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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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Mice with implanted glioblastoma (SB28;\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200936 early-stage,\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200939 late-stage; GFP(+)) were injected with the TSPO tracer [\n                      <jats:sup>18<\/jats:sup>\n                      F]GE-180 (21 MBq\u2009\u00b1\u20091.5 MBq). Dynamic 60\u00a0min microPET scans were performed with and without prior blocking by excessive cold radiotracer. Tumors were dissociated, followed by cell sorting of tumor cells, tumor-associated microglia\/macrophages (TAMs, CD11b(+)) and non-tumor\/non-TAM (i.e. remaining) cells with subsequent gamma emission measures and flow cytometry (scRadiotracing) to calculate radioactivity per single cell. PET signals and single-cell tracer uptake in tumors and non-lesional hemispheres were compared between blocked and unblocked conditions.\n                      <jats:italic>N<\/jats:italic>\n                      \u2009=\u200910 mice were intravenously injected with fluorescent Dextran to investigate BBB disruption by confocal microscopy in correlation with TSPO-PET signals of the same animals.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      TSPO-PET indicated strong but incomplete signal reduction after blocking in tumors (early-stage: -72%; late-stage: -59%,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001) and contralateral hemispheres (early stage: -65%, late-stage: -63%,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001) compared to unblocked animals. We found nearly complete blocking of radiotracer uptake across all analyzed cell fractions (tumor cells: -95%,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.0039; TAMs: -98%,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.0001; remaining cells: -99%,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.0033) compared to unblocked mice, regardless of tumor stages. There was a significant correlation of PET signal reduction (\n                      <jats:italic>R<\/jats:italic>\n                      =-0.824,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.0034) as well as residual PET signal upon blocking (\n                      <jats:italic>R<\/jats:italic>\n                      \u2009=\u20090.809,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.0046) with Dextran intensity.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Specificity 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.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s00259-026-08187-5","type":"journal-article","created":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T02:50:57Z","timestamp":1790218257000},"page":"8675-8685","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Allocation of TSPO-PET signals to cellular and extracellular compartments in dependence of blood-brain barrier disruption in experimental glioblastoma"],"prefix":"10.1007","volume":"53","author":[{"given":"Leonie","family":"Hoermann","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fatma Burcu","family":"Seker","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emanuel","family":"Joseph","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sabrina V","family":"Kirchleitner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jens","family":"Blobner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lea H","family":"Kunze","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Justus F","family":"Thevis","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Selina","family":"Hummel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amelie L","family":"Englert","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karin","family":"Wind-Mark","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adrien","family":"Holzgreve","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Simon","family":"Lindner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rudolf A","family":"Werner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Louisa","family":"von Baumgarten","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nathalie L","family":"Albert","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nikolaus","family":"Plesnila","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthias","family":"Brendel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-6158-319X","authenticated-orcid":false,"given":"Laura M","family":"Bartos","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,9,24]]},"reference":[{"issue":"3","key":"8187_CR1","first-page":"165","volume":"9","author":"JT Low","year":"2022","unstructured":"Low JT, et al. 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RAW has received speaker honoraria from and reports advisory board work for Novartis\/AAA. NLA has received honoraria for lectures, consultation or advisory board participation from ABX, Advanced Accelerator Applications, Carthera, ITM Oncologics GmbH, Medsir, Novartis, OncLive, Servier and Telix Pharmaceuticals, and research funding from Novocure, Telix Pharmaceuticals and Servier. MB is a member of the Neuroimaging Committee of the EANM. MB has received speaker honoraria from Roche, GE Healthcare, Iba, Miltenyi, and Life Molecular Imaging; has advised Life Molecular Imaging, MIAC, Cenos, and GE healthcare; and is currently on the advisory or imaging review boards of AC Immune and ZRO Imaging. All other authors do not report conflicts of interest.","order":3,"name":"Ethics","label":"Competing interests","group":{"name":"EthicsHeading","label":"Declarations"}}]}}