Evidence map›Paper›PMID 25345894›Full record

ReviewBrain pathology (Zurich, Switzerland)2014

The 18 kDa translocator protein, microglia and neuroinflammation.

Guo-Jun Liu, Ryan J Middleton, Claire R Hatty, Winnie Wai-Ying Kam, Ronald Chan, Tien Pham, Meredith Harrison-Brown, Eoin Dodson, Kelly Veale, Richard B Banati

Open access · hybridAbstract readReview
In one paragraph

Review in Brain pathology (Zurich, Switzerland), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers.

0numbers the graph read from it
0cells of the map it votes in
120citing papers in PubMed
14.5field-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

120 citing papers in PubMed, 205 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. In vivo translocator protein in females with autism spectrum disorder: a pilot study.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    Article
  8. Observational
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

60 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

10 authors at 2 institutions in 1 country.

Guo-Jun LiuLife Sciences, Australian Nuclear Science and Technology Organisation, NSW, Australia; Brain & Mind Research Institute, The University of Sydney, NSW, Australia; Discipline of Medical Imaging & Radiation Sciences, Faculty of Health Sciences, The University of Sydney, NSW, Australia.
Ryan J Middleton
Claire R Hatty
Winnie Wai-Ying Kam
Ronald Chan
Tien Pham
Meredith Harrison-Brown
Eoin Dodson
Kelly Veale
Richard B Banati
Australian Nuclear Science and Technology Organisation · AUUniversity of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The 18 kDa translocator protein (TSPO), previously known as the peripheral benzodiazepine receptor, is expressed in the injured brain. It has become known as an imaging marker of "neuroinflammation" indicating active disease, and is best interpreted as a nondiagnostic biomarker and disease staging tool that refers to histopathology rather than disease etiology. The therapeutic potential of TSPO as a drug target is mostly based on the understanding that it is an outer mitochondrial membrane protein required for the translocation of cholesterol, which thus regulates the rate of steroid synthesis. This pivotal role together with the evolutionary conservation of TSPO has underpinned the belief that any loss or mutation of TSPO should be associated with significant physiological deficits or be outright incompatible with life. However, against prediction, full Tspo knockout mice are viable and across their lifespan do not show the phenotype expected if cholesterol transport and steroid synthesis were significantly impaired. Thus, the "translocation" function of TSPO remains to be better substantiated. Here, we discuss the literature before and after the introduction of the new nomenclature for TSPO and review some of the newer findings. In light of the controversy surrounding the function of TSPO, we emphasize the continued importance of identifying compounds with confirmed selectivity and suggest that TSPO expression is analyzed within specific disease contexts rather than merely equated with the reified concept of "neuroinflammation."

Indexed as

AnimalsBrainHumansInflammationMicrogliaNeuroimmunomodulationReceptors, GABAReceptors, GABATSPO protein, humanmicroglianeuroinflammationPBR111PETPK11195TSPO

Identifiers

PMID25345894
PMCPMC8029074
OpenAlexW1574200406

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.