scholarly journals Differential Regulation of Macrophage Glucose Metabolism by Macrophage Colony-stimulating Factor and Granulocyte-Macrophage Colony-stimulating Factor: Implications for 18F FDG PET Imaging of Vessel Wall Inflammation

Radiology ◽  
2017 ◽  
Vol 283 (1) ◽  
pp. 87-97 ◽  
Author(s):  
Sina Tavakoli ◽  
John D. Short ◽  
Kevin Downs ◽  
Huynh Nga Nguyen ◽  
Yanlai Lai ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Pet Imaging ◽  
Fdg Pet ◽  
Vessel Wall ◽  
Differential Regulation ◽  
Colony Stimulating Factor ◽  
Macrophage Colony Stimulating Factor ◽  
18F Fdg ◽  
Macrophage Colony ◽  
Stimulating Factor

Interaction of Colony-Stimulating Factors and Fluorodeoxyglucose F18 Positron Emission Tomography

2002 ◽  
Vol 36 (11) ◽  
pp. 1796-1799 ◽  
Author(s):  
Dmitri Mayer ◽  
Edward M Bednarczyk
Keyword(s):  
Positron Emission Tomography ◽  
Pet Imaging ◽  
Fdg Pet ◽  
Emission Tomography ◽  
Colony Stimulating Factor ◽  
Colony Stimulating Factors ◽  
Positron Emission ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

OBJECTIVE: To evaluate reports of altered diagnostic images with fluorodeoxyglucose F18 (FDG) positron emission tomography (PET) after treatment with colony-stimulating factors (CSFs). DATA SOURCES: Literature was identified by a MEDLINE search (1966–December 2001). Key search terms included granulocyte colony-stimulating factor, granulocyte—macrophage colony-stimulating factor, macrophage colony-stimulating factor, fluorodeoxyglucose, and emission-computed tomography. English language literature was reviewed. DATA SYNTHESIS: Reports have suggested altered FDG PET images following CSF treatment. Studies that assessed the effect of CSF administration on FDG PET imaging of the bone and bone marrow were reviewed. CONCLUSIONS: Administration of CSFs may interfere with accurate FDG PET imaging. Separating FDG PET imaging from CSF therapy by ≥5 days may diminish this interference.

scholarly journals PET imaging of microglia by targeting macrophage colony-stimulating factor 1 receptor (CSF1R)

2019 ◽  
Vol 116 (5) ◽  
pp. 1686-1691 ◽  
Author(s):  
Andrew G. Horti ◽  
Ravi Naik ◽  
Catherine A. Foss ◽  
Il Minn ◽  
Varia Misheneva ◽  
...  
Keyword(s):  
Brain Injury ◽  
Pet Imaging ◽  
Murine Model ◽  
Specific Radioactivity ◽  
Postmortem Brain ◽  
Colony Stimulating Factor ◽  
Postmortem Brain Tissue ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

While neuroinflammation is an evolving concept and the cells involved and their functions are being defined, microglia are understood to be a key cellular mediator of brain injury and repair. The ability to measure microglial activity specifically and noninvasively would be a boon to the study of neuroinflammation, which is involved in a wide variety of neuropsychiatric disorders including traumatic brain injury, demyelinating disease, Alzheimer’s disease (AD), and Parkinson’s disease, among others. We have developed [11C]CPPC [5-cyano-N-(4-(4-[11C]methylpiperazin-1-yl)-2-(piperidin-1-yl)phenyl)furan-2-carboxamide], a positron-emitting, high-affinity ligand that is specific for the macrophage colony-stimulating factor 1 receptor (CSF1R), the expression of which is essentially restricted to microglia within brain. [11C]CPPC demonstrates high and specific brain uptake in a murine and nonhuman primate lipopolysaccharide model of neuroinflammation. It also shows specific and elevated uptake in a murine model of AD, experimental allergic encephalomyelitis murine model of demyelination and in postmortem brain tissue of patients with AD. Radiation dosimetry in mice indicated [11C]CPPC to be safe for future human studies. [11C]CPPC can be synthesized in sufficient radiochemical yield, purity, and specific radioactivity and possesses binding specificity in relevant models that indicate potential for human PET imaging of CSF1R and the microglial component of neuroinflammation.

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