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Non-invasive Imaging and Analysis of Cerebral Ischemia in Living Rats Using Positron Emission Tomography with 18F-FDG
Published on: December 28, 2014
A feasibility study for quantitative assessment of cerebrovascular malformations using flutriciclamide ([18F]GE-180)
Sally Ji Who Kim1,2, Janine M Lupo1, Yicheng Chen1
1Department of Radiology and Biomedical Imaging, University of California, San Francisco, San Francisco, CA, United States.
Aim:
Neuroinflammation plays a key role in both the pathogenesis and the progression of cerebral cavernous malformations (CCM). Flutriciclamide ([18F]GE-180) is a translocator protein (TSPO) targeting positron emission tomography (PET) tracer, developed for imaging neuroinflammation. The objectives of this study were to describe characteristics of flutriciclamide uptake in different brain tissue regions in CCM patients compared to controls, and to evaluate flutriciclamide uptake and iron deposition within CCM lesions.
Materials And Methods:
Five patients with CCM and six controls underwent a 60 or 90 min continuous PET/MRI scan following 315 ± 68.9 MBq flutriciclamide administration. Standardized uptake value (SUV) and standardized uptake value ratio (SUVr) were obtained using the striatum as a pseudo-reference. Quantitative susceptibility maps (QSM) were used to define the location of the vascular malformation and calculate the amount of iron deposition in each lesion.
Results:
Increased flutriciclamide uptake was observed in all CCM lesions. The temporal pole demonstrated the highest radiotracer uptake; the paracentral lobule, cuneus and hippocampus exhibited moderate uptake; while the striatum had the lowest uptake, with average SUVs of 0.66, 0.55, 0.63, 0.55, and 0.33 for patient with CCM and 0.57, 0.50, 0.48, 0.42, and 0.32 for controls, respectively. Regional SUVr showed similar trends. The average SUV and QSM values in CCM lesions were 0.58 ± 0.23 g/ml and 0.30 ± 0.10 ppm. SUVs and QSM were positively correlated in CCM lesions (r = 0.53, p = 0.03).
Conclusion:
The distribution of flutriciclamide ([18F]GE-180) in the human brain and CCM lesions demonstrated the potential of this TSPO PET tracer as a marker of neuroinflammation that may be relevant for characterizing CCM disease progression along with QSM.
Insights
This study shows that flutriciclamide (a TSPO PET tracer) uptake is increased in cerebral cavernous malformations (CCM) lesions, correlating with iron deposition. This highlights its potential for imaging neuroinflammation in CCM disease progression.
Area of Science:
- Neuroimaging
- Neurology
- Radiochemistry
Background:
- Neuroinflammation is a critical factor in the development and progression of cerebral cavernous malformations (CCM).
- Flutriciclamide ([18F]GE-180) is a novel positron emission tomography (PET) tracer designed to visualize neuroinflammation by targeting translocator protein (TSPO).
Purpose of the Study:
- To characterize flutriciclamide uptake in various brain regions of CCM patients compared to healthy controls.
- To assess the relationship between flutriciclamide uptake and iron deposition within CCM lesions.
Main Methods:
- Five CCM patients and six controls underwent PET/MRI scans after receiving flutriciclamide.
- Standardized uptake values (SUV) and SUV ratios (SUVr) were calculated, using the striatum as a reference region.
- Quantitative susceptibility mapping (QSM) was employed to identify lesions and quantify iron content.
Main Results:
- Elevated flutriciclamide uptake was detected in all CCM lesions, with the highest concentrations in the temporal pole.
- Average SUV and QSM values in CCM lesions were 0.58 g/ml and 0.30 ppm, respectively.
- A significant positive correlation was found between flutriciclamide SUV and QSM values in CCM lesions (r = 0.53, p = 0.03).
Conclusions:
- Flutriciclamide PET imaging reveals increased neuroinflammation in CCM lesions.
- The tracer's distribution in the brain and lesions suggests its utility as a biomarker for neuroinflammation in CCM.
- Combined with QSM, flutriciclamide shows promise for characterizing CCM disease progression.
