In vivo imaging of the 18-kDa translocator protein (TSPO) with [18F]FEDAA1106 and PET does not show increased binding in Alzheimer’s disease patients

2013 ◽  
Vol 40 (6) ◽  
pp. 921-931 ◽  
Author(s):  
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Patrik Mattsson ◽  
Anton Forsberg ◽  
Akihiro Takano ◽  
Sangram Nag ◽  
...  
2010 ◽  
Vol 6 ◽  
pp. S429-S430
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Nobuyuki Okamura ◽  
Shozo Furumoto ◽  
Katsutoshi Furukawa ◽  
Hiroyuki Arai ◽  
Kazuhiko Yanai ◽  
...  

2018 ◽  
Vol 9 ◽  
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Paul Edison ◽  
Cornelius K. Donat ◽  
Magdalena Sastre

2019 ◽  
Vol 47 (2) ◽  
pp. 390-402 ◽  
Author(s):  
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Mohamed Ali Bahri ◽  
François Meyer ◽  
Marine Manard ◽  
Emma Delhaye ◽  
...  

2007 ◽  
Vol 7 (4) ◽  
pp. 393-400 ◽  
Author(s):  
Nobuyuki Okamura ◽  
Shozo Furumoto ◽  
Yoshihito Funaki ◽  
Takahiro Suemoto ◽  
Motohisa Kato ◽  
...  

Methods ◽  
2011 ◽  
Vol 53 (3) ◽  
pp. 201-207 ◽  
Author(s):  
Tara L. Spires-Jones ◽  
Alix de Calignon ◽  
Melanie Meyer-Luehmann ◽  
Brian J. Bacskai ◽  
Bradley T. Hyman

2008 ◽  
Vol 4 ◽  
pp. T300-T301
Author(s):  
Paul B. Rosenberg ◽  
Y. Zhou ◽  
A. Kumar ◽  
H.T. Ravert ◽  
J. Brasic ◽  
...  

2020 ◽  
Vol 77 (3) ◽  
pp. 1043-1056 ◽  
Author(s):  
Benjamin B. Tournier ◽  
Stergios Tsartsalis ◽  
Kelly Ceyzériat ◽  
Ben H. Fraser ◽  
Marie-Claude Grégoire ◽  
...  

Background: In vivo PET/SPECT imaging of neuroinflammation is primarily based on the estimation of the 18 kDa-translocator-protein (TSPO). However, TSPO is expressed by different cell types which complicates the interpretation. Objective: The present study evaluates the cellular origin of TSPO alterations in Alzheimer’s disease (AD). Methods: The TSPO cell origin was evaluated by combining radioactive imaging approaches using the TSPO radiotracer [125I]CLINDE and fluorescence-activated cell sorting, in a rat model of AD (TgF344-AD) and in AD subjects. Results: In the hippocampus of TgF344-AD rats, TSPO overexpression not only concerns glial cells but the increase is visible at 12 and 24 months in astrocytes and only at 24 months in microglia. In the temporal cortex of AD subjects, TSPO upregulation involved only glial cells. However, the mechanism of this upregulation appears different with an increase in the number of TSPO binding sites per cell without cell proliferation in the rat, and a microglial cell population expansion with a constant number of binding sites per cell in human AD. Conclusion: These data indicate an earlier astrocyte intervention than microglia and that TSPO in AD probably is an exclusive marker of glial activity without interference from other TSPO-expressing cells. This observation indicates that the interpretation of TSPO imaging depends on the stage of the pathology, and highlights the particular role of astrocytes.


2002 ◽  
Vol 109 (5-6) ◽  
pp. 837-855 ◽  
Author(s):  
H. Hampel ◽  
S. J. Teipel ◽  
G. E. Alexander ◽  
O. Pogarell ◽  
S. I. Rapoport ◽  
...  

1997 ◽  
pp. 451-456
Author(s):  
B. Tavitian ◽  
S. Pappatà ◽  
F. Branly ◽  
A. Jobert ◽  
A. Dalger ◽  
...  

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