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Why are depressed patients inflamed? A reflection on 20 years of research on depression, glucocorticoid resistance and inflammation
Open accessAbstract
Studies over the last 20 years have demonstrated that increased inflammation and hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis are two of the most consistent biological findings in major depression and are often associated: but the molecular and clinical mechanisms underlying these abnormalities are still unclear. These findings are particularly enigmatic, especially considering the accepted notion that high levels of cortisol have an anti-inflammatory action, and therefore the coexistence of inflammation and hypercortisolemia in the same diagnostic group appears counter-intuitive. To celebrate the 2015 Anna-Monika Foundation Award to our laboratory, this review will discuss our own 20 years of research on the clinical and molecular evidence underlying the increased inflammation in depression, especially in the context of a hyperactive HPA axis, and discuss its implications for the pathogenesis and treatment of this disorder.
Overview
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Written from the paper’s full text.
TL;DR
This narrative review reflects on 20 years of the author's laboratory research on why a subgroup of depressed patients shows both increased inflammation and HPA-axis abnormalities, proposing glucocorticoid resistance as the linking mechanism. It argues that inflammation in depression is often a "biological scar" of early-life stress and can be used to predict antidepressant non-response.
Key findings
- Increased inflammation and HPA-axis hyperactivity coexist in depression despite cortisol's expected anti-inflammatory action; the author's in vitro work showed IL-1 induces glucocorticoid resistance (impaired GR translocation), while antidepressants reverse it.
- In the GENDEP sample, depressed patients showed increased mRNA of pro-inflammatory cytokines (IL-1, IL-6, TNF-alpha, MIF) and reduced IL-4, together with reduced GR mRNA and increased FKBP5 — a molecular signature of GR resistance.
- In depressed patients with coronary heart disease, higher IL-6 mRNA and CRP and reduced GR mRNA were found, but associated with HPA-axis hypoactivity rather than hyperactivity.
- Baseline mRNA levels of IL-1, MIF and TNF-alpha predicted roughly half the variance in antidepressant response; in a replication using absolute mRNA values, cut-offs predicted non-response with positive predictive values and specificity of 100%.
- Early-life adversity (childhood maltreatment, and prenatal maternal depression in the South London Child Development Cohort) was associated with raised inflammation markers (CRP, white cell counts, fibrinogen); a randomized controlled trial found prophylactic EPA/DHA prevented or delayed interferon-alpha-induced depression.
Methods
- Design: narrative, self-referential review of the author's own 20 years of research (1991–2017), framed around the 2015 Anna-Monika Foundation Award.
- Evidence base: in vitro models (mouse fibroblasts, human peripheral blood mononuclear cells, human neurons/hippocampal progenitor cells), animal studies, and clinical cohorts including GENDEP, the Dunedin study, and the South London Child Development Cohort, plus an RCT of omega-3 fatty acids.
- Analysis: descriptive synthesis of findings across these studies; no systematic search or meta-analysis is described.
Limitations
- Stated: the review is explicitly self-referential ("the narrative and the citations are self-referential"), and the author lists outstanding unanswered questions, including the epigenetic mechanisms linking early-life events to long-term inflammation, how anti-inflammatories help depression, and whether normalising GR function is helpful for patients.
- Evident from the text: as a single-laboratory narrative review it is not a systematic or exhaustive synthesis, and several cited findings (e.g., the 100% predictive values, preliminary genetic and in utero evidence) are described by the author as preliminary or requiring replication.
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Claims the paper makes
43 Not checked yet · 6 Own interpretation · 1 Partly supported · accuracy not yet measured
In the paper
“these same subjects have glucocorticoid resistance, as shown by a reduced in vitro ability of their peripheral blood mononuclear cells to respond to dexamethasone and cortisol during an immune stimulus (Carvalho et al., 2009).”
§ ANNA-MONIKA > 3. From cells to humans
What the sources say
- Not checked yetcites Carvalho et al., 2009
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Patients with the highest IL-6 levels are also the least likely to respond to antidepressants (Carvalho et al., 2013).”
§ ANNA-MONIKA > 3. From cells to humans
What the sources say
- Not checked yetcites Carvalho et al., 2013 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“In 2008 we described increased plasma cortisol levels and increased inflammation (plasma IL-6) in the same depressed individuals, a group of severely depressed inpatients with treatment-resistant depression (Carvalho et al., 2008)”
§ ANNA-MONIKA > 3. From cells to humans
What the sources say
- Not checked yetcites Carvalho et al., 2008 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“we showed that these same patients also have molecular evidence of GR resistance as shown by a reduced expression of GR mRNA together with an increased expression of the GR chaperone protein, FKBP5 (Cattaneo et al., 2013).”
§ ANNA-MONIKA > 3. From cells to humans
What the sources say
- Not checked yetcites Cattaneo et al., 2013 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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In the paper
“we replicated the increased inflammation in depression as shown by increased mRNA expression of proinflammatory cytokines (IL-1, IL-6, TNF-alpha and macrophage inhibiting factor, MIF) together with a reduced expression of the anti-inflammatory cytokines, IL-4”
§ ANNA-MONIKA > 3. From cells to humans
What the sources say
- Not checked yetcites Cattaneo et al., 2013 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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In the paper
“we were able to demonstrate that p-glycoprotein regulates the effects of antidepressants on GR expression (Yau et al., 2007)”
§ ANNA-MONIKA > 2. Inflammation and the glucocorticoid receptor: love at first sight
What the sources say
- Not checked yetcites Yau et al., 2007 source
boosteddirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“In two studies in healthy volunteers, we were also able to confirm that antidepressants reverse GR resistance, that is, increase GR function as measured by the HPA axis negative feedback (Pariante et al., 2004a) and the effects of cortisol on the EEG (Pariante et al., 2012).”
§ ANNA-MONIKA > 3. From cells to humans
What the sources say
- Not checked yetcites Pariante et al., 2004a
- Not checked yetcites Pariante et al., 2012 source
plaindirectn = 2- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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None of the sources cited for this claim have been checked yet.
In the paper
“We also showed that the detrimental effects of these inflammatory stimuli can be reversed by antidepressant treatments as diverse as inhibitors of the kynurenine pathways, antioxidants and mitochondrial modulators, and omega-3 polyunsaturated fatty acids”
§ ANNA-MONIKA > 4. And from humans to cells
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“an effect that is mediated by an increased production of neurotoxic tryptophan metabolites as well as an increased oxidative stress”
§ ANNA-MONIKA > 4. And from humans to cells
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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In the paper
“we indeed demonstrated that antidepressants not only increase neurogenesis, but do so by activating a downstream cascade of second messenger mechanisms that requires the GR (Anacker et al., 2011).”
§ ANNA-MONIKA > 4. And from humans to cells
What the sources say
- Not checked yetcites Anacker et al., 2011 source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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- It may state two separate claims as one. 19
- Probably not a substantial claim. 1
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“we found that two proinflammatory cytokines, IL-1 and interferon-alpha, reduce human neurogenesis and human neuronal survival”
§ ANNA-MONIKA > 4. And from humans to cells
What the sources say
- Not checked yetcites Alboni et al., 2013
- Not checked yetcites Horowitz et al., 2014
- Partly supportedcites Zunszain et al., 2012 sourceExperimental — accuracy not yet measured
The Results section ('IL-1b Decreases Neuronal Differentiation of Human Hippocampal Progenitor Cells'; page not available) reports that IL-1β reduced neuroblasts and mature neurons in human hippocampal cell cultures, supporting reduced neurogenesis. Our copy does not report an experiment showing that interferon-alpha reduces human neurogenesis or that either cytokine reduces human neuronal survival; the interferon-alpha mention found is in a reference title. (LLM, conf=0.88)
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“we demonstrated that the effects of antidepressants potentiating GR translocation and function is not only directly mediated through steroid-independent activation of the GR, but also indirectly by inhibition of the pglycoprotein transporter that expels cortisol from cells (and, in vivo, from the brain).”
§ ANNA-MONIKA > 2. Inflammation and the glucocorticoid receptor: love at first sight
What the sources say
- Not checked yetcites Pariante et al., 2001
- Not checked yetcites Pariante et al., 2003a
- Not checked yetcites Pariante et al., 2003b
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“we also demonstrated that antidepressants in vitro increase GR activation and function, that is, reverse glucocorticoid resistance, thus confirming the crucial role of the GR as a target of both depressogenic (inflammation) and therapeutic (antidepressants) stimuli (Pariante et al., 1997).”
§ ANNA-MONIKA > 2. Inflammation and the glucocorticoid receptor: love at first sight
What the sources say
- Not checked yetcites Pariante et al., 1997 source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“these effects are common to all tested antidepressants and are present not only in mouse fibroblasts but also in rat neurons”
§ ANNA-MONIKA > 2. Inflammation and the glucocorticoid receptor: love at first sight
What the sources say
- Not checked yetcites Pariante et al., 2001
- Not checked yetcites Pariante et al., 2003a
- Not checked yetcites Pariante et al., 2003b
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“we found that incubating L929 mouse fibroblasts cells with the pro-inflammatory cytokine interleukin (IL)-1 leads to glucocorticoid resistance, i.e., to an impairment of GR activation and translocation from the cytoplasm to the nucleus, resulting in reduced expression of GR-stimulated genes (Pariante et al., 1999).”
§ ANNA-MONIKA > 2. Inflammation and the glucocorticoid receptor: love at first sight
What the sources say
- Not checked yetcites Pariante et al., 1999 source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“but not, however, that pglycoprotein or indeed antidepressants regulate cortisol levels in the brain (Mason et al., 2008(Mason et al., , 2011)).”
§ ANNA-MONIKA > 2. Inflammation and the glucocorticoid receptor: love at first sight
What the sources say
- Not checked yetcites Mason et al., 2008
- Not checked yetcites Mason et al., 2011
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“depressed patients with coronary heart disease have higher inflammation (higher IL-6 mRNA and higher levels of c-reactive protein (CRP), an acute phase response protein produced by the liver in response to IL-6) together with a reduced expression of GR mRNA”
§ ANNA-MONIKA > 3. From cells to humans
What the sources say
- Not checked yetcites Nikkheslat et al., 2015
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“antidepressants increase neurogenesis via a GR-dependent mechanism that requires protein kinase A (PKA) signalling and upregulation of genes such as p11 and the cyclin-dependent kinase-2 (CDK2) inhibitors, p27and p57 (Anacker et al., 2011)”
§ ANNA-MONIKA > 4. And from humans to cells
What the sources say
- Not checked yetcites Anacker et al., 2011 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“both antidepressants and cortisol require the GR to exert their effects on neurogenesis: but with antidepressants activating the GR in order to increase neurogenesis, while cortisol activating the GR in order to decrease neurogenesis.”
§ ANNA-MONIKA > 4. And from humans to cells
What the sources say
- Not checked yetcites Anacker et al., 2011 source
- Not checked yetcites Anacker et al., 2013a
- Not checked yetcites Anacker et al., 2013b
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“we were able to replicate both the antidepressant-induced upregulation of p11 and the cortisol-induced upregulation of SGK1 in the blood (mRNA) of depressed patients, and the cortisolinduced downregulation of TGFβ-SMAD2/3 and Hedgehog signalling in the hippocampus of adult rats exposed to prenatal stress (Anacker et al., 2013a(Anacker et al., , 2013b)).”
§ ANNA-MONIKA > 4. And from humans to cells
What the sources say
- Not checked yetcites Anacker et al., 2013a
- Not checked yetcites Anacker et al., 2013b
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“we showed that this increased inflammation is present not only in subjects who are depressed and have a history of childhood maltreatment but also in those who have experienced maltreatment but are not depressed (Danese et al., 2008)”
§ ANNA-MONIKA > 5. Why are some depressed patients inflamed?
What the sources say
- Not checked yetcites Danese et al., 2008 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In this second cohort, we have confirmed and extended the predictive ability of IL-1 and MIF, and have identified cut-off values for the absolute mRNA measures that accurately predict response probability at an individual level, with positive predictive values and specificity for nonresponders of 100% (Cattaneo et al., 2016).”
§ ANNA-MONIKA > 6. Are these findings clinically relevant?
What the sources say
- Not checked yetcites Cattaneo et al., 2016
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Together, the levels of these three cytokines predict approximately half of the variance in antidepressant response, although IL-1 and MIF explain most of the variance.”
§ ANNA-MONIKA > 6. Are these findings clinically relevant?
What the sources say
- Not checked yetcites Cattaneo et al., 2013 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“in depression, a dysfunction of the GR leads to an impaired HPA axis negative feedback (a phenomenon called glucocorticoid resistance), which in turn leads to the HPA axis hyperactivity (Pariante and Lightman, 2008;Pariante and Miller, 2001).”
§ ANNA-MONIKA > 2. Inflammation and the glucocorticoid receptor: love at first sight
What the sources say
- Not checked yetcites Pariante and Lightman, 2008 source
- Not checked yetcites Pariante and Miller, 2001
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Both these findings indicate the possible molecular signature underlying GR resistance and increased inflammation in depression: a reduced GR expression (that is, less receptor available) together with a decreased GR responsivity (as FKBP5 binds to the GR and maintains it in an unresponsive state).”
§ ANNA-MONIKA > 3. From cells to humans
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These findings confirmed the notion that glucocorticoid resistance, cortisol hypersecretion and increased inflammation are indeed coexistent and related biological abnormalities.”
§ ANNA-MONIKA > 3. From cells to humans
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“This biological picture, perhaps due to the advanced age of the subjects in questions and thus to the long chronicity of their depression, introduces a different type of GR resistance: an ineffective GR together with lower levels of cortisol (Nikkheslat et al., 2015).”
§ ANNA-MONIKA > 3. From cells to humans
What the sources say
- Not checked yetcites Nikkheslat et al., 2015
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Together, these findings indicate that the increased inflammation is a 'biological scar' of the early exposure to high levels of stress, which originates in childhood and is characterised by abnormalities in both mental and physical health (Baumeister et al., 2016).”
§ ANNA-MONIKA > 5. Why are some depressed patients inflamed?
What the sources say
- Not checked yetcites Baumeister et al., 2016 source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“There is consistent evidence from candidate gene studies that genetic variants that increase immune responses are more frequent in patients with depression, or characterise a group of individuals who are at risk of developing a depressive phenotype in the context of an immune challenge (Barnes et al., 2017).”
§ ANNA-MONIKA > 5. Why are some depressed patients inflamed?
What the sources say
- Not checked yetcites Barnes et al., 2017
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The strong impact of the immune system on emotions and behaviour demonstrates that mental health is the health of the whole body.”
§ ANNA-MONIKA > 7. Conclusions
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence. The paper may give no reason why it holds.
The paper relies on this without support.
The molecular and clinical mechanisms underlying the association between increased inflammation and HPA axis hyperactivity in major depression are still unclear.
“the molecular and clinical mechanisms underlying these abnormalities are still unclear.”
The paper relies on this without support.
Not all depressed patients have increased inflammation.
“Not all depressed patients have increased inflammation: so, who are these patients that present with this biological phenotype?”
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?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Abundant evidence supports the role of neuroinflammation and altered immune processes in the aetiopathogeneses of various mental conditions (Mazza, Lucchi, Rossetti, & Clerici, 2020; Pariante, 2017).”
From Can epigenetics shine a light on the biological pathways underlying major mental disorders? (2022) · cites this paper as Pariante, 2017
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“It is important to take into account that some of these processes participate in disease pathogenesis in a parallel manner, such as via the redox system and through the glutamatergic/GABAergic imbalance (Hardingham & Do, 2016); or the immune system and the stress response (Pariante, 2017).”
From Can epigenetics shine a light on the biological pathways underlying major mental disorders? (2022) · cites this paper as Pariante, 2017
In the citing paper
“A group of determinants touched upon by several studies included adverse childhood or early life experiences: ex. conflict with parents, early exposure to traumatic life events, bullying and childhood trauma were found to increase the risk of depression (ex. through pathways, such as inflammation, interaction effects, or cognitive biases) [161,182,258,358,362,380].”
From Biological, Psychological, and Social Determinants of Depression: A Review of Recent Literature (2021) · cites this paper as [182]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ ANNA-MONIKA > 2. Inflammation and the glucocorticoid receptor: love at first sight
“Two subsequent papers demonstrated similar findings in human peripheral blood mononuclear cells (Carvalho et al., 2008(Carvalho et al., , 2010)).”
§ ANNA-MONIKA > References
“Clomipramine in vitro reduces glucocorticoid receptor function in healthy subjects but not in patients with major depression.”
Citations
Cites
The HPA axis in major depression: classical theories and new developments
Pariante, C. M., & Lightman, S. L. (2008) · Trends in Neurosciences · doi:10.1016/j.tins.2008.06.006 · Cited by 2,009
Self-citationChildhood maltreatment predicts adult inflammation in a life-course study
Danese, A., Pariante, C. M., Caspi, A., Taylor, A., & Poulton, R. (2007) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0610362104 · Cited by 1,264 · cited 1×
“…with Avshalom Caspi and Terrie Moffitt on the Dunedin study, we were the first to demonstrate that young adults with a history of childhood trauma show increased inflammation, as demonstrated by increased CRP, increased white blood cell counts and increased fibrinogen levels (Danese et al., 2007).”
Self-citationDanese, A., Moffitt, T. E., Harrington, H., Milne, B. J., Polanczyk, G., Pariante, C. M., Poulton, R., & Caspi, A. (2009) · Archives of Pediatrics & Adolescent Medicine · doi:10.1001/archpediatrics.2009.214 · Cited by 1,165
Self-citationGlucocorticoid receptors in major depression: relevance to pathophysiology and treatment
Pariante, C. M., & Miller, A. H. (2001) · Biological Psychiatry · doi:10.1016/s0006-3223(00)01088-x · Cited by 1,147
Self-citationBaumeister, D., Akhtar, R., Ciufolini, S., Pariante, C. M., & Mondelli, V (2016) · Molecular Psychiatry · doi:10.1038/mp.2015.67 · Cited by 1,084
Self-citationElevated inflammation levels in depressed adults with a history of childhood maltreatment
Danese, A., Moffitt, T. E., Pariante, C. M., Ambler, A., Poulton, R., & Caspi, A. (2008) · Archives of General Psychiatry · doi:10.1001/archpsyc.65.4.409 · Cited by 641 · cited 2×
“In subsequent reports, we showed that this increased inflammation is present not only in subjects who are depressed and have a history of childhood maltreatment but also in those who have experienced maltreatment but are not depressed (Danese et al., 2008); moreover, the increased inflammation clusters with metabolic…”
Self-citationCattaneo, A., Gennarelli, M., Uher, R., Breen, G., Farmer, A., Aitchison, K. J., Craig, I. W., Anacker, C., Zunsztain, P. A., McGuffin, P., et al. (2013) · Neuropsychopharmacology · doi:10.1038/npp.2012.191 · Cited by 436
Self-citationAntidepressants increase human hippocampal neurogenesis by activating the glucocorticoid receptor
Anacker, C., Zunszain, P. A., Cattaneo, A., Carvalho, L. A., Garabedian, M. J., Thuret, S., Price, J., & Pariante, C. M. (2011) · Molecular Psychiatry · doi:10.1038/mp.2011.26 · Cited by 435
Self-citationInterleukin-1β: A New Regulator of the Kynurenine Pathway Affecting Human Hippocampal Neurogenesis
Zunszain, P. A., Anacker, C., Cattaneo, A., Choudhury, S., Musaelyan, K., Myint, A. M., Thuret, S., Price, J., & Pariante, C. M. (2012) · Neuropsychopharmacology · doi:10.1038/npp.2011.277 · Cited by 388
Self-citationGlucocorticoid-Related Molecular Signaling Pathways Regulating Hippocampal Neurogenesis
Anacker, C., Cattaneo, A., Luoni, A., Musaelyan, K., Zunszain, P. A., Milanesi, E., Rybka, J., Berry, A., Cirulli, F., Thuret, S., et al. (2012) · Neuropsychopharmacology · doi:10.1038/npp.2012.253 · Cited by 331
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Items 201–300 of 380
Bottaccioli, A. G., Bologna, M., & Bottaccioli, F. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26062759 · Cited by 15
“The vicious circle between stress, inflammation and depression has also been extensively analyzed in molecular detail over the past 25 years [78,79].”
Nadar, P., Merrill, M. A., Austin, K., Strakowski, S. M., & Halpern, J. M. (2022) · Translational Psychiatry · doi:10.1038/s41398-022-02138-y · Cited by 11
“Animal models and preliminary clinical studies have expanded our understanding of depression from merely an imbalance in serotonin and other monoamines in the central nervous symptoms to include neuroimmune modulation, interruption of the hypothalamic–pituitary–adrenal (HPA) axis, and growth factor dysregulation may a…”
Esalatmanesh, S., Kashani, L., Khooshideh, M., Moghaddam, H. S., Ansari, S., & Akhondzadeh, S. (2023) · Archives of Gynecology and Obstetrics · doi:10.1007/s00404-023-07042-4 · Cited by 12
“A growing body of evidence has demonstrated inflammation plays a role in the pathophysiology of depression [4, 19, 34, 37].”
Wunram, H. L., Oberste, M., Hamacher, S., Neufang, S., Grote, N., Krischer, M., Bloch, W., Schönaü, E., Bender, S., & Fricke, O. (2021) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph18126527 · Cited by 11
“The role of PICs as biomarkers for depression and as response-predictors to antidepressant treatment is particularly interesting in adolescents, where antidepressant treatment is often unsatisfactory [17].”
BackgroundDepression and Anxiety Symptoms Are Associated with Mean Platelet Volume in Autoimmune Disorders
Fábián, B., Horváth, I. F., Shemirani, A. H., & Csiki, Z. (2022) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph191711006 · Cited by 11
Xu, X., Yan, Y., Yang, Z. R., & Zhang, T. (2024) · Journal of Affective Disorders · doi:10.1016/j.jad.2024.08.088 · Cited by 10
Borroni, E., Buoli, M., Nosari, G., Ceresa, A., Fedrizzi, L., Antonangeli, L. M., Monti, P., Bollati, V., Pesatori, A. C., & Carugno, M. (2024) · European Psychiatry · doi:10.1192/j.eurpsy.2024.1767 · Cited by 11
“Finally, air pollution could trigger the activation of the hypothalamic – pituitary – adrenal axis and the release of certain hormones (e.g., cortisol), which characterizes subjects affected by MDD [33].”
BackgroundDixon, R. S., Malave, L. B., Thompson, R., Wu, S. S., Li, Y., Sadik, N., & Anacker, C. (2024) · Neuropsychopharmacology · doi:10.1038/s41386-024-01999-9 · Cited by 12
Łapińska, L., Stachurska, Z., Raczkowski, A., Waszkiewicz, N., Kamiński, K. A., & Kowalska, I. (2022) · Polskie Archiwum Medycyny Wewnętrznej · doi:10.20452/pamw.16261 · Cited by 10
Manosso, L. M., Broseghini, L. D. R., Campos, J. M. B., Padilha, A. P. Z., Botelho, M. E. M., da Costa, M. D. A., Abelaira, H. M., Gonçalves, C. L., & Réus, G. Z. (2022) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2022.09.024 · Cited by 10
Charles, S. J., Farias, M., & Dunbar, R. (2019) · Brain Behavior & Immunity - Health · doi:10.1016/j.bbih.2019.100003 · Cited by 10
Ghaffari, S., Ghobadi, A., Jamshidi, A. H., Mortazavi, S. H., Naderi, S., Aqamolaei, A., Mortezaei, A., Sahebolzamani, E., Shamabadi, A., Jalilvand, S., et al. (2019) · Advances in Integrative Medicine · doi:10.1016/j.aimed.2019.12.002 · Cited by 9
Kong, H., Xu, T., Wang, S., Zhang, Z., Li, M., Qu, S., Li, Q., Gao, P., & Cong, Z. (2023) · International Journal of Biological Macromolecules · doi:10.1016/j.ijbiomac.2023.129067 · Cited by 9
Associations of inflammatory cytokines and cortisol with nonmotor features of Huntington's disease
Bilal, H., McDonald, S. J., Stout, J. C., & Harding, I. H. (2024) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.52016 · Cited by 9
Wang, G., Wu, Y., Chen, A., Hu, L., Wang, Z., Xie, X., He, Q., Xue, Y., Jia, Y., & Zheng, Z. (2025) · Journal of Affective Disorders · doi:10.1016/j.jad.2025.119429 · Cited by 9
Yang, J., Song, G., Zhang, M., Liu, H., & Hou, M. (2025) · BMJ Mental Health · doi:10.1136/bmjment-2025-301749 · Cited by 9
“19 Increased oxidative stress and neuroendocrine imbalances associated with physical decline may further disrupt neurotransmitter systems involved in mood regulation, such as serotonin and dopamine pathways.”
Geng, C., Hao, G., Qiao, Y., Guo, Y., Chen, D., Han, W., Zhang, J., Yang, M., & Jiang, P. (2020) · Prostaglandins & Other Lipid Mediators · doi:10.1016/j.prostaglandins.2020.106464 · Cited by 9
Anxiety in post-covid-19 syndrome – prevalence, mechanisms and treatment
Burkauskas, J., Branchi, I., Pallanti, S., & Domschke, K. (2023) · Neuroscience Applied · doi:10.1016/j.nsa.2023.103932 · Cited by 13
“The interplay between the immune system and the brain has recently emerged as being profoundly implicated in mental disorders (Leboyer et al., 2016; Pariante, 2017).”
Peters, A. T., Jenkins, L. M., Stange, J. P., Bessette, K. L., Skerrett, K. A., Kling, L. R., Welsh, R. C., Milad, M. R., Phan, K. L., & Langenecker, S. A. (2019) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2019.03.007 · Cited by 9
“…that controls reactions to stress and regulates many psychophysiological responses including mood and emotions (Langenecker et al., 2012; Parker et al., 2003; Peters et al., 2016b), the immune system (Brown et al., 2004; Pariante, 2017), and energy storage and expenditure (Young et al., 1998).”
BackgroundGómez-Pérez, L., Cumsille, P., & Román, C. (2020) · Journal of Psychosomatic Research · doi:10.1016/j.jpsychores.2020.110280 · Cited by 9
Dahrendorff, J., Currier, G. W., & Uddin, M. (2024) · American Journal of Medical Genetics Part B Neuropsychiatric Genetics · doi:10.1002/ajmg.b.32985 · Cited by 9
“A large body of literature has characterized the role of inflammatory processes in MDD (reviewed in Beurel et al., 2020; Pariante, 2017).”
Affective scaffolding and chronic illness
Byrne, E. A. (2022) · Philosophical Psychology · doi:10.1080/09515089.2022.2147422 · Cited by 8
“…more widely recognized that some cases of depression are likewise associated with elevated levels of certain inflammatory cytokines by white blood cells in response to stress, which may be suggestive of an inflammatory sub-type of depression (Bullmore, 2018; Harrison et al., 2009; Pariante, 2017).”
BackgroundBorroni, E., Pesatori, A. C., Nosari, G., Monti, P., Ceresa, A., Fedrizzi, L., Bollati, V., Buoli, M., & Carugno, M. (2023) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph20065196 · Cited by 8
“Over-inflammation, in turn, triggers oxidative stress [24] and the activation of the hypothalamus–pituitary–adrenal (HPA) axis and the related hypercortisolemia typical of subjects affected by MDD [25].”
BackgroundWalther, A., Penz, M. S., Ijacic, D., & Rice, T. (2017) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2017.00207 · Cited by 8
“Attenuated responses indicate a dysregulation of the HPA negative feedback and glucocorticoid resistance (40).”
BackgroundKang, H., Bae, K., Kim, S., Shin, I., Kim, H. R., Shin, M., Hong, Y. J., Ahn, Y., Jeong, M. H., Yoon, J., et al. (2018) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2018.10.024 · Cited by 7
Lazzari, D., Bottaccioli, A., & Bottaccioli, F. (2020) · Brain, behavior, and immunity · doi:10.1016/j.bbi.2020.05.036 · Cited by 4
“Depression can be seen as a form of low-grade inflammation (Pariante, 2017) that is particularly active in the brain circuits involved in adaptive behaviour and processing emotional states.”
BackgroundA Brief Historic Review of Research on Early Life Stress and Inflammation across the Lifespan
Entringer, S., & Heim, C. C. (2024) · NeuroImmunoModulation · doi:10.1159/000542676 · Cited by 9
“…effects of cortisol on the HPA axis and down-regulates the production of pro-in fl ammatory cytokines by immune cells – is less sensitive for the effects of cortisol, resulting in HPA axis hyperactivity and higher levels of pro-in fl ammatory cytokines, especially after acute stress exposure [36].”
Constantino, J. L., van Dalfsen, J. H., Massetti, S., Kamphuis, J., & Schoevers, R. A. (2025) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2025.111251 · Cited by 9
Qin, B., Li, Z., Xia, G., Wang, X., & Bai, R. (2025) · Journal of Affective Disorders · doi:10.1016/j.jad.2025.01.122 · Cited by 8
Stress and the gut microbiota-brain axis
Hyder, N., & Raza, M. L. (2025) · Progress in brain research · doi:10.1016/bs.pbr.2025.01.002 · Cited by 7
Influence of gender on cytokine induced depression and treatment
Sarkar, S., Kemper, J., Sarkar, R., Brants, L., Friebe, A., Spengler, U., Schläpfer, T. E., Reimer, J., Buggisch, P., Ockenga, J., et al. (2021) · Journal of Affective Disorders · doi:10.1016/j.jad.2021.05.087 · Cited by 9
Ariza, M., Béjar, J., Barruè, C., Cano, N., Segura, B., NAUTILUS Project Collaborative Group, Bernia, J. A., Arauzo, V., Balagué‐Marmaña, M., Pérez-Pellejero, C., et al. (2024) · European Archives of Psychiatry and Clinical Neuroscience · doi:10.1007/s00406-023-01748-x · Cited by 9
“However, several characteristic markers of people with PCC, such as increased cortisol levels or increased pro-inflammatory factors [5], are associated with depression [89].”
Moving toward affective immunology: Legacy and future directions
Graham‐Engeland, J. E. (2024) · Comprehensive Psychoneuroendocrinology · doi:10.1016/j.cpnec.2024.100241 · Cited by 7
Altered cellular immune reactivity in traumatized women with and without major depressive disorder
Hellmann‐Regen, J., Spitzer, C., Kuehl, L. K., Schultebraucks, K., Otte, C., & Wingenfeld, K. (2018) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2018.10.023 · Cited by 7
“Additionally, GR resistance might reduce the regulatory effects of corticoids on immune cell activity (Pariante, 2017).”
InfluentialProtective effect of Hypericum perforatum on dexamethasone-induced diabetic depression in rats
Elhadidy, M., Salama, A. A., EL-Kassaby, M. I., & Omara, E. (2019) · Journal of The Arab Society for Medical Research · doi:10.4103/jasmr.jasmr_7_19 · Cited by 7
Inflammation predicts sexual arousability in healthy women
Clephane, K., Wilson, M. C., Craig, A. N., Heiman, J. R., & Lorenz, T. K. (2021) · Comprehensive Psychoneuroendocrinology · doi:10.1016/j.cpnec.2021.100086 · Cited by 16
RIPK3-MLKL dependent necroptosis mediates depressive-like behavior by facilitating neuroinflammation
Zheng, H., Xu, Z.-Y., Hu, T., Wu, Y., Huang, C.-W., Li, J., Cao, Z., Wang, W., Jiang, C., & Su, W. (2025) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2025.578643 · Cited by 6
Korthauer, L. E., Goveas, J. S., Rapp, S. R., Espeland, M. A., Shumaker, S. A., Garcia, K. R., Rossom, R. C., García, L., Tindle, H. A., Salmoirago‐Blotcher, E., et al. (2022) · International Journal of Geriatric Psychiatry · doi:10.1002/gps.5817 · Cited by 6
“to a variety of pathological processes that increase risk for cognitive decline, including metabolic syndrome, disrupted endothelial functioning, elevated cytokine levels, neuroinflammation, and oxidative stress.(51) Each of these processes has also been linked to risk for AD(52) and elevated glucocorticoid levels hav…”
Background5E Mental Health? Notes on an emerging style of thought
Rose, N. (2025) · Transcultural Psychiatry · doi:10.1177/13634615251327862 · Cited by 7
Magri, C., Giacopuzzi, E., Sacco, C., Bocchio‐Chiavetto, L., Minelli, A., & Gennarelli, M. (2021) · Scientific Reports · doi:10.1038/s41598-020-80374-2 · Cited by 6
Mechanism of Depression through Brain Function Imaging of Depression Patients and Normal People
Tang, C., Zhang, Y., Zhai, Z., Zhu, X., Wang, C., & Yang, G. (2022) · Journal of Healthcare Engineering · doi:10.1155/2022/1125049 · Cited by 6
RetractedLópez‐Arnau, R., Camarasa, J., Carbó, M., Nadal‐Gratacós, N., Puigseslloses, P., Espinosa‐Velasco, M., Urquizu, E., Escubedo, E., & Pubill, D. (2022) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2022.990405 · Cited by 6
Chen, X., Chen, J., Han, X., Zhao, Y. W., Cao, J., Jiao, X.-Z., Liu, H., Guo, C.-L., Meng, S., Liang, S., et al. (2022) · Chinese Journal of Integrative Medicine · doi:10.1007/s11655-022-3685-6 · Cited by 6
Paganin, W., & Signorini, S. (2024) · Biomarkers in Neuropsychiatry · doi:10.1016/j.bionps.2024.100098 · Cited by 7
Cowell, W., Colicino, E., Lee, A., Enlow, M. B., Flom, J. D., Berin, M. C., Wright, R. O., & Wright, R. J. (2019) · Stress · doi:10.1080/10253890.2019.1686612 · Cited by 6
“depression) to hyper-inflammation in the CNS (Pariante, 2017) have fueled research, largely conducted in murine models, investigating fractalkine signaling in relation to stress and stress-related psychopathologies.”
BackgroundInfluentialChaves, R. D. C., Mallmann, A. S. V., de Oliveira, N. F., Capibaribe, V. C. C., da Silva, D. M. A., Lopes, I. S., Valentim, J. T., Riello, G. B. C., de Carvalho, A. M. R., Fonteles, M. M. D. F., et al. (2020) · Hormones and Behavior · doi:10.1016/j.yhbeh.2020.104758 · Cited by 6
Brambila‐Tapia, A. J. L., Gutiérrez-García, M. M., Ruíz‐Sandoval, J. L., Vázquez-Vázquez, D., Ramírez-Martínez, J. F., Macías-Islas, M. Á., Mireles-Ramírez, M. A., De-Santos-Fonseca, A. D., Chávez, A. P., & Lara, R. M. M. (2020) · EXPLORE · doi:10.1016/j.explore.2020.10.002 · Cited by 6
Choi, W., Stewart, R. J., Kang, H., Kim, J., Kim, H. K., Kang, H., Lee, J., Kim, S., & Kim, J. (2021) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2021.01.029 · Cited by 6
Commentary: Sex Differences in the Peripheral Immune System in Patients with Depression
Breidenstein, J., Przyborowski, C., & Walther, A. (2017) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2017.00145 · Cited by 6
“However, the molecular mechanisms underlying this relationship remain to be further investigated (3, 4).”
BackgroundFiori, V., Lombardo, C., & Ballesio, A. (2025) · Sleep Medicine · doi:10.1016/j.sleep.2025.108735 · Cited by 6
Alhazzaa, O. A., Abahussin, H. M., Majrashi, M. A., Alotaibi, M. S., Alkhrayef, M. N., Alhamdan, Z. A., & Alawad, A. O. (2026) · Frontiers in Aging · doi:10.3389/fragi.2026.1743142 · Cited by 5
“Chronic elevation of cortisol and related hormones leads immune cells to become less sensitive to the anti-inflammatory effects of glucocorticoids, thereby impairing their ability to suppress inflammation (Pariante, 2017).”
Zhang, W., Wang, Y., Wei, Z. C., Chang, G., Luo, Q., Abudusailamu, N., Nurula, M., Tao, S., Li, H., & Chen, Y. (2019) · Springer eBooks · doi:10.1007/978-981-15-0591-1_9 · Cited by 5
Almeida, S. S., Oliveira, M. A., Medeiros, R., Guerra, M. P., Pariante, C. M., & Fernandes, L. P. N. S. (2023) · PLoS ONE · doi:10.1371/journal.pone.0279344 · Cited by 5
Self-citationSun, Y., Zhao, H., Chang, M., Yue, T., Yuan, Y., & Shi, Y. (2024) · Journal of the Science of Food and Agriculture · doi:10.1002/jsfa.13825 · Cited by 5
The Relationship between Low Carbohydrate Diet Score and Mental Health in Overweight and Obese Women
Yarizadeh, H., Setayesh, L., Askarpour, M., Keshavarz, S. A., & Mirzaei, K. (2020) · Qom Univ Med Sci J · doi:10.29252/qums.14.2.47 · Cited by 5
Bottaccioli, F., Bottaccioli, A., Marzola, E., Longo, P., Minelli, A., & Abbate-Daga, G. (2021) · Endocrines · doi:10.3390/endocrines2030022 · Cited by 6
“Immunopsychiatry is an emerging research area investigating immune dysregulation in the pathogenesis of mental disorders, with specific regard to depression [24,25].”
BackgroundUse of Extracellular Monomeric Ubiquitin as a Therapeutic Option for Major Depressive Disorder
Maldonado-García, J. L., García-Mena, L. H., Cabrera, D. M., Pérez‐Sánchez, G., Becerril‐Villanueva, E., Álvarez-Herrera, S., Homberg, T. A., Vallejo‐Castillo, L., Pérez‐Tapia, S. M., Moreno-Lafont, M. C., et al. (2024) · Pharmaceuticals · doi:10.3390/ph17070841 · Cited by 5
Effects of hydrocortisone and yohimbine on selective attention to emotional cues
Metz, S., Chae, W. R., Deuter, C. E., Otte, C., & Wingenfeld, K. (2021) · Journal of Psychopharmacology · doi:10.1177/0269881121997100 · Cited by 6
“As there are no studies investigating these effects on sad stimuli and depression is primarily associated with glucocorticoid resistance (Pariante, 2017) and an attentional bias to sad faces (Dai et al., 2016), an attentional bias to sad faces in association with HPA axis and SNS activation is…”
BackgroundCárdenas-Cloud, E., Brambila‐Tapia, A. J. L., Lara, R. M. M., Pérez-Vázquez, F., Chavarría-Ávila, E., Romero-Abundis, F. J., & Mercado, M. V.-D. (2021) · Reumatismo · doi:10.4081/reumatismo.2021.1400 · Cited by 5
Pathogenicity of Endocrine Dysregulation in AutismPreprint
Swierczynski, A. (2018) · Preprints.org · doi:10.20944/preprints201805.0359.v1 · Cited by 4
“In humans, women who were depressed while pregnant subsequently gave birth to children with increased inflammation persisting into early adulthood [187].”
BackgroundLin, W., Wang, Q., Liu, J., & Tan, Q. (2025) · International Journal of Women s Health · doi:10.2147/ijwh.s500846 · Cited by 4
“22,23 Therefore, maintaining a positive and stable emotional state in patients may be a crucial part of disease control.”
Zhang, J., Liu, Y., & Zhao, K. (2026) · Behavioural Brain Research · doi:10.1016/j.bbr.2026.116268 · Cited by 5
Bidirectional mechanism of comorbidity of depression and insomnia based on synaptic plasticity.
Meng, F., & Wang, L. (2023) · PubMed Central · doi:10.11817/j.issn.1672-7347.2023.230082 · Cited by 5
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Yamalı, C., Nenni, M., Sakarya, M. T., & Kaplan, H. A. (2024) · Mini-Reviews in Medicinal Chemistry · doi:10.2174/0113895575319878240612070850 · Cited by 4
The Potential of Biophilic Design and Nature to Improve Health, Creativity and Well-Being
Sjövall, I. A. K., & Spiers, H. J. (2024) · Springer eBooks · doi:10.1007/978-3-031-64699-7_11 · Cited by 5
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Zhu, W., Chang, J.-L., Tian, L., Yang, X., & Li, W.-F. (2025) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.70394 · Cited by 5
“Furthermore, elevated CORT levels can activate neuroinflammatory pathways, exacerbate synaptic pruning, and impair cognitive functions, which are commonly observed in individuals with depression [41, 42].”
Peters, A. T., Smith, R. A., Kassel, M. T., Hagan, M. J., Maki, P. M., Meter, A. V., Briceño, E. M., Ryan, K. A., Weldon, A. L., Weisenbach, S. L., et al. (2018) · Journal of Affective Disorders · doi:10.1016/j.jad.2018.07.006 · Cited by 4
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Depression and Inflammation: Is There any Role for Biomarkers?
Akhondzadeh, S. (2019) · Europe PMC (PubMed Central) · Cited by 4
Inflammation, Sickness Behaviour and Depression
Khandaker, G. M., Colasanti, A., & Harrison, N. A. (2021) · Cambridge University Press eBooks · doi:10.1017/9781108539623.008 · Cited by 5
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Celecoxib in Treatment of Postpartum Depression: A Case Report
Esalatmanesh, S., Kashani, L., & Akhondzadeh, S. (2023) · Archives of Iranian Medicine · doi:10.34172/aim.2023.42 · Cited by 4
“13 Depression is associated with an increase in inflammation and hyperactivity of the hypothalamic-pituitary-adrenocortical (HPA) axis 14 and inflammatory disease is related to depression.”
BackgroundPromoting the Resilience of the Italian Population Against SARS-CoV-2
Bottaccioli, A. G., Lazzari, D., & Bottaccioli, F. (2021) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2020.560017 · Cited by 4
“Depression, in these cases, can, therefore, be seen as a form of low-grade inflammation (57) particularly active in brain circuits involved in adaptive behavior and emotional state processing (limbic and prefrontal cortex); this leads to a pathological condition that, in its chronicization, is continuously fed by inad…”
BackgroundCan some microbes promote host stress and benefit evolutionarily from this strategy?
Aktipis, A., & Beltrán, D. G. (2020) · BioEssays · doi:10.1002/bies.202000188 · Cited by 4
“One way that hosts can respond to chronic stress is to blunt the stress response – reducing glucose levels in the blood,[58] down-regulating glucocorticoid receptors[59] and muting the cardiovascular response to stress.”
BackgroundScience and fashion: inflammation and oxidative stress in psychiatry
Arango, C. (2018) · European Archives of Psychiatry and Clinical Neuroscience · doi:10.1007/s00406-018-0871-9 · Cited by 4
Dahrendorff, J., Pages, K. P., Currier, G. W., Sarker, M. H., Graham, Z., Louis‐Jacques, A. F., Dagne, G. A., & Uddin, M. (2025) · BMC Medical Genomics · doi:10.1186/s12920-025-02240-2 · Cited by 3
“…response model comparing responders and non-responders to TMS treatment, we identified a total 67 significant DMRs that occur in genes belonging to pathways previously implicated in MDD [34] and TRD [69] including DMRs involved with the regulation of monoamines [70] and inflammation [71, 72].”
Genetics and Neurobiology of Treatment-Resistant Depression—A Review
Płaza, O., Gałecki, P., Bliźniewska-Kowalska, K. M., Gałecka, M., Brońska, A., Jornet-Plaza, J., Szurek, A., & Szulc, A. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms262211016 · Cited by 7
“Additionally, inflammatory proteins increase glucocorticoid receptor resistance and impair feedback inhibition within the HPA axis, thus leading to a continuous state of hypercortisolemia that is linked to hippocampal atrophy and emotional dysregulation [84–86].”
Santoni, M., Mastio, A., Concas, L., Mostallino, R., Herres, A., Sagheddu, C., Castelli, M. P., Frau, R., Muntoni, A. L., & Pistis, M. (2026) · Translational Psychiatry · doi:10.1038/s41398-026-03926-6 · Cited by 3
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The Philosophical and Scientific Basis for the Integration of Medicine and Psychology
Bottaccioli, F., & Bottaccioli, A. G. (2024) · Integrated science · doi:10.1007/978-3-031-73061-0_3 · Cited by 4
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“Increased inflammation has been demonstrated in a subset of patients with a “neurodevelopmentally-based” form of depression, originating from early exposure to stress.(10,13) It is widely shared that stress can increase the risk of depression.”
BackgroundMerolla, A., LORENZO, R. D., L., P. G., Critelli, S., Palladini, M., Damanti, S., Vitali, G., Canti, V., Cilla, M., Martinenghi, S., et al. (2024) · International Clinical Psychopharmacology · doi:10.1097/yic.0000000000000537 · Cited by 3
“Similarly, an unsynchronized and exaggerated production of inflammatory mediators including interleukin (IL)-1, IL-6 and tumor necrosis factor α is involved in the pathogenesis of major depression (Pariante, 2017; Müller, 2013).”
BackgroundLow-grade inflammation and serotonin 4 receptor binding in the healthy and the depressed brain
Clausen, M. R., Larsen, S. V., Høgsted, E. S., Nasser, A., Svarer, C., Knudsen, G. M., & Frøkjær, V. G. (2024) · Neuroscience Applied · doi:10.1016/j.nsa.2024.104078 · Cited by 3
“Over the last two decades, the role of inflammation in the etiology of MDD has been extensively investigated and emphasized (Verduijn et al., 2015; Wium-Andersen et al., 2013; Pariante, 2017).”
Murata, S., Murphy, M. L. M., Khanna, R., Hoppensteadt, D., Fareed, J., & Halaris, A. E. (2021) · Journal of Affective Disorders Reports · doi:10.1016/j.jadr.2021.100117 · Cited by 3
Paradoxos de Retroalimentação da Pandemia da Covid-19: quebrando o ciclo
Sartório, C. L., Juíz, P. J. L., Rodrigues, L. C. D. M., & da Silva, A. M. Á. (2020) · Cadernos de Prospecção · doi:10.9771/cp.v13i2.36157 · Cited by 5
Adolescent depression, childhood maltreatment, and the immune system; a role for epigenetic aging?
Tollenaar, M. S., Creasey, N., Wever, M. C. M., Knipping, K., Garssen, J., van Houtum, L. A. E. M., Wentholt, W. G. M., Janssen, L. H. C., Lax, E., & Elzinga, B. M. (2025) · Brain Behavior & Immunity - Health · doi:10.1016/j.bbih.2025.101080 · Cited by 2
“It is thought that these somatic health issues may be due to chronic low-grade inflammation, which has often been found in individuals with depression (Dantzer, 2012; Lamers et al., 2019; Lindqvist et al., 2017; Pariante, 2017).”
Yang, Z., Zhang, J., Zhao, Z., & Zhang, N. (2026) · Journal of Affective Disorders · doi:10.1016/j.jad.2026.121176 · Cited by 3
Microglia associated research in depression: an exploratory trends analysis
Chen, Y.-J., Zhu, Q.-Q., Xie, M.-R., Zhang, D., SHUAI, Y.-F., Li, Y. H., Zhang, N., He, W., Liao, Y., Zeng, Q.-J., et al. (2026) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2026.1757943 · Cited by 3
“Studies suggest a vicious cycle in depression involving “stress–HPA axis activation–microglia–mediated neuroinflamma-tion-depression” (Pariante, 2017).”
Inflammation in treatment-resistant depression: From mechanisms to therapeutics
Wu, S., Gao, X., Zhou, Y., Lin, Z., Chen, C. H., Luo, J., Liu, X., Lin, L., 邵红伟, & Liu, S. (2026) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2026.111953 · Cited by 3
Literature Review: Immune System and Its Relation to Depression
Evilia, W., Wahyuni, A. A. S., & Aryani, L. N. A. (2021) · Jurnal Psikiatri Surabaya · doi:10.20473/jps.v10i2.28416 · Cited by 5
Lombardo, G., Belcastro, S., Mondelli, V., & Gianotti, L. (2023) · L Endocrinologo · doi:10.1007/s40619-023-01379-3 · Cited by 4
Li, K., You, L., Zhen, J., Huang, G., Wang, T., Cai, Y., Zhang, Y., & Xu, A. (2023) · Journal of Traditional Chinese Medical Sciences · doi:10.1016/j.jtcms.2023.12.001 · Cited by 2
Zhang, Y., Xia, M., Song, W., Li, D., Wei, X., & Wang, D. (2024) · Journal of Innovative Optical Health Sciences · doi:10.1142/s1793545825500087 · Cited by 2
Immune links in comorbid depression and psoriasis: A narrative mini-review and perspective
Lada, G. (2025) · Brain Behavior & Immunity - Health · doi:10.1016/j.bbih.2025.100949 · Cited by 2
Chen, Y.-L., Huang, J., Chen, X., & Zheng, R. (2025) · Medicine · doi:10.1097/md.0000000000045557 · Cited by 2
“[8] Third, stress-induced alterations in deiodinase activity modified local thyroid hormone metabolism, potentially predisposing to cystic changes.”
The Antidepressants and the Metabolic Syndrome
Kolcsár, M., Gáll, Z., Bába, L.-I., & Zoltán, K. I. (2018) · Orvostudományi Értesítö · doi:10.2478/orvtudert-2018-0009 · Cited by 2
Metadata
- Authors
- Pariante, C. M.
- Affiliations
- King's College London (GB)
- Corresponding author
- Pariante, Carmine M.
- ORCID
- Pariante, Carmine M.
- Venue
- European Neuropsychopharmacology
- Publisher
- Elsevier BV
- Published
- 2017-06
- Volume
- 27
- Issue
- 6
- Pages
- 554-559
- ISSN
- 0924-977X (ISSN-L)
- OpenAlex
- W2611710834
- Cited by
- 382
- References
- 50
- Citations by year
- 2026: 29 · 2025: 31 · 2024: 56 · 2023: 32 · 2022: 40 · 2021: 44 · 2020: 59 · 2019: 43 · 2018: 39 · 2017: 9
- FWCI
- 3.63
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- European Neuropsychopharmacology (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Research Portal (King's College London) (publishedVersion, cc-by-nc-nd)
- Funders
- mmunopsychiatry (MR/L014815/1)
- Medical Research Council (MR/J002739/1)
- National Institute for Health Research Mental Health Biomedical Research Centre
- Maudsley NHS Foundation Trust
- King׳s College London
- Wellcome Trust Consortium
- NARSAD
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
- Keywords
- major depressive disorder, inflammation, glucocorticoid resistance, hypothalamic-pituitary-adrenal axis, hypercortisolism, cortisol, depression pathogenesis, depression treatment
- MeSH terms
- Anti-Inflammatory Agents, Depression, Glucocorticoids, Humans, Hydrocortisone, Hypothalamo-Hypophyseal System, Inflammation, Metabolism, Inborn Errors, Pituitary-Adrenal System, Receptors, Glucocorticoid, Time Factors, Inflammation Mediators, Biomedical Research
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