The DOI matches its Crossref record; 148 of the 151 references it cites were found in a registry or an index; none of the 199 sources its claims cite is checked for support yet.
The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology
Open accessAbstract
Volumetric reductions in the hippocampus and medial prefrontal cortex (mPFC) are among the most well-documented neural abnormalities in major depressive disorder (MDD). Hippocampal and mPFC structural reductions have been specifically tied to MDD illness progression markers, including greater number of major depressive episodes (MDEs), longer illness duration, and nonremission/treatment resistance. Chronic stress plays a critical role in the development of hippocampal and mPFC deficits, with some studies suggesting that these deficits occur irrespective of MDE occurrence. However, preclinical and human research also points to other stress-mediated neurotoxic processes, including enhanced inflammation and neurotransmitter disturbances, which may require the presence of an MDE and contribute to further brain structural decline as the illness advances. Specifically, hypothalamic-pituitary-adrenal axis dysfunction, enhanced inflammation and oxidative stress, and neurotransmitter abnormalities (e.g., serotonin, glutamate, gamma-aminobutyric acid) likely interact to facilitate illness progression in MDD. Congruent with stress sensitization models of MDD, with each consecutive MDE it may take lower levels of stress to trigger these neurotoxic pathways, leading to more pronounced brain volumetric reductions. Given that stress and MDD have overlapping and distinct influences on neurobiological pathways implicated in hippocampal and mPFC structural decline, further work is needed to clarify which precise mechanisms ultimately contribute to MDD development and maintenance.
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In the paper
“With respect to mPFC volume reductions, small to large effect sizes have been reported (Figure 2).”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Hippocampus and mPFC volume reductions: Cause versus consequence of MDD?
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“each successive episode carries a 10–20% risk of failing to remit with current therapeutic approaches (1).”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Abstract
What the sources say
- Not checked yetcites [1] Monroe, 2011, Recurrence in major depression: A conceptual analysis, Psychol Rev source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Major depressive disorder (MDD) is frequently a chronic, progressive illness.”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Abstract
What the sources say
- Not checked yetcites [1] Monroe, 2011, Recurrence in major depression: A conceptual analysis, Psychol Rev source
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In the paper
“Additionally, these estimates are likely impacted by antidepressant use and presence of other psychiatric comorbidities, given that they were not exclusionary in most studies.”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Hippocampus and mPFC volume reductions: Cause versus consequence of MDD?
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In the paper
“These meta-analyses have reported moderate effect sizes for reduced hippocampal volume in MDD (Cohen’s d range = −0.41 to −0.47; 6,8,9).”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Hippocampus and mPFC volume reductions: Cause versus consequence of MDD?
What the sources say
- Not checked yetcites [6] Koolschijn, 2009, Brain volume abnormalities in major depressive disorder: A meta-analysis of magnetic resonance imaging studies, Hum Brain Mapp source
- Not checked yetcites [8] Kempton, 2011, Structural neuroimaging studies in major depressive disorder, Arch Gen Psychiatry source
- Not checked yetcites [9] Arnone, 2012, Magnetic resonance imaging studies in unipolar depression: Systematic review and meta-regression analyses, Eur Neuropsychopharmacol source
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In the paper
“several meta-analyses have demonstrated that, relative to healthy controls (HCs), individuals with MDD show reduced hippocampus and mPFC volumes, including dorsal and ventral mPFC portions (dmPFC/vmPFC) extending into the medial orbital frontal cortex (mOFC) as well as dorsal and rostral portions of the anterior cingulate cortex (rACC/dACC) (2,4–14).”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Hippocampus and mPFC volume reductions: Cause versus consequence of MDD?
What the sources say
- Not checked yetcites [2] McKinnon, 2009, A meta-analysis examining clinical predictors of hippocampal volume in patients with major depressive disorder, J Psychiatry Neurosci source
- Not checked yetcites [4] Videbech, 2004, Hippocampal volume and depression: A meta-analysis of MRI studies, Am J Psychiatry source
- Not checked yetcites [5] Campbell, 2004, Lower hippocampal volume in patients suffering from depression: A meta-analysis, Am J Psychiatry source
- Not checked yetcites [6] Koolschijn, 2009, Brain volume abnormalities in major depressive disorder: A meta-analysis of magnetic resonance imaging studies, Hum Brain Mapp source
- Not checked yetcites [7] Cole, 2011, Hippocampal atrophy in first episode depression: A meta-analysis of magnetic resonance imaging studies, J Affect Disord source
- Not checked yetcites [8] Kempton, 2011, Structural neuroimaging studies in major depressive disorder, Arch Gen Psychiatry source
- Not checked yetcites [9] Arnone, 2012, Magnetic resonance imaging studies in unipolar depression: Systematic review and meta-regression analyses, Eur Neuropsychopharmacol source
- Not checked yetcites [10] Bora, 2012, Gray matter abnormalities in major depressive disorder: A meta-analysis of voxel based morphometry studies, J Affect Disord source
- Not checked yetcites [11] Du, 2012, Voxelwise meta-analysis of gray matter reduction in major depressive disorder, Prog Neuropsychopharmacol Biol Psychiatry source
- Not checked yetcites [12] Lai, 2013, Gray matter volume in major depressive disorder: A meta-analysis of voxel-based morphometry studies, Psychiatry Res Neuroimaging source
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In the paper
“the hippocampus and medial prefrontal cortex (mPFC) have been repeatedly implicated in the pathophysiology and progression of this illness (2,3).”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Abstract
What the sources say
- Not checked yetcites [2] McKinnon, 2009, A meta-analysis examining clinical predictors of hippocampal volume in patients with major depressive disorder, J Psychiatry Neurosci source
- Not checked yetcites [3] Treadway, 2015, Illness progression, recent stress, and morphometry of hippocampal subfields and medial prefrontal cortex in major depression, Biol Psychiatry source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Notably, longitudinal studies have shown that common antidepressants lead to increases in hippocampus and mPFC volumes (17).”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Hippocampus and mPFC volume reductions: Cause versus consequence of MDD?
What the sources say
- Not checked yetcites [17] Frodl, 2008, Effect of hippocampal and amygdala volumes on clinical outcomes in major depression: A 3-year prospective magnetic resonance imaging study, J Psychiatry Neurosci source
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In the paper
“greater baseline life stress was associated with the development of smaller hippocampal volumes three months later in a sample of HCs (48).”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Hippocampus and mPFC volume reductions: Cause versus consequence of MDD?
What the sources say
- Not checked yetcites [48] Papagni, 2011, Effects of stressful life events on human brain structure: A longitudinal voxel-based morphometry study, Stress source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“and non-remission/treatment resistance (28,31–38).”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Hippocampus and mPFC volume reductions: Cause versus consequence of MDD?
What the sources say
- Not checked yetcites [28] Sheline, 2003, Untreated depression and hippocampal volume loss, Am J Psychiatry source
- Not checked yetcites [31] Hsieh, 2002, Hippocampal volume and antidepressant response in geriatric depression, Int J Geriatr Psychiatry source
- Not checked yetcites [32] Frodl, 2004, Hippocampal and amygdala changes in patients with major depressive disorder and healthy controls during a 1-year follow-up, J Clin Psychiatry source
- Not checked yetcites [33] MacQueen, 2008, Posterior hippocampal volumes are associated with remission rates in patients with major depressive disorder, Biol Psychiatry source
- Not checked yetcites [34] Hoogenboom, 2012, Feasibility of studying brain morphology in major depressive disorder with structural magnetic resonance imaging and clinical data from the electronic medical record, Psychiatry Res source
- Not checked yetcites [35] Taylor, 2014, Hippocampus atrophy and the longitudinal course of late-life depression, Am J Geriatr Psychiatry source
- Not checked yetcites [36] Phillips, 2015, A prospective, longitudinal study of the effect of remission on cortical thickness and hippocampal volume in patients with treatment-resistant depression, Int J Neuropsychopharmacol source
- Not checked yetcites [37] Serra-Blasco, 2016, Naturalistic course of major depressive disorder predicted by clinical and structural neuroimaging data: A 5-year follow-up, Depress Anxiety source
- Not checked yetcites [38] Frodl, 2008, Depression-related variation in brain morphology over 3 years, Arch Gen Psychiatry source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- It may state two separate claims as one. 30
- Probably not a substantial claim. 4
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In the paper
“those that have parcellated the hippocampus into different subfields have found evidence for reduced cornu ammonis 1–3, dentate gyrus/cornu ammonis 4, and subiculum volumes as well as both anterior and posterior subdivisions in MDD (e.g., 15,16).”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Hippocampus and mPFC volume reductions: Cause versus consequence of MDD?
What the sources say
- Not checked yetcites [15] Han, 2016, Hippocampal subfield analysis in medication-naïve female patients with major depressive disorder, J Affect Disord source
- Not checked yetcites [16] Malykhin, 2010, Structural changes in the hippocampus in major depressive disorder: Contributions of disease and treatment, J Psychiatry Neurosci source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Approximately 60% of individuals with MDD will experience recurrent episodes”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Abstract
What the sources say
- Not checked yetcites [1] Monroe, 2011, Recurrence in major depression: A conceptual analysis, Psychol Rev source
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“the stress autonomy model posits that successive MDEs develop independently of stressful life events.”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Stress and hippocampal/mPFC volume reduction in MDD
What the sources say
- Not checked yetcites [50] Monroe, 2005, Life stress, the “kindling” hypothesis, and the recurrence of depression: Considerations from a life stress perspective, Psychol Rev source
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Instead, this study suggests that hippocampal changes result from stress and are likely independent of MDE development.”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Hippocampus and mPFC volume reductions: Cause versus consequence of MDD?
What the sources say
- Not checked yetcites [46] Jayatissa, 2010, A reduced number of hippocampal granule cells does not associate with an anhedonia-like phenotype in a rat chronic mild stress model of depression, Stress source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Rests on an assumption: Findings from animal models of stress and depression can be generalized to human major depressive disorder neurobiology.
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 results contradict both causal and consequence hypotheses of hippocampal abnormalities in MDD.”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Hippocampus and mPFC volume reductions: Cause versus consequence of MDD?
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“the stress sensitization model hypothesizes that with recurrent episodes of depression, more minor stressors are capable of triggering MDEs”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Stress and hippocampal/mPFC volume reduction in MDD
What the sources say
- Not checked yetcites [50] Monroe, 2005, Life stress, the “kindling” hypothesis, and the recurrence of depression: Considerations from a life stress perspective, Psychol Rev source
plaindirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Both models posit that while first MDEs are highly likely to follow periods of severe stress, the strength of this relationship declines as a function of illness course.”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Stress and hippocampal/mPFC volume reduction in MDD
What the sources say
- Not checked yetcites [50] Monroe, 2005, Life stress, the “kindling” hypothesis, and the recurrence of depression: Considerations from a life stress perspective, Psychol Rev source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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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
“A possible explanation for these seemingly contradictory findings may be that chronic stress drives initial hippocampal and mPFC abnormalities, but other risk factors need to be present (e.g., genetic, abnormal physiological response to stress) for development of a MDE.”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Hippocampus and mPFC volume reductions: Cause versus consequence of MDD?
hedgeddirect- Asserted: passes — The authors put it forward as true.
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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 suggest that hippocampal and mPFC volume reductions may be a selective marker for the propensity towards and/or the consequence of episodic recurrence.”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Hippocampus and mPFC volume reductions: Cause versus consequence of MDD?
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“A lower cortisol output may reflect its bioavailability or it may be an indicator of reduced responsiveness to the presence of glucocorticoids (77).”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > The role of HPA axis dysregulation in stress-mediated hippocampal and mPFC deficits
What the sources say
- Not checked yetcites [77] Raison, 2003, When not enough is too much: The role of insufficient glucocorticoid signaling in the pathophysiology of stress-related disorders, Am J Psychiatry source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“a meta-analysis found that a history of childhood maltreatment was associated with a greater probability of developing recurrent and persistent cycles of depression as well as treatment-resistance (56).”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Stress and hippocampal/mPFC volume reduction in MDD
What the sources say
- Not checked yetcites [56] Nanni, 2012, Childhood maltreatment predicts unfavorable course of illness and treatment outcome in depression: A meta-analysis, Am J Psychiatry source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“individuals with a history of multiple MDEs exhibited smaller hippocampal and mPFC volumes, yet reported less perceived life stress, compared to those with fewer episodes (3).”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Stress and hippocampal/mPFC volume reduction in MDD
What the sources say
- Not checked yetcites [3] Treadway, 2015, Illness progression, recent stress, and morphometry of hippocampal subfields and medial prefrontal cortex in major depression, Biol Psychiatry source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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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
“This suggests that while high levels of stress may have an important role in initiating hippocampal vulnerabilities amongst individuals with a first MDE, this relationship may be weaker amongst those with recurrent MDEs.”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Stress and hippocampal/mPFC volume reduction in MDD
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“Animal models have established that prolonged stress can lead to HPA axis hyperreactivity and depressive behaviors along with hippocampal and mPFC abnormalities (68,69).”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > The role of HPA axis dysregulation in stress-mediated hippocampal and mPFC deficits
What the sources say
- Not checked yetcites [68] Moylan, 2013, The neuroprogressive nature of major depressive disorder: Pathways to disease evolution and resistance, and therapeutic implications, Mol Psychiatry source
- Not checked yetcites [69] Saaltink, 2014, Stress, glucocorticoid receptors, and adult neurogenesis: A balance between excitation and inhibition?, Cell Mol Life Sci source
boosteddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Rests on an assumption: Findings from animal models of stress and depression can be generalized to human major depressive disorder neurobiology.
None of the sources cited for this claim have been checked yet.
In the paper
“increased oxidative stress, lower antioxidant levels, and imbalanced oxidant:antioxidant levels have been well documented within the hippocampus (103,104) and mPFC (104–106), resulting in associated markers of DNA/RNA damage in these regions.”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Oxidative stress as a mechanism contributing to MDD-related brain structural deficits
What the sources say
- Not checked yetcites [103] Che, 2010, Oxidative damage to RNA but not DNA in the hippocampus of patients with major mental illness, J Psychiatry Neurosci source
- Not checked yetcites [104] Meyer, 2009, Brain monoamine oxidase A binding in major depressive disorder, Arch Gen Psychiatry source
- Not checked yetcites [105] Michel, 2007, Evidence for oxidative stress in the frontal cortex in patients with recurrent depressive disorder—A postmortem study, Psychiatry Res source
- Not checked yetcites [106] Gawryluk, 2011, Decreased levels of glutathione, the major brain antioxidant, in post-mortem prefrontal cortex from patients with psychiatric disorders, Int J Neuropsychopharmacol source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“preclinical studies have also demonstrated that chronic stress initiates production of oxidative stress and impairment of antioxidant defense mechanisms in the hippocampus and mPFC (102).”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Oxidative stress as a mechanism contributing to MDD-related brain structural deficits
What the sources say
- Not checked yetcites [102] Filipović, 2017, Oxidative and nitrosative stress pathways in the brain of socially isolated adult male rats demonstrating depressive- and anxiety-like symptoms, Brain Struct Funct source
boosteddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Rests on an assumption: Findings from animal models of stress and depression can be generalized to human major depressive disorder neurobiology.
In the paper
“This can result in hippocampal and mPFC cellular damage and reduced hippocampal neurogenesis (102), likely contributing to hippocampal and mPFC atrophy.”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Oxidative stress as a mechanism contributing to MDD-related brain structural deficits
What the sources say
- Not checked yetcites [102] Filipović, 2017, Oxidative and nitrosative stress pathways in the brain of socially isolated adult male rats demonstrating depressive- and anxiety-like symptoms, Brain Struct Funct source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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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
“This suggests that some stress-related serotonergic abnormalities are independent of the development of depressive behavior, whereas others were specific to anhedonia development.”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Serotonin dysfunction contribute to brain structural decline and MDD illness progression
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“a study comparing stress-resilient mice versus those exhibiting anhedonic behavior noted that stress-elevated expression of 5HT2A receptors within the mPFC occurred in both groups of mice, whereas additional 5-HT transporter elevations occurred exclusively in the depression-susceptible mice (90).”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Serotonin dysfunction contribute to brain structural decline and MDD illness progression
What the sources say
- Not checked yetcites [90] Couch, 2013, Microglial activation, increased TNF and SERT expression in the prefrontal cortex define stress-altered behaviour in mice susceptible to anhedonia, Brain Behav Immun 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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It may state two separate claims as one.
- Rests on an assumption: Findings from animal models of stress and depression can be generalized to human major depressive disorder neurobiology.
In the paper
“Discrepancies may be due to clinical heterogeneity, including illness stage, particularly since greater serotonin dysfunction has been described amongst individuals with MDD who have experienced a greater number of past MDEs (120).”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Serotonin dysfunction contribute to brain structural decline and MDD illness progression
What the sources say
- Not checked yetcites [120] Maes, 2012, Increased autoimmune activity against 5-HT: A key component of depression that is associated with inflammation and activation of cell-mediated immunity, and with severity and staging of depression, J Affect Disord source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
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In the paper
“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).”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Stress-mediated inflammatory pathways to hippocampal and mPFC deficits in MDD
What the sources say
- Not checked yetcites [95] Frodl, 2012, Reduced expression of glucocorticoid-inducible genes GILZ and SGK-1: High IL-6 levels are associated with reduced hippocampal volumes in major depressive disorder, Transl Psychiatry source
- Not checked yetcites [96] van Velzen, 2017, Immunometabolic dysregulation is associated with reduced cortical thickness of the anterior cingulate cortex, Brain Behav Immun source
- Not checked yetcites [97] Savitz, 2013, Inflammation and neurological disease-related genes are differentially expressed in depressed patients with mood disorders and correlate with morphometric and functional imaging abnormalities, Brain Behav Immun source
plaincorrelational- 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
“greater oxidative stress, lower antioxidant, and greater oxidative stress-related DNA/RNA damage have been linked to clinical markers of MDD illness progression, including greater chronicity, more MDEs, and treatment resistance (98,108–113).”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Oxidative stress as a mechanism contributing to MDD-related brain structural deficits
What the sources say
- Not checked yetcites [98] Sowa-Kućma, 2018, Are there differences in lipid peroxidation and immune biomarkers between major depression and bipolar disorder: Effects of melancholia, atypical depression, severity of illness, episode number, suicidal ideation and prior suicide attempts, Prog Neuropsychopharmacol Biol Psychiatry source
- Not checked yetcites [108] Baek, 2016, Decreased total antioxidant activity in major depressive disorder patients non-responsive to antidepressant treatment, Psychiatry Investig source
- Not checked yetcites [109] Śliwiński, 2015, Elevated level of DNA damage and impaired repair of oxidative DNA damage in patients with recurrent depressive disorder, Med Sci Monit source
- Not checked yetcites [110] Czarny, 2017, Impact of single nucleotide polymorphisms of base excision repair genes on DNA damage and efficiency of DNA repair in recurrent depression disorder, Mol Neurobiol source
- Not checked yetcites [111] Jorgensen, 2013, Systemic oxidatively generated DNA/RNA damage in clinical depression: Associations to symptom severity and response to electroconvulsive therapy, J Affect Disord source
- Not checked yetcites [112] Stefanescu, 2012, The relevance of oxidative stress status in first episode and recurrent depression, J Affect Disord source
- Not checked yetcites [113] Talarowska, 2014, Manganese superoxide dismutase gene expression and cognitive functions in recurrent depressive disorder, Neuropsychobiology 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
“the stimulating effects of peripheral pro-inflammatory cytokines on brain microglia can result in reduced hippocampal neurogenesis (92).”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Stress-mediated inflammatory pathways to hippocampal and mPFC deficits in MDD
What the sources say
- Not checked yetcites [92] Chesnokova, 2016, Chronic peripheral inflammation, hippocampal neurogenesis, and behavior, Brain Behav Immun 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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“IDO is an enzyme that catabolizes tryptophan leading to serotonin depletion and production of kynurenine.”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > A common pathway leading to MDD illness progression-related hippocampal and mPFC volume reductions
What the sources say
- Not checked yetcites [68] Moylan, 2013, The neuroprogressive nature of major depressive disorder: Pathways to disease evolution and resistance, and therapeutic implications, Mol Psychiatry 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.
- 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
“Some studies have reported enhanced chronic stress-related glutamate release and glutamate receptor expression, but reduced glutamate clearance/metabolism in the hippocampus (122,123).”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Glutamatergic contributions to MDD-related brain structural decline
What the sources say
- Not checked yetcites [122] Sun, 2017, Hippocampal GR- and CB1-mediated mGluR5 differentially produces susceptibility and resilience to acute and chronic mild stress in rats, Neuroscience source
- Not checked yetcites [123] De Vasconcellos-Bittencourt, 2011, Chronic stress and lithium treatments alter hippocampal glutamate uptake and release in the rat and potentiate necrotic cellular death after oxygen and glucose deprivation, Neurochem Res source
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
“Chronic stress disrupts glutamate release, glutamate clearance from the synapse, and glutamate transmitter expression, but the direction of the effects is region-specific (121).”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Glutamatergic contributions to MDD-related brain structural decline
What the sources say
- Not checked yetcites [121] Grimm, 2012, Region-specific glutamate changes in patients with unipolar depression, J Psychiatr Res 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.
- 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
“Reduced mPFC GABA levels in MDD have been associated with smaller hippocampal volumes (139) and treatment resistance (142,143).”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > GABAergic disturbances associated with brain structural decline and chronic MDD
What the sources say
- Not checked yetcites [139] Abdallah, 2015, Prefrontal cortical GABA abnormalities are associated with reduced hippocampal volume in major depressive disorder, Eur Neuropsychopharmacol source
- Not checked yetcites [142] Levinson, 2010, Evidence of cortical inhibitory deficits in major depressive disorder, Biol Psychiatry source
- Not checked yetcites [143] Price, 2009, Amino acid neurotransmitters assessed by proton magnetic resonance spectroscopy: Relationship to treatment resistance in major depressive disorder, Biol Psychiatry 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
“A different pattern has been described in the mPFC, with some reporting reduced chronic stress-related glutamate receptor expression, which has been speculated as a potential protective mechanism against excessive glutamate signaling and excitoxicity (e.g., 124–125).”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Glutamatergic contributions to MDD-related brain structural decline
What the sources say
- Not checked yetcites [124] Jett, 2017, Deficits in cognitive flexibility induced by chronic unpredictable stress are associated with impaired glutamate neurotransmission in the rat medial prefrontal cortex, Neuroscience source
- Not checked yetcites [125] Yuen, 2012, Repeated stress causes cognitive impairment by suppressing glutamate receptor expression and function in prefrontal cortex, Neuron source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. 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 production of neurotoxic 3HK and QA leads to increased glutamate and oxidative stress as well as reduced GABAergic inhibitory control.”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > A common pathway leading to MDD illness progression-related hippocampal and mPFC volume reductions
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
“a study found that a lower KynA/3HK ratio correlated with reduced hippocampal volumes in MDD and partially mediated the relationship between MDD and mPFC cortical thinning (146,147).”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > A common pathway leading to MDD illness progression-related hippocampal and mPFC volume reductions
What the sources say
- Not checked yetcites [146] Savitz, 2015, Putative neuroprotective and neurotoxic kynurenine pathway metabolites are associated with hippocampal and amygdalar volumes in subjects with major depressive disorder, Neuropsychopharmacology source
- Not checked yetcites [147] Meier, 2016, Relationship between neurotoxic kynurenine metabolites and reductions in right medial prefrontal cortical thickness in major depressive disorder, Brain Behav Immun 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
“a human imaging study noted associations between increased extracellular glutamate levels and hippocampal volume reductions (130).”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Glutamatergic contributions to MDD-related brain structural decline
What the sources say
- Not checked yetcites [130] Cavus, 2008, Decreased hippocampal volume on MRI is associated with increased extracellular glutamate in epilepsy patients, Epilepsia source
plaincorrelational- 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.
- 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
“when the serotonin system is dysregulated, this can contribute to reduced GABAergic inhibitory control, resulting in enhanced glutamate and HPA axis reactivity, and ultimately reduced hippocampal neurogenesis (124,138).”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > GABAergic disturbances associated with brain structural decline and chronic MDD
What the sources say
- Not checked yetcites [124] Jett, 2017, Deficits in cognitive flexibility induced by chronic unpredictable stress are associated with impaired glutamate neurotransmission in the rat medial prefrontal cortex, Neuroscience source
- Not checked yetcites [138] Rubio-Casillas, 2016, The dose makes the poison: From glutamate-mediated neurogenesis to neuronal atrophy and depression, Rev Neurosci 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.
- 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
“Generally, studies have found reduced Glx/glutamate levels in the mPFC and hippocampus in MDD, with those having a more chronic course showing greater declines compared to individuals experiencing a first episode (127,128).”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > Glutamatergic contributions to MDD-related brain structural decline
What the sources say
- Not checked yetcites [127] de Diego-Adeliño, 2013, Hippocampal abnormalities of glutamate/glutamine, N-acetylaspartate and choline in patients with depression are related to past illness burden, J Psychiatry Neurosci source
- Not checked yetcites [128] Portella, 2011, Ventromedial prefrontal spectroscopic abnormalities over the course of depression: A comparison among first episode, remitted recurrent and chronic patients, J Psychiatr Res 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.
The paper relies on this without support.
Findings from animal models of stress and depression can be generalized to human major depressive disorder neurobiology.
“Animal models have established that prolonged stress can lead to HPA axis hyperreactivity and depressive behaviors along with hippocampal and mPFC abnormalities (68,69).”
The paper relies on this without support.
Hippocampal and medial prefrontal cortex volume reductions measured by MRI reflect cellular damage or atrophy relevant to major depressive disorder.
“Volumetric reductions in the hippocampus and medial prefrontal cortex (mPFC) are among the most well documented neural abnormalities in major depressive disorder (MDD).”
The paper relies on this without support.
Peripheral and central measures of inflammation, oxidative stress, cortisol, and neurotransmitters index the same brain processes relevant to hippocampal and medial prefrontal cortex structure.
“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).”
The paper relies on this without support.
The stress sensitization and stress autonomy models apply to structural brain changes, not only to the onset of major depressive episodes.
“Two classes of stress-related models, the stress sensitization and stress autonomy models, have been proposed to explain how relationships between stress and depression change as a function of illness course (50).”
The paper relies on this without support.
The proposed indoleamine 2,3-dioxygenase-kynurenine pathway operates in humans with major depressive disorder as described.
“One possible common pathway involves chronic stress triggering HPA axis dysfunction and enhanced production of cell-mediated immune cytokines, which activate indoleamine 2,3-dioxygenase (IDO;68).”
The paper relies on this without support.
Major depressive disorder illness progression markers such as episode count, illness duration, and treatment resistance reflect a common progressive disease process.
“they have been consistently associated with markers of a progressive course of MDD characterized by more recurrent episodes/relapses (3,19–25), longer illness duration (24,26–30), and non-remission/treatment resistance (28,31–38).”
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?
In the citing paper
“and the significantly reduced mPFC volume spanning across dorsomedial PFC, ventromedial (VM) PFC and ACC 205.”
From Mechanisms of synaptic transmission dysregulation in the prefrontal cortex: pathophysiological implications (2022) · cites this paper as [205]
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
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > The role of HPA axis dysregulation in stress-mediated hippocampal and mPFC deficits
“Additionally, given that these studies are cross-sectional, and brain structural changes may occur long after stress exposure, prospective studies are needed to link distinct cortisol trajectories with different life stress profiles, structural deficits, and illness course.”
§ The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology > References
“83. O’Brien JT, Lloyd A, McKeith I, Gholkar A, Ferrier N (2004): A longitudinal study of hippocampal volume, cortisol levels, and cognition in older depressed subjects.”
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“In this model, intestinal T cells migrate to the meninges after a stroke, which is reversed by the depletion of particular groups of gut bacteria (Benakis et al. 2016).”
Background
Metadata
- Authors
- Belleau, E. L., Treadway, M. T., & Pizzagalli, D. A.
- Affiliations
- Harvard University (US)
- Emory University (US)
- Corresponding author
- Pizzagalli, Diego A.
- Venue
- Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2019-03
- Volume
- 85
- Issue
- 6
- Pages
- 443-453
- ISSN
- 0006-3223 (ISSN-L)
- PMC
- PMC6380948
- OpenAlex
- W2895959992
- Cited by
- 550
- References
- 151
- Citations by year
- 2026: 67 · 2025: 94 · 2024: 83 · 2023: 85 · 2022: 89 · 2021: 70 · 2020: 41 · 2019: 20
- FWCI
- 3.68
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Harvard Medical School
- McLean Hospital
- Klingenstein Third Generation Foundation
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- major depressive disorder, chronic stress, hippocampal volume, medial prefrontal cortex, brain structure, hippocampal atrophy, disease progression, major depressive episode, treatment resistance, hypothalamic-pituitary-adrenal axis, neuroinflammation, oxidative stress, neurotransmitter abnormalities, stress sensitization, structural neuroplasticity
- MeSH terms
- Animals, Depressive Disorder, Major, Major Depressive Disorder, Hippocampus, Humans, Stress, Psychological, Prefrontal Cortex
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.
A language model drew the claims from the paper on 2026-10-04, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-04 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
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 ›
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