The neuroinflammation marker translocator protein is not elevated in individuals with mild-to-moderate depression: A [11C]PBR28 PET study

•Individuals with mild-to-moderate depression without systemic inflammation do not have neuroinflammation, as measured with PET imaging. Depression is associated with systemic inflammation. In animals, systemic inflammation can induce neuroinflammation and activation of microglia; however, postmorte...

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Published inBrain, behavior, and immunity Vol. 33; pp. 131 - 138
Main Authors Hannestad, Jonas, DellaGioia, Nicole, Gallezot, Jean-Dominique, Lim, Keunpoong, Nabulsi, Nabeel, Esterlis, Irina, Pittman, Brian, Lee, Jae-Yun, O’Connor, Kevin C., Pelletier, Daniel, Carson, Richard E.
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier Inc 01.10.2013
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ISSN0889-1591
1090-2139
DOI10.1016/j.bbi.2013.06.010

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Abstract •Individuals with mild-to-moderate depression without systemic inflammation do not have neuroinflammation, as measured with PET imaging. 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 18kDa (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.
AbstractList •Individuals with mild-to-moderate depression without systemic inflammation do not have neuroinflammation, as measured with PET imaging. 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 18kDa (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.
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 [ 11 C]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 ( V T ) of [ 11 C]PBR28 was used as a measure of total ligand binding. The primary outcome was the difference in V T 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 [ 11 C]PBR28 binding ( V T ) between the two groups. In fact, 7 of 10 individuals with depression had lower [ 11 C]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.
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.
Highlight • Individuals with mild-to-moderate depression without systemic inflammation do not have neuroinflammation, as measured with PET imaging.
Author Esterlis, Irina
Lee, Jae-Yun
Carson, Richard E.
Hannestad, Jonas
O’Connor, Kevin C.
Pittman, Brian
Pelletier, Daniel
DellaGioia, Nicole
Lim, Keunpoong
Nabulsi, Nabeel
Gallezot, Jean-Dominique
AuthorAffiliation a Department of Psychiatry, Yale School of Medicine, New Haven, CT, USA
c Department of Neurology, Program in Human and Translational Immunology, Yale School of Medicine, New Haven, CT, USA
b Department of Diagnostic Radiology, Yale School of Medicine, New Haven, CT, USA
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/23850810$$D View this record in MEDLINE/PubMed
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Elsevier Inc.
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2013 Elsevier Inc. All rights reserved. 2013
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Keywords Depression
Neuroinflammation
Translocator protein 18kDa
PET
Microglia
Translocator protein 18 kDa
Language English
License https://www.elsevier.com/tdm/userlicense/1.0
Copyright © 2013 Elsevier Inc. All rights reserved.
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OpenAccessLink https://www.ncbi.nlm.nih.gov/pmc/articles/3899398
PMID 23850810
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  year: 2013
  text: 2013-10-01
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PublicationTitle Brain, behavior, and immunity
PublicationTitleAlternate Brain Behav Immun
PublicationYear 2013
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Snippet •Individuals with mild-to-moderate depression without systemic inflammation do not have neuroinflammation, as measured with PET imaging. Depression is...
Highlight • Individuals with mild-to-moderate depression without systemic inflammation do not have neuroinflammation, as measured with PET imaging.
Depression is associated with systemic inflammation. In animals, systemic inflammation can induce neuroinflammation and activation of microglia; however,...
SourceID pubmedcentral
pubmed
crossref
elsevier
SourceType Open Access Repository
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Enrichment Source
Publisher
StartPage 131
SubjectTerms Adolescent
Adult
Allergy and Immunology
Biomarkers - metabolism
C-Reactive Protein - metabolism
Carbon Radioisotopes
Case-Control Studies
Depression
Depression - blood
Depression - immunology
Depression - pathology
Female
Genotype
Humans
Magnetic Resonance Imaging
Male
Microglia
Microglia - immunology
Microglia - metabolism
Microglia - pathology
Middle Aged
Neurogenic Inflammation - blood
Neurogenic Inflammation - immunology
Neurogenic Inflammation - pathology
Neuroinflammation
PET
Positron-Emission Tomography - methods
Protein Binding - immunology
Psychiatry
Receptors, GABA - blood
Translocator protein 18 kDa
Young Adult
Title The neuroinflammation marker translocator protein is not elevated in individuals with mild-to-moderate depression: A [11C]PBR28 PET study
URI https://www.clinicalkey.com/#!/content/1-s2.0-S0889159113002341
https://www.clinicalkey.es/playcontent/1-s2.0-S0889159113002341
https://dx.doi.org/10.1016/j.bbi.2013.06.010
https://www.ncbi.nlm.nih.gov/pubmed/23850810
https://pubmed.ncbi.nlm.nih.gov/PMC3899398
Volume 33
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