54 Chapter 2 interpretation of increased TSPO PET signal also may reflect differences in relative abundance of microglia and astrocytes. Based on this and our previous work, we raise the possibility that a successful therapeutic intervention, which modulates the microglia from proinflammatory to neuroprotective or homeostatic phenotypes, might potentially have no effect on the TSPO PET signal, although interventions that reduce the density of activated glial cells may. Understanding the cellular neuropathology of TSPO expression quantitatively is a fundamental step in the evaluation of TSPO as a potential therapeutic target. Acknowledgements The authors thank the UK MS society for financial support (grant number: C008-16.1). PMM acknowledges generous support from Edmond J Safra Foundation and Lily Safra, the NIHR Investigator programme and the UK Dementia Research Institute. PMM and DRJO thank the Imperial College Healthcare Trust-NIHR Biomedical Research Centre for infrastructure support and the Medical Research Council for support of TSPO studies.
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