Positron emission tomography demonstrates dopamine D2receptor supersensitivity in the striatum of patients with early Parkinson's disease

1990 ◽  
Vol 5 (1) ◽  
pp. 55-59 ◽  
Author(s):  
U. K. Rinne ◽  
A. Laihinen ◽  
J. O. Rinne ◽  
K. Naågren ◽  
J. Bergman ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Positron Emission Tomography ◽  
Parkinson's Disease ◽  
Emission Tomography ◽  
Positron Emission ◽  
Early Parkinson’S Disease

scholarly journals Spared Caudal Brainstem SERT Binding in Early Parkinson's Disease

2007 ◽  
Vol 28 (3) ◽  
pp. 441-444 ◽  
Author(s):  
Roger L Albin ◽  
Robert A Koeppe ◽  
Nicolaas I Bohnen ◽  
Kristine Wernette ◽  
Michael A Kilbourn ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Positron Emission Tomography ◽  
Parkinson's Disease ◽  
Serotonin Transporter ◽  
Emission Tomography ◽  
Serotoninergic Neurons ◽  
Positron Emission ◽  
Brainstem Nuclei ◽  
Early Parkinson’S Disease ◽  
Normal Controls

Postmortem data indicate loss of serotoninergic neurons in Parkinson's disease (PD). We used the serotonin transporter (SERT) radioligand 3-amino-4-(2-dimethylaminomethyl-phenylsulfaryl)-benzonitril (DASB) and positron emission tomography to examine SERT distribution and changes in early PD subjects. We studied five PD subjects (H&Y 1 to 2.5) and eight normal controls. There is reduced SERT binding in PD. The magnitude of DASB binding reductions was greater in the forebrain than in the brainstem regions. There was no asymmetry of diminished SERT binding. DASB binding in the medulla was relatively spared, inconsistent with the description of early prominent pathologic study in these caudal brainstem nuclei.

scholarly journals Observation of magnetic susceptibility changes within the thalamus: a comparative study between healthy and Parkinson’s disease afflicted cynomolgus monkeys using 7 T MRI

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Sangwoo Kim ◽  
Youngjeon Lee ◽  
Chang-Yeop Jeon ◽  
Yeung Bae Jin ◽  
Sukhoon Oh ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Parkinson’S Disease ◽  
Positron Emission Tomography ◽  
Parkinson's Disease ◽  
Magnetic Resonance ◽  
Disease Model ◽  
Emission Tomography ◽  
Resonance Imaging ◽  
Cynomolgus Monkeys ◽  
Positron Emission

Abstract Background Although the thalamus is known to modulate basal ganglia function related to motor control activity, the abnormal changes within the thalamus during distinct medical complications have been scarcely investigated. In order to explore the feasibility of assessing iron accumulation in the thalamus as an informative biomarker for Parkinson’s disease (PD), this study was designed to employ quantitative susceptibility mapping using a 7 T magnetic resonance imaging system in cynomolgus monkeys. A 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-injected cynomolgus monkey and a healthy control (HC) were examined by 7 T magnetic resonance imaging. Positron emission tomography with 18F-N-(3-fluoro propyl)-2ß-carboxymethoxy-3ß-(4-iodophenyl) nortropane was also employed to identify the relationship between iron deposits and dopamine depletion. All acquired values were averaged within the volume of interest of the nigrostriatal pathway. Findings Compared with the HC, the overall elevation of iron deposition within the thalamus in the Parkinson’s disease model (about 53.81% increase) was similar to that in the substantia nigra (54.81%) region. Substantial susceptibility changes were observed in the intralaminar part of the thalamus (about 70.78% increase). Additionally, we observed that in the Parkinson’s disease model, binding potential values obtained from positron emission tomography were considerably decreased in the thalamus (97.51%) and substantia nigra (92.48%). Conclusions The increased iron deposition in the thalamus showed negative correlation with dopaminergic activity in PD, supporting the idea that iron accumulation affects glutaminergic inputs and dopaminergic neurons. This investigation indicates that the remarkable susceptibility changes in the thalamus could be an initial major diagnostic biomarker for Parkinson’s disease-related motor symptoms.

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