative or hereditary conditions. Clinical features may include bradykinesia, rigidity, parkinsonian gait, and masked facies. In general, tremor is less prominent in secondary parkinsonism than in the primary form. (From Joynt, Clinical Neurology, 1998, Ch38, pp39-42)
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