ArticleEuropean journal of nuclear medicine and molecular imaging2026
Allocation of TSPO-PET signals to cellular and extracellular compartments in dependence of blood-brain barrier disruption in experimental glioblastoma.
Article in European journal of nuclear medicine and molecular imaging, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundTranslocator protein (TSPO)-PET imaging facilitates monitoring of glioblastoma in preclinical models and patients. However, specificity of TSPO-PET signals remains to be investigated. In this study, we aimed to decipher exact contributions of cellular and extracellular compartments including the impact of blood-brain barrier (BBB) disruption to TSPO-PET signals in an experimental glioblastoma mouse model.
methodsMice with implanted glioblastoma (SB28; n = 36 early-stage, n = 39 late-stage; GFP(+)) were injected with the TSPO tracer [
resultsTSPO-PET indicated strong but incomplete signal reduction after blocking in tumors (early-stage: -72%; late-stage: -59%, p < 0.001) and contralateral hemispheres (early stage: -65%, late-stage: -63%, p < 0.001) compared to unblocked animals. We found nearly complete blocking of radiotracer uptake across all analyzed cell fractions (tumor cells: -95%, p = 0.0039; TAMs: -98%, p < 0.0001; remaining cells: -99%, p = 0.0033) compared to unblocked mice, regardless of tumor stages. There was a significant correlation of PET signal reduction (R=-0.824, p = 0.0034) as well as residual PET signal upon blocking (R = 0.809, p = 0.0046) with Dextran intensity.
conclusionSpecificity of TSPO-PET signals in experimental glioblastoma reaches 72% in early-stage tumors, but decreases to 59% in late-stage SB28 tumors, due to progressive contributions of BBB disruption. Non-specific TSPO tracer uptake is driven by BBB disruption and fully allocated to the extracellular compartment, whereas cellular TSPO tracer uptake shows strong specificity.
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