Inflammation and neurological disease-related genes are differentially expressed in depressed patients with mood disorders and correlate with morphometric and functional imaging abnormalities
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Depressed patients show evidence of both proinflammatory changes and neurophysiological abnormalities such as increased amygdala reactivity and volumetric decreases of the hippocampus and ventromedial prefrontal cortex (vmPFC). However, very little is known about the relationship between inflammation and neuroimaging abnormalities in mood disorders. A whole genome expression analysis of peripheral blood mononuclear cells yielded 12 protein-coding genes (ADM, APBB3, CD160, CFD, CITED2, CTSZ, IER5, NFKBIZ, NR4A2, NUCKS1, SERTAD1, TNF) that were differentially expressed between 29 unmedicated depressed patients with a mood disorder (8 bipolar disorder, 21 major depressive disorder) and 24 healthy controls (HCs). Several of these genes have been implicated in neurological disorders and/or apoptosis. Ingenuity Pathway Analysis yielded two genes networks, one centered around TNF with NFKβ, TGFβ, and ERK as connecting hubs, and the second network indicating cell cycle and/or kinase signaling anomalies. fMRI scanning was conducted using a backward-masking task in which subjects were presented with emotionally-valenced faces. Compared with HCs, the depressed subjects displayed a greater hemodynamic response in the right amygdala, left hippocampus, and the ventromedial prefrontal cortex to masked sad versus happy faces. The mRNA levels of several genes were significantly correlated with the hemodynamic response of the amygdala, vmPFC and hippocampus to masked sad versus happy faces. Differentially-expressed transcripts were significantly correlated with thickness of the left subgenual ACC, and volume of the hippocampus and caudate. Our results raise the possibility that molecular-level immune dysfunction can be mapped onto macro-level neuroimaging abnormalities, potentially elucidating a mechanism by which inflammation leads to depression.
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In major depressive disorder, higher peripheral pro-inflammatory cytokines, more inflammation-related gene expression, and less neuroprotective gene expression are associated with greater hippocampal volume loss and medial prefrontal cortex thinning.
“higher levels of peripheral pro-inflammatory cytokines, greater expression of inflammation-related genes, and reduced expression of neuroprotective genes, have all been associated with greater hippocampal volume decline and mPFC thinning in MDD (95–97).”
From The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology (2019) · cites this paper as [97]
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- Authors
- Savitz, J., Frank, M. B., Victor, T., Bebak, M., Marino, J. H., Bellgowan, P. S. F., McKinney, B. A., Bodurka, J., Kent Teague, T., & Drevets, W. C.
- Affiliations
- Laureate Institute for Brain Research (US)
- Oklahoma Medical Research Foundation (US)
- University of Oklahoma (US)
- University of Tulsa (US)
- Corresponding author
- Savitz, Jonathan
- ORCID
- Venue
- Brain, Behavior, and Immunity
- Publisher
- Elsevier BV
- Published
- 2013-07
- Volume
- 31
- Pages
- 161-171
- ISSN
- 0889-1591 (ISSN-L)
- PMC
- PMC3577998
- OpenAlex
- W2012930576
- Cited by
- 146
- References
- 76
- Citations by year
- 2026: 8 · 2025: 6 · 2024: 12 · 2023: 9 · 2022: 11 · 2021: 12 · 2020: 13 · 2019: 13 · 2018: 10 · 2017: 7 · 2016: 14 · 2015: 11 · 2014: 14 · 2013: 5 · 2012: 1
- FWCI
- 3.04
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Brain Behavior and Immunity (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Foundation for the National Institutes of Health
- John D. and Catherine T. MacArthur Foundation
- William K. Warren Foundation
- National Institute for Materials Science
- National Institute of Mental Health (K01MH096077)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- depression, mood disorders, inflammation, gene expression, peripheral blood mononuclear cells, major depressive disorder, bipolar disorder, amygdala, hippocampus, ventromedial prefrontal cortex, subgenual anterior cingulate cortex, caudate nucleus, TNF-α, NF-κB, emotional face processing, neuroinflammation
- MeSH terms
- Adult, Bipolar Disorder, Brain, Depressive Disorder, Emotions, Facial Expression, Female, Humans, Image Processing, Computer-Assisted, Inflammation, Magnetic Resonance Imaging, Male, Middle Aged, Organ Size, Photic Stimulation, Gene Expression Profiling, Functional Neuroimaging
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