The neuroinflammation marker translocator protein is not elevated in individuals with mild-to-moderate depression: A [11C]PBR28 PET study
Open accessAbstract
Depression is associated with systemic inflammation. In animals, systemic inflammation can induce neuroinflammation and activation of microglia; however, postmortem studies have not convincingly shown that there is neuroinflammation in depression. The purpose of this study was to use positron emission tomography (PET) with [¹¹C]PBR28, which binds to the neuroinflammation marker translocator protein 18 kDa (TSPO), to compare the level of TSPO between individuals with depression and control subjects. Ten individuals who were in an acute episode of major depression and 10 control subjects matched for TSPO genotype and other characteristics had a PET scan with arterial input function to quantify levels of TSPO in brain regions of interest (ROIs). Total volume of distribution (VT) of [¹¹C]PBR28 was used as a measure of total ligand binding. The primary outcome was the difference in VT between the two groups; this was assessed using a linear mixed model with group as a between-subject factor and region as a within-subject factor. There was no statistically significant difference in [¹¹C]PBR28 binding (VT) between the two groups. In fact, 7 of 10 individuals with depression had lower [¹¹C]PBR28 binding in all ROIs compared to their respective genotype-matched control subjects. Future studies are needed to determine whether individuals with mild-to-moderate depression have lower TSPO levels and to assess whether individuals with severe depression and/or with elevated levels of systemic inflammation might have higher TSPO levels than control subjects.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Not all studies have revealed increased TSPO binding in patients with depression, possibly owing to effects of medication and/or a paucity of subjects with increased inflammation.
“not all studies have revealed increased TSPO binding in patients with depression, possibly owing to effects of medication and/or a paucity of subjects with increased inflammation61,62.”
From The role of inflammation in depression: from evolutionary imperative to modern treatment target (2016) · cites this paper as [62]
The Discussion reports no significant increase in TSPO binding in the study’s mild-to-moderately depressed group and says people with elevated inflammation were excluded; it raises the possibility that such people might have higher binding. The Results note that two participants took antidepressants, but the paper does not identify medication effects as a possible explanation for its null finding. (LLM, conf=0.86)
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 58 · Cited by 204
- Authors
- Hannestad, J., DellaGioia, N., Gallezot, J.-D., Lim, K., Nabulsi, N., Esterlis, I., Pittman, B., Lee, J.-Y., O’Connor, K. C., Pelletier, D., & Carson, R. E.
- Affiliations
- Yale University (US)
- Corresponding author
- Hannestad, Jonas
- ORCID
- Venue
- Brain, Behavior, and Immunity
- Publisher
- Elsevier BV
- Published
- 2013-10
- Volume
- 33
- Pages
- 131-138
- ISSN
- 0889-1591 (ISSN-L)
- PMC
- PMC3899398
- OpenAlex
- W1989435867
- Cited by
- 204
- References
- 58
- Citations by year
- 2026: 4 · 2025: 9 · 2024: 5 · 2023: 4 · 2022: 9 · 2021: 42 · 2020: 20 · 2019: 17 · 2018: 23 · 2017: 26 · 2016: 13 · 2015: 18 · 2014: 12 · 2013: 1
- FWCI
- 4.96
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Brain Behavior and Immunity (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Mental Health (K01MH092681)
- National Institute on Drug Abuse (K12 DA00167, K12DA000167)
- National Center for Research Resources (UL1RR024139)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Keywords
- depression, neuroinflammation, translocator protein (TSPO), TSPO, [11C]PBR28, microglial activation, systemic inflammation, major depressive disorder, volume of distribution, arterial input function
- MeSH terms
- Adolescent, Adult, C-Reactive Protein, Carbon Radioisotopes, Depression, Female, Genotype, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Protein Binding, Biomarkers, Case-Control Studies, Microglia, Receptors, GABA, Neurogenic Inflammation, Positron-Emission Tomography, Young Adult
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
