Evidence map›Paper›PMID 29203847›Full record

ReviewMolecular psychiatry2018

Reconceptualization of translocator protein as a biomarker of neuroinflammation in psychiatry.

T Notter, J M Coughlin, A Sawa, U Meyer

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

89 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Development and evaluation of [European journal of nuclear medicine and molecular imaging · 2025
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. In vivo translocator protein in females with autism spectrum disorder: a pilot study.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    Article
  11. Impact of repeated blast exposure on active-duty United States Special Operations Forces.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  12. Article
  13. Nicotinic regulation of microglia: potential contributions to addiction.Journal of neural transmission (Vienna, Austria : 1996) · 2024
    Review
  14. Article
  15. Microglia-neuron interactions in schizophrenia.Frontiers in cellular neuroscience · 2024
    Review
  16. Article
  17. Article
  18. Article
  19. Molecular Imaging of Pulmonary Inflammation in Users of Electronic and Combustible Cigarettes: A Pilot Study.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2023
    Article
  20. Review

29 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

4 authors.

T NotterInstitute of Pharmacology and Toxicology, University of Zurich-Vetsuisse, Zurich, Switzerland.
J M CoughlinDepartment of Psychiatry and Behavioral Sciences, Johns Hopkins Medical Institutions, Baltimore, MD, USA.
A SawaDepartment of Psychiatry and Behavioral Sciences, Johns Hopkins Medical Institutions, Baltimore, MD, USA.
U MeyerInstitute of Pharmacology and Toxicology, University of Zurich-Vetsuisse, Zurich, Switzerland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A great deal of interest in psychiatric research is currently centered upon the pathogenic role of inflammatory processes. Positron emission tomography (PET) using radiolabeled ligands selective for the 18 kDa translocator protein (TSPO) has become the most widely used technique to assess putative neuroimmune abnormalities in vivo. Originally used to detect discrete neurotoxic damages, TSPO has generally turned into a biomarker of 'neuroinflammation' or 'microglial activation'. Psychiatric research has mostly accepted these denotations of TSPO, even if they may be inadequate and misleading under many pathological conditions. A reliable and neurobiologically meaningful diagnosis of 'neuroinflammation' or 'microglial activation' is unlikely to be achieved by the sole use of TSPO PET imaging. It is also very likely that the pathological meanings of altered TSPO binding or expression are disease-specific, and therefore, not easily generalizable across different neuropathologies or inflammatory conditions. This difficulty is intricately linked to the varying (and still ill-defined) physiological functions and cellular expression patterns of TSPO in health and disease. While altered TSPO binding or expression may indeed mirror ongoing neuroinflammatory processes in some cases, it may reflect other pathophysiological processes such as abnormalities in cell metabolism, energy production and oxidative stress in others. Hence, the increasing popularity of TSPO PET imaging has paradoxically introduced substantial uncertainty regarding the nature and meaning of neuroinflammatory processes and microglial activation in psychiatry, and likely in other neuropathological conditions as well. The ambiguity of conceiving TSPO simply as a biomarker of 'neuroinflammation' or 'microglial activation' calls for alternative interpretations and complimentary approaches. Without the latter, the ongoing scientific efforts and excitement surrounding the role of the neuroimmune system in psychiatry may not turn into therapeutic hope for affected individuals.

Indexed as

AnimalsBiomarkersEncephalitisHumansMental DisordersModels, MolecularPositron-Emission TomographyReceptors, GABABiomarkersReceptors, GABATSPO protein, human

Identifiers

PMID29203847

What OpenQuestion holds

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Registered trials

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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.