scholarly journals Neuroinflammation in neocortical epilepsy measured by PET imaging of translocator protein

Epilepsia ◽  
2019 ◽  
Author(s):  
Leah P. Dickstein ◽  
Jeih‐San Liow ◽  
Alison Austermuehle ◽  
Sami Zoghbi ◽  
Sara K. Inati ◽  
...  
Keyword(s):  
Pet Imaging ◽  
Translocator Protein ◽  
Neocortical Epilepsy

scholarly journals Translocator Protein PET Imaging for Glial Activation in Multiple Sclerosis

2010 ◽  
Vol 6 (3) ◽  
pp. 354-361 ◽  
Author(s):  
Unsong Oh ◽  
Masahiro Fujita ◽  
Vasiliki N. Ikonomidou ◽  
Iordanis E. Evangelou ◽  
Eiji Matsuura ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Pet Imaging ◽  
Glial Activation ◽  
Translocator Protein

[18F]DPA-714 PET imaging of translocator protein TSPO (18 kDa) in the normal and excitotoxically-lesioned nonhuman primate brain

2014 ◽  
Vol 42 (3) ◽  
pp. 478-494 ◽  
Author(s):  
S. Lavisse ◽  
K. Inoue ◽  
C. Jan ◽  
M. A. Peyronneau ◽  
F. Petit ◽  
...  
Keyword(s):  
Pet Imaging ◽  
Nonhuman Primate ◽  
Translocator Protein ◽  
Primate Brain

scholarly journals The 18-kDa Mitochondrial Translocator Protein in Human Gliomas: An 11C-(R)PK11195 PET Imaging and Neuropathology Study

2015 ◽  
Vol 56 (4) ◽  
pp. 512-517 ◽  
Author(s):  
Z. Su ◽  
F. Roncaroli ◽  
P. F. Durrenberger ◽  
D. J. Coope ◽  
K. Karabatsou ◽  
...  
Keyword(s):  
Pet Imaging ◽  
Translocator Protein ◽  
Human Gliomas

P4-172: Pet imaging of translocator protein (TSPO) in elderly controls using [11C]DPA-713

2009 ◽  
Vol 5 (4S_Part_16) ◽  
pp. P482-P482
Author(s):  
Paul B. Rosenberg ◽  
Constantine G. Lyketsos ◽  
Chris Endres ◽  
Dima Hammoud ◽  
Martin Pomper
Keyword(s):  
Pet Imaging ◽  
Translocator Protein

scholarly journals In vivo (R)-[11C]PK11195 PET imaging of 18kDa translocator protein in recent onset psychosis

2016 ◽  
Vol 2 (1) ◽  
Author(s):  
Thalia F van der Doef ◽  
Lot D de Witte ◽  
Arjen L Sutterland ◽  
Ellen Jobse ◽  
Maqsood Yaqub ◽  
...  
Keyword(s):  
Pet Imaging ◽  
Translocator Protein ◽  
Recent Onset

scholarly journals A Novel PET Imaging Probe for the Detection and Monitoring of Translocator Protein 18 kDa Expression in Pathological Disorders

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Mara Perrone ◽  
Byung Seok Moon ◽  
Hyun Soo Park ◽  
Valentino Laquintana ◽  
Jae Ho Jung ◽  
...  
Keyword(s):  
Pet Imaging ◽  
Translocator Protein ◽  
Imaging Probe ◽  
Translocator Protein 18 Kda

scholarly journals PET Imaging of Translocator Protein (18 kDa) in a Mouse Model of Alzheimer's Disease Using N-(2,5-Dimethoxybenzyl)-2-18F-Fluoro-N-(2-Phenoxyphenyl)Acetamide

2015 ◽  
Vol 56 (2) ◽  
pp. 311-316 ◽  
Author(s):  
M. L. James ◽  
N. P. Belichenko ◽  
T.-V. V. Nguyen ◽  
L. E. Andrews ◽  
Z. Ding ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Pet Imaging ◽  
Translocator Protein ◽  
Model Of Alzheimer’S Disease ◽  
Translocator Protein 18 Kda

scholarly journals Evaluation of the PBR/TSPO Radioligand [18F]DPA-714 in a Rat Model of Focal Cerebral Ischemia

2009 ◽  
Vol 30 (1) ◽  
pp. 230-241 ◽  
Author(s):  
Abraham Martín ◽  
Raphaël Boisgard ◽  
Benoit Thézé ◽  
Nadja Van Camp ◽  
Bertrand Kuhnast ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Pet Imaging ◽  
Time Course ◽  
Focal Cerebral Ischemia ◽  
Quantitative Information ◽  
Translocator Protein ◽  
Experimental Stroke ◽  
Tspo Expression

Focal cerebral ischemia leads to an inflammatory reaction involving an overexpression of the peripheral benzodiazepine receptor (PBR)/18-kDa translocator protein (TSPO) in the cerebral monocytic lineage (microglia and monocyte) and in astrocytes. Imaging of PBR/TSPO by positron emission tomography (PET) using radiolabeled ligands can document inflammatory processes induced by cerebral ischemia. We performed in vivo PET imaging with [18F]DPA-714 to determine the time course of PBR/TSPO expression over several days after induction of cerebral ischemia in rats. In vivo PET imaging showed significant increase in DPA ( N,N-diethyl-2-(2-(4-(2-fluoroethoxy)phenyl)-5,7-dimethylpyrazolo[1,5-a]pyrimidin-3-yl)acetamide) uptake on the injured side compared with that in the contralateral area on days 7, 11, 15, and 21 after ischemia; the maximal binding value was reached 11 days after ischemia. In vitro autoradiography confirmed these in vivo results. In vivo and in vitro [18F]DPA-714 binding was displaced from the lesion by PK11195 and DPA-714. Immunohistochemistry showed increased PBR/TSPO expression, peaking at day 11 in cells expressing microglia/macrophage antigens in the ischemic area. At later times, a centripetal migration of astrocytes toward the lesion was observed, promoting the formation of an astrocytic scar. These results show that [18F]DPA-714 provides accurate quantitative information of the time course of PBR/TSPO expression in experimental stroke.

scholarly journals Insights into smouldering MS brain pathology with multimodal diffusion tensor and PET imaging

2020 ◽  
Author(s):  
Svetlana Bezukladova ◽  
Jouni Tuisku ◽  
Markus Matilainen ◽  
Anna Vuorimaa ◽  
Marjo Nylund ◽  
...  
Keyword(s):  
White Matter ◽  
Pet Imaging ◽  
Microglial Activation ◽  
Diffusion Tensor ◽  
Volume Ratio ◽  
Translocator Protein ◽  
Control Group ◽  
In Vivo Evaluation ◽  
Conventional Mri

Objective: To evaluate in vivo the co-occurrence of microglial activation and microstructural white matter damage in multiple sclerosis (MS) brain, and to examine their association with clinical disability. Methods: 18-kDa translocator protein (TSPO) brain PET imaging was performed for evaluation of microglial activation by using the radioligand [11C](R)-PK11195. TSPO-binding was evaluated as the distribution volume ratio (DVR) from dynamic PET images. Diffusion tensor imaging (DTI) and conventional MRI were performed at the same time. Mean fractional anisotropy (FA) and mean (MD), axial (AD) and radial (RD) diffusivities were calculated within the whole normal appearing white matter (NAWM) and segmented NAWM regions appearing normal in conventional MRI. 55 MS patients and 15 healthy controls were examined. Results: Microstructural damage was observed in the NAWM of MS brain. DTI parameters of MS patients were significantly altered in the NAWM, when compared to an age- and sex-matched healthy control group: mean FA was decreased, and MD, AD and RD were increased. These structural abnormalities correlated with increased TSPO binding in the whole NAWM and in the temporal NAWM (p<0.05 for all correlations; p<0.01 for RD in the temporal NAWM). Both compromised WM integrity and increased microglial activation in the NAWM correlated significantly with higher clinical disability measured with expanded disability status scale (EDSS). Conclusions: Widespread structural disruption in the NAWM is linked to neuroinflammation, and both phenomena associate with clinical disability. Multimodal PET and DTI imaging allows in vivo evaluation of widespread MS pathology not visible using conventional MRI.

scholarly journals Insights into disseminated MS brain pathology with multimodal diffusion tensor and PET imaging

2020 ◽  
Vol 7 (3) ◽  
pp. e691 ◽  
Author(s):  
Svetlana Bezukladova ◽  
Jouni Tuisku ◽  
Markus Matilainen ◽  
Anna Vuorimaa ◽  
Marjo Nylund ◽  
...  
Keyword(s):  
Pet Imaging ◽  
Microglial Activation ◽  
Diffusion Tensor ◽  
Volume Ratio ◽  
Translocator Protein ◽  
In Vivo Evaluation ◽  
Conventional Mri ◽  
Disability Status ◽  
Distribution Volume Ratio

ObjectiveTo evaluate in vivo the co-occurrence of microglial activation and microstructural white matter (WM) damage in the MS brain and to examine their association with clinical disability.Methods18-kDa translocator protein (TSPO) brain PET imaging was performed for evaluation of microglial activation by using the radioligand [11C](R)-PK11195. TSPO binding was evaluated as the distribution volume ratio (DVR) from dynamic PET images. Diffusion tensor imaging (DTI) and conventional MRI (cMRI) were performed at the same time. Mean fractional anisotropy (FA) and mean (MD), axial, and radial (RD) diffusivities were calculated within the whole normal-appearing WM (NAWM) and segmented NAWM regions appearing normal in cMRI. Fifty-five patients with MS and 15 healthy controls (HCs) were examined.ResultsMicrostructural damage was observed in the NAWM of the MS brain. DTI parameters of patients with MS were significantly altered in the NAWM compared with an age- and sex-matched HC group: mean FA was decreased, and MD and RD were increased. These structural abnormalities correlated with increased TSPO binding in the whole NAWM and in the temporal NAWM (p < 0.05 for all correlations; p < 0.01 for RD in the temporal NAWM). Both compromised WM integrity and increased microglial activation in the NAWM correlated significantly with higher clinical disability measured with the Expanded Disability Status Scale score.ConclusionsWidespread structural disruption in the NAWM is linked to neuroinflammation, and both phenomena associate with clinical disability. Multimodal PET and DTI allow in vivo evaluation of widespread MS pathology not visible using cMRI.

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