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![25 (a) In vitro autoradiogram of [ 125 I]33 in sagittal sections of rat brain. (b) Quantified values of the autoradiogram in cerebral cortex (CTX), hippocampus (HIP), striatum (STR), thalamus (THA), and cerebellum (CB). Nonspecific binding was determined in the presence of nonradioactive 33 (10 μM). (c) Effect of nonradioactive 33 and Ro 25–6981 (NR2B antagonist) on the brain tissue to blood ratio in mice at 180 min after intravenous injection of [ 125 I]33. Drugs were pretreated 30 min before the tracer injection. * P < 0.01 in comparison to the control group (Fuchigami et al. 2010)](profile/Takeshi-Fuchigami-2/publication/300881580/figure/fig16/AS:373753558126601@1466121200595/a-In-vitro-autoradiogram-of-125-I33-in-sagittal-sections-of-rat-brain-b.png)
25 (a) In vitro autoradiogram of [ 125 I]33 in sagittal sections of rat brain. (b) Quantified values of the autoradiogram in cerebral cortex (CTX), hippocampus (HIP), striatum (STR), thalamus (THA), and cerebellum (CB). Nonspecific binding was determined in the presence of nonradioactive 33 (10 μM). (c) Effect of nonradioactive 33 and Ro 25–6981 (NR2B antagonist) on the brain tissue to blood ratio in mice at 180 min after intravenous injection of [ 125 I]33. Drugs were pretreated 30 min before the tracer injection. * P < 0.01 in comparison to the control group (Fuchigami et al. 2010)
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![Fig. 18.20 Typical autoradiogram of in vitro binding of [ 11 C]22 (a)...](profile/Takeshi-Fuchigami-2/publication/300881580/figure/fig11/AS:373753558126596@1466121200286/Typical-autoradiogram-of-in-vitro-binding-of-11-C22-a-and-11-C23-b-Effect-of_Q320.jpg)
![Fig. 18.23 (a) In vitro autoradiogram of [ 11 C]26 in sagittal sections...](profile/Takeshi-Fuchigami-2/publication/300881580/figure/fig14/AS:373753558126599@1466121200532/a-In-vitro-autoradiogram-of-11-C26-in-sagittal-sections-of-rat-brain-b-Quantified_Q320.jpg)
N-methyl-d-aspartate receptors (NMDARs) play an important role in the neurotransmission of the central nervous system (CNS). On the other hand, aberrant functioning of the NMDARs has been implicated in various CNS disorders. Positron emission tomography (PET) and single photon emission computed tomography (SPECT) imaging of NMDARs may provide novel...
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Citations
... NMDARs are a family of ionotropic receptors (ion channels) activated by glutamate -the principal excitatory neurotransmitter in the brain (Fuchigami et al. 2021). Overactive glutamatergic neurotransmission is thought to underlie LID, and NMDAR inhibition reduces LID in preclinical PD models (Niccolini et al. 2015b). ...
Parkinson's disease (PD) is a neurodegenerative disorder that affects millions of people worldwide. Two hallmarks of PD are the accumulation of alpha‐synuclein and the loss of dopaminergic neurons in the brain. There is no cure for PD, and all existing treatments focus on alleviating the symptoms. PD diagnosis is also based on the symptoms, such as abnormalities of movement, mood, and cognition observed in the patients. Molecular imaging methods such as magnetic resonance imaging (MRI), single‐photon emission computed tomography (SPECT), and positron emission tomography (PET) can detect objective alterations in the neurochemical machinery of the brain and help diagnose and study neurodegenerative diseases. This review addresses the application of functional MRI, PET, and SPECT in PD patients. We provide an overview of the imaging targets, discuss the rationale behind target selection, the agents (tracers) with which the imaging can be performed, and the main findings regarding each target's state in PD. Molecular imaging has proven itself effective in supporting clinical diagnosis of PD and has helped reveal that PD is a heterogeneous disorder, which has important implications for the development of future therapies. However, the application of molecular imaging for early diagnosis of PD or for differentiation between PD and atypical parkinsonisms has remained challenging. The final section of the review is dedicated to new imaging targets with which one can detect the PD‐related pathological changes upstream from dopaminergic degeneration. The foremost of those targets is alpha‐synuclein. We discuss the progress of tracer development achieved so far and challenges on the path toward alpha‐synuclein imaging in humans.
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