In vivo cell tracking via 18F-fluorodeoxyglucose labeling: a review of the preclinical and clinical applications in cell-based diagnosis and therapy

Wu, Chenxi; Ma, Guotao; Li, Jing; Zheng, Kun; Dang, Yongyan; Shi, Ximin; Sun, Yi; Li, Fang; Zhu, Zhaohui

doi:10.1016/j.clinimag.2012.02.023

Cited by 19 publications

(14 citation statements)

References 42 publications

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“…The relatively long half-life (67 h) and high in vivo stability of 111 In-oxine provides the option to acquire images after 24 h or more, whereas 99m Tc chelated agents have a relatively short half-life (6 h). 18 F-fluorodeoxyglucose (FDG) also can be taken up and metabolically trapped by the cells and subsequently tracked in vivo 43, 44 .…”

Section: Cell Labelingmentioning

confidence: 99%

Clinical imaging in regenerative medicine

et al. 2014

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In regenerative medicine, clinical imaging is indispensable for characterizing damaged tissue and for measuring the safety and efficacy of therapy. However, the ability to track the fate and function of transplanted cells with current technologies is limited. Exogenous contrast labels such as nanoparticles give a strong signal in the short term but are unreliable long term. Genetically encoded labels are good both short- and long-term in animals, but in the human setting they raise regulatory issues related to the safety of genomic integration and potential immunogenicity of reporter proteins. Imaging studies in brain, heart and islets share a common set of challenges, including developing novel labeling approaches to improve detection thresholds and early delineation of toxicity and function. Key areas for future research include addressing safety concerns associated with genetic labels and developing methods to follow cell survival, differentiation and integration with host tissue. Imaging may bridge the gap between cell therapies and health outcomes by elucidating mechanisms of action through longitudinal monitoring.

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Section: Cell Labelingmentioning

confidence: 99%

Clinical imaging in regenerative medicine

et al. 2014

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“…The most popular tracers investigated to date bind to translocator protein (TPSO) which is expressed on activated microglia, astrocytes, and other infiltrating immune cells in the brain. TPSO signal has been shown to increase with microglia activation in tauopathies including AD, PSP, PiD, and FTDP-17 [111–113] as well as several other neurodegenerative diseases and injury models such as other frontotemporal dementias (FTDs), Parkinson’s disease, stroke and TBI [114]. Interestingly, despite many reports characterizing microglial activation in response to Aβ plaque deposition, Maeda et al observed stronger correlation of TPSO tracer 11 C–AC-5216 binding in response to NFTs and NTs in AD and non-AD tauopathy brains.…”

Section: Introductionmentioning

confidence: 99%

Glial contributions to neurodegeneration in tauopathies

Leyns

Holtzman

2017

Mol Neurodegeneration

300

240

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Tauopathies are a broad set of neurodegenerative dementias characterized by aggregation of the tau protein into filamentous inclusions that can be found in neurons and glial cells. Activated microglia, astrocytes and elevated levels of proinflammatory molecules are also pathological hallmarks that are found in brain regions affected by tau pathology. There has been abundant research in recent years to understand the role of gliosis and neuroinflammation in neurodegenerative diseases, particularly in Alzheimer’s disease (AD) which is the most common form of dementia. AD is a tauopathy characterized by both extracellular amyloid-β plaques in addition to intracellular neurofibrillary tangles and neuropil threads containing aggregated tau protein. Accumulating evidence suggests that neuroinflammation offers a possible mechanistic link between these pathologies. Additionally, there appears to be a role for neuroinflammation in aggravating tau pathology and neurodegeneration in tauopathies featuring tau deposits as the predominant pathological signature. In this review, we survey the literature regarding inflammatory mechanisms that may impact neurodegeneration in AD and related tauopathies. We consider a physical role for microglia in the spread of tau pathology as well as the non-cell autonomous effects of secreted proinflammatory cytokines, specifically interleukin 1 beta, interleukin 6, tumor necrosis factor alpha and complement proteins. These molecules appear to have direct effects on tau pathophysiology and overall neuronal health. They also indirectly impact neuronal homeostasis by altering glial function. We conclude by proposing a complex role for gliosis and neuroinflammation in accelerating the progression of AD and other tauopathies.

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“…[ 64 Cu]‐PTSM proved to be superior to [ 18 F]‐fluorodeoxyglucose‐labelled leukocytes with a higher and more reproducible labelling efficiency . The short physical half‐life of 18 F is not suitable for long‐term observations, and non‐specific uptake was observed with [ 18 F]‐fluorodeoxyglucose‐labelled leukocytes partly because of high efflux of 18 F after injection . In addition, carbon‐11 ( 11 C, t 1/2 = 20.3 min) has been utilised for macrophage imaging in rheumatoid synovitis using the PET tracer [ 11 C]PK11195, which is a ligand for the translocator protein 18 kDa that is expressed on macrophages.…”

Section: Introductionmentioning

confidence: 99%

A new technique for the radiolabelling of mixed leukocytes with zirconium‐89 for inflammation imaging with positron emission tomography

Fairclough¹,

Prenant²,

Ellis

et al. 2016

Labelled Comp Radiopharmac

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Mixed leukocyte (white blood cells [WBCs]) trafficking using positron emission tomography (PET) is receiving growing interest to diagnose and monitor inflammatory conditions. PET, a high sensitivity molecular imaging technique, allows precise quantification of the signal produced from radiolabelled moieties. We have evaluated a new method for radiolabelling WBCs with either zirconium‐89 (89Zr) or copper‐64 (64Cu) for PET imaging. Chitosan nanoparticles (CNs) were produced by a process of ionotropic gelation and used to deliver radiometals into WBCs. Experiments were carried out using mixed WBCs freshly isolated from whole human blood. WBCs radiolabelling efficiency was higher with [89Zr]‐loaded CN (76.8 ± 9.6% (n = 12)) than with [64Cu]‐loaded CN (26.3 ± 7.0 % (n = 7)). [89Zr]‐WBCs showed an initial loss of 28.4 ± 5.8% (n = 2) of the radioactivity after 2 h. This loss was then followed by a plateau as 89Zr remains stable in the cells. [64Cu]‐WBCs showed a loss of 85 ± 6% (n = 3) of the radioactivity after 1 h, which increased to 96 ± 6% (n = 3) loss after 3 h. WBC labelling with [89Zr]‐loaded CN showed a fast kinetic of leukocyte association, high labelling efficiency and a relatively good retention of the radioactivity. This method using 89Zr has a potential application for PET imaging of inflammation.

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In vivo cell tracking via 18F-fluorodeoxyglucose labeling: a review of the preclinical and clinical applications in cell-based diagnosis and therapy

Cited by 19 publications

References 42 publications

Clinical imaging in regenerative medicine

Clinical imaging in regenerative medicine

Glial contributions to neurodegeneration in tauopathies

A new technique for the radiolabelling of mixed leukocytes with zirconium‐89 for inflammation imaging with positron emission tomography

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