Abstract

AbstractBackgroundRecent evidence indicates that activated microglial cells contribute to the brain FDG‐PET signal changes in neurodegenerative disorders. Radiopharmaceuticals targeting the 18‐kDa translocator protein (TSPO) have been used to measure microglial activation. The combination of FDG‐PET and TSPO‐PET allows for assessing, in‐vivo and non‐invasively, whether they associate in brain regions vulnerable to neurodegeneration. So far, multiple studies have used FDG‐PET and TSPO‐PET concomitantly, but to our knowledge, no systematic evaluation has been conducted to assess whether they are associated. We aimed to systematically summarize the current data on brain TSPO‐PET and FDG‐PET signals in individuals with neurodegenerative disorders.MethodStudies performing TSPO‐ and FDG‐PET in neurodegenerative disorders were searched in PubMed and Web of Science. Included articles must have performed PET images concomitantly with both tracers in healthy controls and individuals presenting with neurodegenerative disorders. This review complied with PRISMA (2020) guidelines and was registered at PROSPERO (CRD42022354523).ResultA total of 272 articles were found after a search on PubMed and Web of Science, with eight meeting the inclusion criteria. We included clinical studies with individuals presenting Alzheimer’s Disease (AD), Parkinson’s Disease (PD), corticobasal syndrome and progressive supranuclear palsy, behavioral variant frontotemporal dementia, and progressive nonfluent aphasia. In AD, five studies presented negative associations, and one presented a positive association between TSPO and FDG signals in brain regions vulnerable to AD. In PD (3 studies) and the other related neurodegenerative disorders (2 studies) evaluated, we found a negative correlation between FDG‐PET and TSPO‐PET signals in vulnerable regions.ConclusionAll studies presented associations between FDG‐ and TSPO‐PET signals. These findings suggest that microglia, indexed by TSPO binding, negatively impacts brain glucose metabolism indexed by FDG‐PET. Further studies are needed to address associations between TSPO‐PET and FDG‐PET in the asymptomatic and early stages of neurodegenerative disorders.

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