Disease relevance of FLUORODOPA F 18

• METHODS: We used positron-emission tomography to measure presynaptic accumulation of fluorodopa F 18 tracer in the dopaminergic regions of the brains of 12 patients with Lesch-Nyhan disease (age, 10 to 20 years) and 15 healthy controls (age, 12 to 23) [1].
• Nonlinear progression of Parkinson disease as determined by serial positron emission tomographic imaging of striatal fluorodopa F 18 activity [2].

High impact information on FLUORODOPA F 18

• RESULTS: The fluorodopa F 18 ratio was significantly lower in the putamen (31 percent of control values), caudate nucleus (39 percent), frontal cortex (44 percent), and ventral tegmental complex (substantia nigra and ventral tegmentum; 57 percent) in the patients with Lesch-Nyhan disease than in the controls [1].
• Fluorodopa F 18 positron emission tomography and the progression of Parkinson disease [3].
• Putamen and caudate nucleus fluorodopa F 18 uptake was assessed using regions of interest analysis [4].
• Young-onset Parkinson disease with and without parkin gene mutations: a fluorodopa F 18 positron emission tomography study [4].
• Dopaminergic dysfunction in midbrain dystonia: anatomoclinical study using 3-dimensional magnetic resonance imaging and fluorodopa F 18 positron emission tomography [5].

Chemical compound and disease context of FLUORODOPA F 18

• CONCLUSIONS: The pattern of fluorodopa F 18 uptake in the striatum of YOPD patients is similar to that of patients with idiopathic Parkinson disease and does not depend on the presence or absence of mutations of the parkin gene [4].

Associations of FLUORODOPA F 18 with other chemical compounds

• In parkin patients, no significant correlation was found among fluorodopa F 18 uptake, motor disability, and the type of mutations [4].

References