Abstract
We analyzed (18)F-dopa PET data from 11 members of kindreds with familial progressive supranuclear palsy (PSP) to characterize their cerebral dopaminergic dysfunction. Three clinically-affected PSP patients showed reduced (18)F-dopa uptake in the striatum, orbitofrontal cortex and amygdala. One asymptomatic subject exhibited progressive putamen dopaminergic dysfunction. 60% of subjects with abnormal (18)F-dopa scans developed PSP subsequently. This is the first in vivo documentation of cortical dopaminergic deficiency in PSP. Reduced striatal (18)F-dopa uptake in susceptible relatives may predict later clinical disease.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Aged
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Amygdala / diagnostic imaging
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Amygdala / metabolism
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Amygdala / physiopathology
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Cerebral Cortex / diagnostic imaging
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Cerebral Cortex / metabolism
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Cerebral Cortex / physiopathology
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Corpus Striatum / diagnostic imaging
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Corpus Striatum / metabolism
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Corpus Striatum / physiopathology
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Dihydroxyphenylalanine / analogs & derivatives*
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Dihydroxyphenylalanine / pharmacokinetics
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Disease Progression
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Dopamine / metabolism*
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Down-Regulation / physiology
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Female
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Genetic Predisposition to Disease
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Humans
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Limbic System / diagnostic imaging*
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Limbic System / metabolism*
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Limbic System / physiopathology
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Male
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Neurocognitive Disorders / diagnostic imaging
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Neurocognitive Disorders / metabolism
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Neurocognitive Disorders / physiopathology
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Pedigree
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Positron-Emission Tomography / methods
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Predictive Value of Tests
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Reference Values
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Supranuclear Palsy, Progressive / diagnostic imaging*
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Supranuclear Palsy, Progressive / metabolism*
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Supranuclear Palsy, Progressive / physiopathology
Substances
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fluorodopa F 18
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Dihydroxyphenylalanine
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Dopamine