Evidence map›Paper›PMID 18374421›Full record

ReviewPharmacology & therapeutics2008

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

Ming-Kai Chen, Tomás R Guilarte

Abstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 269 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
269citing papers in PubMed, 1 pooled it
7.7field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

269 citing papers in PubMed, 1 synthesis or guideline pooled it, 493 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Building a database for brain 18 kDa translocator protein imaged using [Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019
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  4. Kinetic modelling of [Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018
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  9. TSPO-PET highlights an atypical mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) phenotype.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Article
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  12. Neuroinflammation demonstrated byAlzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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209 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Ming-Kai ChenNeurotoxicology & Molecular Imaging Laboratory, Department of Environmental Health Sciences, Johns Hopkins University, Bloomberg School of Public Health, Baltimore, Maryland 21205, USA.
Tomás R Guilarte
Johns Hopkins University · US

Funding

ENVIRONMENTAL TOXICOLOGY PRE/POST DOCTORAL RES.TRAININGT32ES007062 · NIEHS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Justin Adam Colacino · 1985 to 2026
$10.5M
TSPO and Neuroinflammation in Alzheimer's DiseaseR01ES007062 · NIEHS · JOHNS HOPKINS UNIVERSITY · PI GUILARTE, TOMAS R · 1995 to 2023
$7.3M
NIEHS NIH HHS ES07062NIEHS NIH HHS R01 ES007062NIEHS NIH HHS T32 ES007062
6 · The paper itself

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.

Indexed as

AnimalsBrain InjuriesDisease Models, AnimalDrug Delivery SystemsGene ExpressionGliosisHumansLigandsPositron-Emission TomographyReceptors, GABALigandsReceptors, GABATSPO protein, human

Identifiers

PMID18374421
PMCPMC2453598
OpenAlexW2077541192

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.