cells Review In Vivo TSPO Signal and Neuroinflammation in Alzheimer’s Disease Benjamin B. Tournier 1,2,* , Stergios Tsartsalis 1 , Kelly Ceyzériat 1,3,4 , Valentina Garibotto 3 and Philippe Millet 1,2 1 Division of Adult Psychiatry, Department of Psychiatry, University Hospitals of Geneva, 1205 Geneva, Switzerland;
[email protected] (S.T.);
[email protected] (K.C.);
[email protected] (P.M.) 2 Department of Psychiatry, University of Geneva, 1211 Geneva, Switzerland 3 Division of Nuclear Medicine and Molecular Imaging, Diagnostic Department, Geneva University and Geneva University Hospitals, 1205 Geneva, Switzerland;
[email protected] 4 Division of Radiation Oncology, Department of Oncology, University Hospitals of Geneva, 1205 Geneva, Switzerland * Correspondence:
[email protected]; Tel.: +41-22-305-5379 Received: 21 July 2020; Accepted: 18 August 2020; Published: 21 August 2020 Abstract: In the last decade, positron emission tomography (PET) and single-photon emission computed tomography (SPECT) in in vivo imaging has attempted to demonstrate the presence of neuroinflammatory reactions by measuring the 18 kDa translocator protein (TSPO) expression in many diseases of the central nervous system. We focus on two pathological conditions for which neuropathological studies have shown the presence of neuroinflammation, which translates in opposite in vivo expression of TSPO. Alzheimer’s disease has been the most widely assessed with more than forty preclinical and clinical studies, showing overall that TSPO is upregulated in this condition, despite differences in the topography of this increase, its time-course and the associated cell types. In the case of schizophrenia, a reduction of TSPO has instead been observed, though the evidence remains scarce and contradictory.