scholarly journals Development of molecular imaging probe targeted at Alzheimer’s disease pathology

2017 ◽  
Vol 150 (4) ◽  
pp. 172-176
Author(s):  
Nobuyuki Okamura ◽  
Ryuichi Harada ◽  
Shozo Furumoto ◽  
Tadaho Nakamura ◽  
Kazuhiko Yanai ◽  
...  
2011 ◽  
Vol 10 (6) ◽  
pp. 7290.2011.00003 ◽  
Author(s):  
Fred Reynolds ◽  
Kimberly A. Kelly

Molecular imaging allows clinicians to visualize disease-specific molecules, thereby providing relevant information in the diagnosis and treatment of patients. With advances in genomics and proteomics and underlying mechanisms of disease pathology, the number of targets identified has significantly outpaced the number of developed molecular imaging probes. There has been a concerted effort to bridge this gap with multidisciplinary efforts in chemistry, proteomics, physics, material science, and biology—all essential to progress in molecular imaging probe development. In this review, we discuss target selection, screening techniques, and probe optimization with the aim of developing clinically relevant molecularly targeted imaging agents.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Se Jong Oh ◽  
Hae-June Lee ◽  
Ye Ji Jeong ◽  
Kyung Rok Nam ◽  
Kyung Jun Kang ◽  
...  

Abstract Alzheimer’s disease (AD) is a chronic neurodegenerative disorder and the leading cause of dementia, but therapeutic treatment options are limited. Taurine has been reported to have neuroprotective properties against dementia, including AD. The present study aimed to investigate the treatment effect of taurine in AD mice by functional molecular imaging. To elucidate glutamate alterations by taurine, taurine was administered to 5xFAD transgenic mice from 2 months of age, known to apear amyloid deposition. Then, we performed glutamate positron emission tomography (PET) imaging studies for three groups (wild-type, AD, and taurine-treated AD, n = 5 in each group). As a result, brain uptake in the taurine-treated AD group was 31–40% higher than that in the AD group (cortex: 40%, p < 0.05; striatum: 32%, p < 0.01; hippocampus: 36%, p < 0.01; thalamus: 31%, p > 0.05) and 3–14% lower than that in the WT group (cortex: 10%, p > 0.05; striatum: 15%, p > 0.05; hippocampus: 14%, p > 0.05; thalamus: 3%, p > 0.05). However, we did not observe differences in Aβ pathology between the taurine-treated AD and AD groups in immunohistochemistry experiments. Our results reveal that although taurine treatment did not completely recover the glutamate system, it significantly increased metabolic glutamate receptor type 5 brain uptake. Therefore, taurine has therapeutic potential against AD.


APOPTOSIS ◽  
2012 ◽  
Vol 18 (2) ◽  
pp. 238-247 ◽  
Author(s):  
Ming-Wei Wang ◽  
Fang Wang ◽  
Yu-Jia Zheng ◽  
Ying-Jian Zhang ◽  
Yong-Ping Zhang ◽  
...  

2017 ◽  
Vol 851 ◽  
pp. 012014 ◽  
Author(s):  
P Moradi Khaniabadi ◽  
A. M. S.A Majid ◽  
M Asif ◽  
B Moradi Khaniabadi ◽  
D Shahbazi-Gahrouei ◽  
...  

2011 ◽  
Vol 6 (1) ◽  
pp. 16
Author(s):  
Karl Herholz ◽  

The most sensitive and accurate method for molecular imaging in human Alzheimer’s disease (AD) is positron emission tomography (PET). The most widely available PET tracer, which is also used in clinical oncology, is 18F-2-fluoro-2-deoxy-D-glucose (FDG). FDG is an imaging biomarker for early and differential diagnosis of AD. Even higher molecular specificity and sensitivity for detection of AD before dementia onset is provided by high-affinity ligands for fibrillary amyloid. 11C-Pittsburgh Compound B is widely being used in research laboratories, while new 18F-labelled ligands are currently undergoing formal clinical trials as amyloid imaging agents and are expected to become commercially available for clinical use in the near future. A large variety of tracers is being developed and used in dementia research for activated microglia and multiple neurotransmitter systems to study disease pathophysiology, biological correlates of clinical symptoms and new possibilities for treatment. Current studies in humans are investigating cholinergic, serotonergic and dopaminergic neurotransmission.


2010 ◽  
Vol 81 (8) ◽  
pp. 882-884 ◽  
Author(s):  
N. Tolboom ◽  
W. M. van der Flier ◽  
J. Boverhoff ◽  
M. Yaqub ◽  
M. P. Wattjes ◽  
...  

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