scholarly journals F-18 Stilbenes as PET Imaging Agents for Detecting β-Amyloid Plaques in the Brain

2005 ◽  
Vol 48 (19) ◽  
pp. 5980-5988 ◽  
Author(s):  
Wei Zhang ◽  
Shunichi Oya ◽  
Mei-Ping Kung ◽  
Catherine Hou ◽  
Donna L. Maier ◽  
...  
2012 ◽  
Vol 22 (13) ◽  
pp. 4332-4337 ◽  
Author(s):  
Britt-Marie Swahn ◽  
Johan Sandell ◽  
David Pyring ◽  
Margareta Bergh ◽  
Fredrik Jeppsson ◽  
...  

CNS Spectrums ◽  
2005 ◽  
Vol 10 (S18) ◽  
pp. 13-16 ◽  
Author(s):  
Mark A. Mintun

AbstractAlzheimer's disease is a degenerative neurological condition characterized by the presence of β-amyloid plaques and neurofibrillary tangles in the limbic and neocortical regions of the brain. Pittsburgh Compound-B (PIB), a benzothiazole analog, has recently been found to specifically label amyloid deposits in positron emission tomography (PET) studies of the brain, opening the door for a wide range of applications related to Alzheimer's disease. In this article, data demonstrating the specificity of PIB as a PET tracer for β-amyloid lesions are reviewed, and the potential clinical applications of PIB PET imaging is discussed. Because amyloid plaques are common even in elderly individuals who are not suffering from dementia, the primary diagnostic function of PIB PET imaging presumably would be to rule out, rather than definitively confirm, Alzheimer's diagnoses in elderly patients. Other possible uses include monitoring plaque loads in patients receiving anti-amyloid therapy for Alzheimer's disease, as well as assessing plaque formation in unaffected individuals as a means of evaluating future Alzheimer's disease.


2010 ◽  
Vol 20 (6) ◽  
pp. 1976-1980 ◽  
Author(s):  
Britt-Marie Swahn ◽  
David Wensbo ◽  
Johan Sandell ◽  
Daniel Sohn ◽  
Can Slivo ◽  
...  

2008 ◽  
Vol 18 (17) ◽  
pp. 4823-4827 ◽  
Author(s):  
Wenchao Qu ◽  
Seok-Rye Choi ◽  
Catherine Hou ◽  
Zhiping Zhuang ◽  
Shunichi Oya ◽  
...  

2011 ◽  
Vol 21 (14) ◽  
pp. 4193-4196 ◽  
Author(s):  
Mengchao Cui ◽  
Masahiro Ono ◽  
Hiroyuki Kimura ◽  
Boli Liu ◽  
Hideo Saji

2010 ◽  
Vol 1 (7) ◽  
pp. 321-325 ◽  
Author(s):  
Yan Cheng ◽  
Masahiro Ono ◽  
Hiroyuki Kimura ◽  
Shinya Kagawa ◽  
Ryuichi Nishii ◽  
...  

2013 ◽  
Vol 21 (13) ◽  
pp. 3708-3714 ◽  
Author(s):  
Hualong Fu ◽  
Lihai Yu ◽  
Mengchao Cui ◽  
Jinming Zhang ◽  
Xiaojun Zhang ◽  
...  

2018 ◽  
Vol 10 (425) ◽  
pp. eaar7522
Author(s):  
Jennifer A. Philips

An in vivo selection strategy identifies an antibody that induces stem cells to differentiate into microglia-like cells, migrate to the brain, and reduce β-amyloid plaques in mice.


2019 ◽  
Vol 2 (1) ◽  
Author(s):  
Oscar L Lopez ◽  
William E Klunk ◽  
Chester A Mathis ◽  
Beth E Snitz ◽  
Yuefang Chang ◽  
...  

Abstract A blood test that predicts the extent of amyloid plaques in the brain and risk of Alzheimer’s disease would have important benefits for the early identification of higher risk of dementia and Alzheimer’s disease and the evaluation of new preventative therapies. The goal of this study was to determine whether plasma levels of amyloid-β1–42, 1–40 and the amyloid-β1–42/1–40 ratio among participants in the Pittsburgh centre of the Ginkgo Evaluation of Memory Study were related to the extent of brain fibrillar amyloid plaques measured in 2009 using Pittsburgh compound-B PET imaging, hippocampal volume, cortical thickness in the temporal lobe and white matter lesions. There were 194 participants who had Pittsburgh compound-B measurements in 2009 with the mean age of 85 years; 96% were white and 60% men. Pittsburgh compound-B positivity was defined as a standardized uptake value ratio of ≥1.57. Amyloid-β in blood was measured using a sandwich enzyme-linked immunosorbent assay developed by Eli Lilly and modified at the University of Vermont. All participants were nondemented as of 2008 at the time of study close out. The study sample included 160 with blood samples drawn in 2000–02 and 133 from 2009 and also had brain amyloid measured in 2009. All blood samples were analysed at the same time in 2009. Plasma amyloid-β1–42 was inversely related to the percent Pittsburgh compound-B positive (standardized uptake value ratio ≥1.57), β −0.04, P = 0.005. Practically all participants who were apolipoprotein-E4 positive at older ages were also Pittsburgh compound-B positive for fibrillar amyloid. Among apolipoprotein-E4-negative participants, quartiles of amyloid-β1–42 were inversely related to Pittsburgh compound-B positivity. In multiple regression models, plasma amyloid-β1–42 measured in 2000–02 or 2009 were significantly and inversely related to Pittsburgh compound-B positivity as was the amyloid-β1–42/1–40 ratio. There was a 4-fold increase in the odds ratio for the presence of Pittsburgh compound-B positivity in the brain in 2009 for the first quartile of amyloid-β1–42 as compared with the fourth quartile in the multiple logistic model. This is one of the first longitudinal studies to evaluate the relationship between amyloid-β1–42 in the blood and the extent of brain amyloid deposition measured by PET imaging using Pittsburgh compound-B. Our findings showed that remote and recent low plasma amyloid-β1–42 levels were inversely associated with brain amyloid deposition in cognitively normal individuals. However, changes in plasma amyloid-β1–42 over time (8 years) were small and not related to the amount of Pittsburgh compound-B.


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