Cited by 506Neuroinflammation and Neurodegeneration MechanismsPharmacological Receptor Mechanisms and EffectsTraumatic Brain Injury and Neurovascular Disturbances

Translocator protein 18 kDa (TSPO): Molecular sensor of brain injury and repair

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Chen, Ming-Kai, Guilarte, Tomás R.·2008·Pharmacology & Therapeutics

Abstract

For over 15 years, the peripheral benzodiazepine receptor (PBR), recently named translocator protein 18 kDa (TSPO) has been studied as a biomarker of reactive gliosis and inflammation associated with a variety of neuropathological conditions. Early studies documented that in the brain parenchyma, TSPO is exclusively localized in glial cells. Under normal physiological conditions, TSPO levels are low in the brain neuropil but they markedly increase at sites of brain injury and inflammation making it uniquely suited for assessing active gliosis. This research has generated significant efforts from multiple research groups throughout the world to apply TSPO as a marker of "active" brain pathology using in vivo imaging modalities such as Positron Emission Tomography (PET) in experimental animals and humans. Further, in the last few years, there has been an increased interest in understanding the molecular and cellular function(s) of TSPO in glial cells. The latest evidence suggests that TSPO may not only serve as a biomarker of active brain disease but also the use of TSPO-specific ligands may have therapeutic implications in brain injury and repair. This review presents an overview of the history and function of TSPO focusing on studies related to its use as a sensor of active brain disease in experimental animals and in human studies.

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Crossref · 10.1016/j.pharmthera.2007.12.004

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  • TSPO-binding radioligands used to assess neuroinflammation via PET imaging may have value as a biosensor of ongoing disease and may also be a target to reduce inflammation-mediated damage in diseases such as HIV-associated neurological disorders and dementia.

    “Use of TSPO-binding radioligands to assess neuroinflammation via PET imaging indicates that they may have value as a biosensor of ongoing disease and may also be a target to reduce inflammation-mediated damage in diseases such as HIV-associated neurological disorders and dementia ([17] and see [15;18] for review).”

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Authors
Chen, M.-K., & Guilarte, T. R.
Affiliations
Johns Hopkins University (US)
Corresponding author
Guilarte, Tomás R.
Venue
Pharmacology & Therapeutics
Publisher
Elsevier BV
Published
2008-04
Volume
118
Issue
1
Pages
1-17
ISSN
0163-7258 (ISSN-L)
OpenAlex
W2077541192
Cited by
506
References
14
Citations by year
2026: 12 · 2025: 16 · 2024: 19 · 2023: 21 · 2022: 26 · 2021: 33 · 2020: 37 · 2019: 27 · 2018: 40 · 2017: 38 · 2016: 44 · 2015: 51 · 2014: 29 · 2013: 16 · 2012: 30
FWCI
1.89
Type
journal article
Language
en
Open access
Locations
  • Pharmacology & Therapeutics (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
  • FIU - Digital Commons (Florida International University) (submittedVersion)
Funders
  • National Institutes of Health (5r01es007062-24)
  • National Institute of Environmental Health Sciences (T32ES007062, R01-ES007062, ES-07062)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pharmacological Receptor Mechanisms and Effects
  • Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
Keywords
translocator protein (TSPO), TSPO, reactive gliosis, neuroinflammation, brain injury, brain repair, TSPO PET imaging, TSPO ligands, glial cells
MeSH terms
Animals, Brain Injuries, Disease Models, Animal, Gliosis, Humans, Ligands, Gene Expression, Drug Delivery Systems, Receptors, GABA, Positron-Emission Tomography

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