In Vivo TSPO Signal and Neuroinflammation in Alzheimer’s Disease
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 ner...
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doaj-db0dd2149e664e71b0c62ea469be7ec12020-11-25T03:39:21ZengMDPI AGCells2073-44092020-08-0191941194110.3390/cells9091941In Vivo TSPO Signal and Neuroinflammation in Alzheimer’s DiseaseBenjamin B. Tournier0Stergios Tsartsalis1Kelly Ceyzériat2Valentina Garibotto3Philippe Millet4Division of Adult Psychiatry, Department of Psychiatry, University Hospitals of Geneva, 1205 Geneva, SwitzerlandDivision of Adult Psychiatry, Department of Psychiatry, University Hospitals of Geneva, 1205 Geneva, SwitzerlandDivision of Adult Psychiatry, Department of Psychiatry, University Hospitals of Geneva, 1205 Geneva, SwitzerlandDivision of Nuclear Medicine and Molecular Imaging, Diagnostic Department, Geneva University and Geneva University Hospitals, 1205 Geneva, SwitzerlandDivision of Adult Psychiatry, Department of Psychiatry, University Hospitals of Geneva, 1205 Geneva, SwitzerlandIn 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. This review focuses on the key characteristics of TSPO as a biomarker of neuroinflammation in vivo, namely, on the cellular origin of the variations in its expression, on its possible biological/pathological role and on its variations across disease phases.https://www.mdpi.com/2073-4409/9/9/1941TSPOAlzheimer’s diseaseschizophreniaastrocytesmicroglia |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Benjamin B. Tournier Stergios Tsartsalis Kelly Ceyzériat Valentina Garibotto Philippe Millet |
spellingShingle |
Benjamin B. Tournier Stergios Tsartsalis Kelly Ceyzériat Valentina Garibotto Philippe Millet In Vivo TSPO Signal and Neuroinflammation in Alzheimer’s Disease Cells TSPO Alzheimer’s disease schizophrenia astrocytes microglia |
author_facet |
Benjamin B. Tournier Stergios Tsartsalis Kelly Ceyzériat Valentina Garibotto Philippe Millet |
author_sort |
Benjamin B. Tournier |
title |
In Vivo TSPO Signal and Neuroinflammation in Alzheimer’s Disease |
title_short |
In Vivo TSPO Signal and Neuroinflammation in Alzheimer’s Disease |
title_full |
In Vivo TSPO Signal and Neuroinflammation in Alzheimer’s Disease |
title_fullStr |
In Vivo TSPO Signal and Neuroinflammation in Alzheimer’s Disease |
title_full_unstemmed |
In Vivo TSPO Signal and Neuroinflammation in Alzheimer’s Disease |
title_sort |
in vivo tspo signal and neuroinflammation in alzheimer’s disease |
publisher |
MDPI AG |
series |
Cells |
issn |
2073-4409 |
publishDate |
2020-08-01 |
description |
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. This review focuses on the key characteristics of TSPO as a biomarker of neuroinflammation in vivo, namely, on the cellular origin of the variations in its expression, on its possible biological/pathological role and on its variations across disease phases. |
topic |
TSPO Alzheimer’s disease schizophrenia astrocytes microglia |
url |
https://www.mdpi.com/2073-4409/9/9/1941 |
work_keys_str_mv |
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