scholarly journals In vivo binding of protoporphyrin IX to rat translocator protein imaged with positron emission tomography

Synapse ◽  
2010 ◽  
Vol 64 (8) ◽  
pp. 649-653 ◽  
Author(s):  
Harushige Ozaki ◽  
Sami S. Zoghbi ◽  
Jinsoo Hong ◽  
Ajay Verma ◽  
Victor W. Pike ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Protoporphyrin Ix ◽  
Translocator Protein ◽  
Emission Tomography ◽  
In Vivo Binding ◽  
Positron Emission

scholarly journals The methodology of TSPO imaging with positron emission tomography

2015 ◽  
Vol 43 (4) ◽  
pp. 586-592 ◽  
Author(s):  
Federico E. Turkheimer ◽  
Gaia Rizzo ◽  
Peter S. Bloomfield ◽  
Oliver Howes ◽  
Paolo Zanotti-Fregonara ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Cellular Heterogeneity ◽  
Translocator Protein ◽  
Emission Tomography ◽  
Expected Improvement ◽  
Positron Emission ◽  
Distribution In Blood ◽  
Methodological Aspects ◽  
Tspo Imaging

The 18-kDA translocator protein (TSPO) is consistently elevated in activated microglia of the central nervous system (CNS) in response to a variety of insults as well as neurodegenerative and psychiatric conditions. It is therefore a target of interest for molecular strategies aimed at imaging neuroinflammation in vivo. For more than 20 years, positron emission tomography (PET) has allowed the imaging of TSPO density in brain using [11C]-(R)-PK11195, a radiolabelled-specific antagonist of the TSPO that has demonstrated microglial activation in a large number pathological cohorts. The significant clinical interest in brain immunity as a primary or comorbid factor in illness has sparked great interest in the TSPO as a biomarker and a surprising number of second generation TSPO radiotracers have been developed aimed at improving the quality of TSPO imaging through novel radioligands with higher affinity. However, such major investment has not yet resulted in the expected improvement in image quality. We here review the main methodological aspects of TSPO PET imaging with particular attention to TSPO genetics, cellular heterogeneity of TSPO in brain tissue and TSPO distribution in blood and plasma that need to be considered in the quantification of PET data to avoid spurious results as well as ineffective development and use of these radiotracers.

Specific in vivo binding in the rat brain of [18F]RP 62203: A selective 5-HT2A receptor radioligand for positron emission tomography

1996 ◽  
Vol 23 (2) ◽  
pp. 169-171 ◽  
Author(s):  
Laurent Besret ◽  
François Dauphin ◽  
Cécile Huard ◽  
Marie-Claire Lasne ◽  
Richard Vivet ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Rat Brain ◽  
Emission Tomography ◽  
In Vivo Binding ◽  
Positron Emission

Positron emission tomography imaging in evaluation of MS pathology in vivo

2018 ◽  
Vol 24 (11) ◽  
pp. 1399-1412 ◽  
Author(s):  
Heidi Högel ◽  
Eero Rissanen ◽  
Anna Vuorimaa ◽  
Laura Airas
Keyword(s):  
Positron Emission Tomography ◽  
Pet Imaging ◽  
Human Subjects ◽  
Positron Emission Tomography Imaging ◽  
Translocator Protein ◽  
Emission Tomography ◽  
Amyloid Pet ◽  
Positron Emission ◽  
Density Evaluation

Positron emission tomography (PET) gives an opportunity to quantitate the expression of specific molecular targets in vivo and longitudinally in brain and thus enhances our possibilities to understand and follow up multiple sclerosis (MS)-related pathology. For successful PET imaging, one needs a relevant target molecule within the brain, to which a blood–brain barrier–penetrating specific radioligand will bind. 18-kDa translocator protein (TSPO)-binding radioligands have been used to detect activated microglial cells at different stages of MS, and remyelination has been measured using amyloid PET. Several PET ligands for the detection of other inflammatory targets, besides TSPO, have been developed but not yet been used for imaging MS patients. Finally, synaptic density evaluation has been successfully tested in human subjects and gives opportunities for the evaluation of the development of cortical and deep gray matter pathology in MS. This review will discuss PET imaging modalities relevant for MS today.

scholarly journals Upregulation of cannabinoid receptor type 2, but not TSPO, in senescence-accelerated neuroinflammation in mice: a positron emission tomography study

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Satoru Yamagishi ◽  
Yurika Iga ◽  
Masato Nakamura ◽  
Chika Takizawa ◽  
Dai Fukumoto ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Cannabinoid Receptor ◽  
Early Stage ◽  
Specific Treatment ◽  
Translocator Protein ◽  
Emission Tomography ◽  
Cortical Region ◽  
Positron Emission

Abstract Background Microglial cells are activated in response to changes in brain homeostasis during aging, dementia, and stroke. Type 2 endocannabinoid receptors (CB2) and translocator protein 18 kD (TSPO) are considered to reflect distinct aspects of microglia-related neuroinflammatory responses in the brain. CB2 activation is considered to relate to the neuroprotective responses that may occur predominantly in the early stage of brain disorders such as Alzheimer’s disease, while an increase in TSPO expression tends to occur later during neuroinflammation, in a proinflammatory fashion. However, this information was deduced from studies with different animal samples under different experimental settings. In this study, we aimed to examine the early microglial status in the inflammation occurring in the brains of senescence-accelerated mouse prone 10 (SAMP10) mice, using positron emission tomography (PET) with CB2 and TSPO tracers, together with immunohistochemistry. Methods Five- and 15-week-old SAMP10 mice that undergo neurodegeneration after 7 months of age were used. The binding levels of the TSPO tracer (R)-[11C]PK11195 and CB2 tracer [11C]NE40 were measured using PET in combination with immunohistochemistry for CB2 and TSPO. To our knowledge, this is the first study to report PET data for CB2 and TSPO at the early stage of cognitive impairment in an animal model. Results The standard uptake value ratios (SUVRs) of [11C]NE40 binding were significantly higher than those of (R)-[11C]PK11195 binding in the cerebral cortical region at 15 weeks of age. At 5 weeks of age, the [11C]NE40 SUVR tended to be higher than the (R)-[11C]PK11195 SUVR. The (R)-[11C]PK11195 SUVR did not significantly differ between 5- and 15-week-old mice. Consistently, immunostaining analysis confirmed the upregulation of CB2, but not TSPO. Conclusions The use of the CB2 tracer [11C]NE40 and/or an immunohistochemical approach allows evaluation of the role of microglia in acute neuroinflammatory processes in the early stage of neurodegeneration. The present results provide in vivo evidence of different responses of two types of microglia to senescence-accelerated neuroinflammation, implying the perturbation of microglial balance by aging. Specific treatment for CB2-positive microglia might help ameliorate senescence-related neuroinflammation and the following neurodegeneration.

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