The DOI matches its Crossref record; 112 of the 124 references it cites were found in a registry or an index; none of the 100 sources its claims cite is checked for support yet.
Glucocorticoids, cytokines and brain abnormalities in depression
Open accessAbstract
Major depression (MD) is a common psychiatric disorder with a complex and multifactor aetiology. Potential mechanisms associated with the pathogenesis of this disorder include monoamine deficits, hypothalamic-pituitary-adrenal (HPA) axis dysfunctions, inflammatory and/or neurodegenerative alterations. An increased secretion and reactivity of cortisol together with an altered feedback inhibition are the most widely observed HPA abnormalities in MD patients. Glucocorticoids, such as cortisol, are vital hormones that are released in response to stress, and regulate metabolism and immunity but also neuronal survival and neurogenesis. Interestingly depression is highly prevalent in infectious, autoimmune and neurodegenerative diseases and at the same time, depressed patients show higher levels of pro-inflammatory cytokines. Since communication occurs between the endocrine, immune and central nervous system, an activation of the inflammatory responses can affect neuroendocrine processes, and vice versa. Therefore, HPA axis hyperactivity and inflammation might be part of the same pathophysiological process: HPA axis hyperactivity is a marker of glucocorticoid resistance, implying ineffective action of glucocorticoid hormones on target tissues, which could lead to immune activation; and, equally, inflammation could stimulate HPA axis activity via both a direct action of cytokines on the brain and by inducing glucocorticoid resistance. In addition, increased levels of pro-inflammatory cytokines also induce the production of neurotoxic end products of the tryptophan–kynurenine pathway. Although the evidence for neurodegeneration in MD is controversial, depression is comorbid with many other conditions where neurodegeneration is present. Since several systems seem to be involved interacting with each other, we cannot unequivocally accept the simple model that glucocorticoids induce neurodegeneration, but rather that elevated cytokines, in the context of glucocorticoid resistance, are probably the offenders. Chronic inflammatory changes in the presence of glucocorticoid resistance may represent a common feature that could be responsible for the enhanced vulnerability of depressed patients to develop neurodegenerative changes later in life. However, further studies are needed to clarify the relative contribution of glucocorticoids and inflammatory signals to MD and other disorders.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
77 Not checked yet · 16 Own interpretation · 16 No basis given · 1 Own method
None of the sources cited for this claim have been checked yet.
In the paper
“Decreased responsiveness to glucocorticoids, a phenomenon known as glucocorticoid resistance, is believed to be related in part to an impaired function of the GR”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 2. The HPA axis in major depression > 2.2. Glucocorticoid resistance
What the sources say
- Not checked yetcites Pariante et al., 1995
- Not checked yetcites Pariante and Miller, 2001 source
- Not checked yetcites Carvalho and Pariante, 2008
hedgedconditional- 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.
None of the sources cited for this claim have been checked yet.
In the paper
“The HPA abnormalities found in MD, extensively studied also in our laboratory, include increased secretion and reactivity of cortisol”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 2. The HPA axis in major depression
What the sources say
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.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“pro-inflammatory cytokines produced in response to peripheral infections act on the brain to cause what is known as ‘sickness behaviour’”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 3. Inflammation and depression
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.
In the paper
“They influence neuronal functioning through changes in apoptosis, oxidative stress and metabolic derangement, as well as by impairing processes of neuronal branching”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 3. Inflammation and depression
What the sources say
- Not checked yetcites Hayley et al., 2005 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.
In the paper
“elevated basal cerebrospinal fluid CRH levels”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 2. The HPA axis in major depression
What the sources say
- Not checked yetcites Nemeroff et al., 1984 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.
In the paper
“Overall, these changes in immune function occurring in depression are said to confer an immune resistance to glucocorticoids”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 2. The HPA axis in major depression > 2.1. Role of glucocorticoids
What the sources say
- Not checked yetcites Maes et al., 1994 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.
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 evidence that cytokine-mediated inflammatory processes play an important role in the development of depression is now strong.”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 3. Inflammation and depression
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.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Evidence supporting the role of glucocorticoid resistance (rather than glucocorticoid excess) in depression comes from a multitude of studies, some of them conducted in our own laboratory, showing that antidepressants in human, animal and cellular models tend to increase (rather than decrease) GR function”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 2. The HPA axis in major depression > 2.2. Glucocorticoid resistance
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.
- Based: passes — The paper gives a reason why it holds.
In the paper
“increased size as well as activity of the pituitary and adrenal glands”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 2. The HPA axis in major depression
What the sources say
- Not checked yetcites Nemeroff et al., 1992 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.
In the paper
“IL-1beta has been shown to inhibit long-term potentiation, a form of neuronal plasticity believed to underlie learning and memory”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 3. Inflammation and depression
What the sources say
- Not checked yetcites Pickering and O’Connor, 2007 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. 58
- Probably not a substantial claim. 5
In the paper
“Cytokines can activate the HPA axis, causing an elevation of systemic glucocorticoid levels, and at the same time, they can inhibit GR function at multiple levels, including GR translocation and induction of GR isoforms with reduced capacity to bind ligand”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 3. Inflammation and depression > 3.1. Mechanisms of cross talk between cytokines and GR
What the sources say
- Not checked yetcites Pace et al., 2007 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.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Actions mediated by both receptors are complementary and operate in different time domains of the stress response: the MR normally prevents stress-induced disturbances, but, if such disturbances occur, the GR can operate and help in the recovery process.”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 2. The HPA axis in major depression > 2.2. Glucocorticoid resistance
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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“A reduction in neurogenesis can theoretically contribute to the cognitive symptoms of depression, even though by itself is unlikely to produce the full mood disorder”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 2. The HPA axis in major depression > 2.4. Effects of glucocorticoids on neurogenesis
What the sources say
- Not checked yetcites Lucassen et al., 2010 source
plainconditional- 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
“dexamethasone administration induced an increase in the number of neutrophils and a decrease in the number of lymphocytes in healthy controls, whereas this effect was not observed in non-suppressors”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 2. The HPA axis in major depression > 2.1. Role of glucocorticoids
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.
- 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
“depressed patients show higher levels of pro-inflammatory cytokines, acute phase proteins, chemokines and cellular adhesion molecules”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 3. Inflammation and depression
What the sources say
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 MR binds cortisol with higher affinity, hence it regulates normal HPA fluctuations, being significantly bound even at the circadian trough, and fully bound at the circadian peak and during stressful episodes. The GR, of lower affinity, gets extensively occupied in times of stress.”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 2. The HPA axis in major depression > 2.2. Glucocorticoid resistance
What the sources say
- Not checked yetcites de Kloet et al., 2005 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
“Depression is highly prevalent in infectious, autoimmune and neurodegenerative diseases, and this co-morbidity cannot be attributed only to the psychological distress of the starting disease”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 3. Inflammation and depression
What the sources say
- Not checked yetcites Pollak and Yirmiya, 2002 source
plain- 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
“Although it is possible that an imbalance between MR and GR could increase the vulnerability to stress-related psychiatric disorders in predisposed individuals”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 2. The HPA axis in major depression > 2.2. Glucocorticoid resistance
What the sources say
- Not checked yetcites de Kloet et al., 2007 source
hedgedconditional- 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.
None of the sources cited for this claim have been checked yet.
In the paper
“severe or chronic stress exposure, both in early life as well as in adulthood, can cause neural cell death and atrophy of neuronal processes, and also affect hippocampal neurogenesis and plasticity”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 2. The HPA axis in major depression > 2.4. Effects of glucocorticoids on neurogenesis
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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“A failure in GR function, as hypothesized to take place in depression, may therefore result from reduced glucocorticoid binding to GR, reduced GR expression, enhanced activation of inflammatory pathways, or lack of co-repressor activity”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 2. The HPA axis in major depression > 2.3. Molecular basis of glucocorticoid action
What the sources say
- Not checked yetcites De Bosscher and Haegeman, 2009 source
hedgedconditional- 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
“if stress is repetitively experienced in an uncontrollable and unpredictable manner, it can cause alterations in dendrite and spine morphology in specific brain regions, and eventually suppress adult neurogenesis”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 2. The HPA axis in major depression > 2.4. Effects of glucocorticoids on neurogenesis
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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“If, during systemic infections, cancer or autoimmune diseases, the activation of the peripheral immune system is prolonged, the immune signalling to the brain could lead to an exacerbation of sickness behaviour and to the development of depressive symptoms in vulnerable individuals”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 3. Inflammation and depression
What the sources say
- Not checked yetcites Dantzer et al., 2008 source
hedgedconditional- 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
“therapeutic administration of the cytokine interferon-alpha (IFN-alpha) leads to a depressive symptomatology in up to 50% of patients, who show similar biological alterations as those found in MD and can be treated with antidepressant medication”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 3. Inflammation and depression
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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“While dexamethasone administration significantly suppressed the mitogen-induced lymphocyte proliferation and the interleukin-1beta (IL-1beta) production in healthy controls, MD patients exhibited dexamethasone non-suppression”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 2. The HPA axis in major depression > 2.1. Role of glucocorticoids
What the sources say
- Not checked yetcites Maes et al, 1991 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
“Glucocorticoids act by binding to the cytosolic GR, which is subsequently activated and is thus able to translocate into the nucleus.”
- Also stated in: § 2.3. Molecular basis of glucocorticoid action · plain
“Once in the nucleus, the GR either binds to DNA and switches on the expression of anti-inflammatory genes, or acts indirectly by protein–protein interaction to repress the activity of a number of distinct signalling pathways such as nuclear factor-kappaB (NF-kappaB)”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 2. The HPA axis in major depression > 2.3. Molecular basis of glucocorticoid action
What the sources say
- Not checked yetcites Revollo and Cidlowski, 2009 source
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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Also stated in: § 2.3. Molecular basis of glucocorticoid action · plain
None of the sources cited for this claim have been checked yet.
In the paper
“Hyperactivity of the HPA axis in MD can be demonstrated by the altered feedback inhibition, as seen by increased circulating cortisol and non-suppression of cortisol following administration of dexamethasone”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 2. The HPA axis in major depression > 2.1. Role of glucocorticoids
What the sources say
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 development of functional glucocorticoid resistance was accompanied by the accumulation of glucocorticoid-insensitive cells in the spleen that exhibit impaired nuclear translocation of the GR and lack of glucocorticoid-induced suppression of NF-kappaB”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 4. Interactions between cytokines and glucocorticoids: what comes first?
What the sources say
- Not checked yetcites Engler et al., 2008 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.
In the paper
“IL-1beta and IL-6, both of which increase during infection, have been described as playing a central role in synaptic plasticity, neurogenesis and neuromodulation”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 3. Inflammation and depression > 3.2. Pro-inflammatory cytokines IL-1beta and IL-6
What the sources say
- Not checked yetcites McAfoose and Baune 2009 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.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Whereas an acute or short-term stressful life event can enhance immune responses, chronic or long-term stress can suppress immunity.”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 4. Interactions between cytokines and glucocorticoids: what comes first? > 4.1. Effect of duration and timing of stress
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
“Stockmeier et al. (2004) observed that the packing density of glia, pyramidal neurons and granule cell neurons is significantly increased in all hippocampal subfields and the dentate gyrus, and pyramidal neuron soma size is significantly decreased, suggesting that a significant reduction in neuropil in MD may account for the decreased hippocampal volume detected by neuroimaging.”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 5. Neurodegeneration
What the sources say
- Not checked yetcites Stockmeier et al. (2004) source
hedgedconditional- 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 administration of corticosterone produced depressive symptoms both in wild type and knockout mice, and the effects of CMS on behavioural depression could be mimicked by exogenous administration of IL-1beta”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 4. Interactions between cytokines and glucocorticoids: what comes first?
What the sources say
- Not checked yetcites Goshen et al., 2008 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
“splenocytes of mice stimulated with the bacterial cell wall component lipopolysaccharide (LPS) and also repeatedly subjected to social disruption were less sensitive to the anti-inflammatory actions of glucocorticoids, showing increased levels of pro-inflammatory cytokines”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 4. Interactions between cytokines and glucocorticoids: what comes first?
What the sources say
- Not checked yetcites Engler et al., 2008 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
“both inhibiting the IL-1 receptor and using IL-1 receptor null mice prevented the anhedonic behaviour caused by chronic stress exposure”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 3. Inflammation and depression > 3.2. Pro-inflammatory cytokines IL-1beta and IL-6
What the sources say
- Not checked yetcites Koo and Duman, 2008 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.
- 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
“HPA axis hyperactivity and inflammation might be part of the same pathophysiological process: HPA axis hyperactivity is a marker of glucocorticoid resistance, implying ineffective action of glucocorticoid hormones on target tissues, which could lead to immune activation; equally, inflammation could stimulate HPA axis activity via both a direct action of cytokines on the brain and by inducing gluc”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 4. Interactions between cytokines and glucocorticoids: what comes first? > 4.1. Effect of duration and timing of stress
hedgedconditional- 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.
- Rests on an assumption: Communication occurs between the endocrine, immune, and central nervous systems, so activation of inflammatory responses can affect neuroendocrine processes and vice versa.
None of the sources cited for this claim have been checked yet.
In the paper
“The caregivers’ patterns of cortisol secretion were similar to those of matched control. However, their monocytes showed diminished expression of transcripts bearing response elements for glucocorticoids, and heightened expression of transcripts with response elements for the key pro-inflammatory transcription factor NF-kappaB”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 4. Interactions between cytokines and glucocorticoids: what comes first?
What the sources say
plain- 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
“exposure to chronic restraint stress prior to the injury exacerbated a depressive-like behaviour causing also an increase in IL-1beta gene expression, whereas a pre-treatment with a corticosteroid synthesis inhibitor before stress was able to eliminate the damaging effects of chronic stress. In addition, interference with IL-1beta signalling, through administration of an IL-1 receptor antagonist,”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 4. Interactions between cytokines and glucocorticoids: what comes first? > 4.1. Effect of duration and timing of stress
What the sources say
- Not checked yetcites Norman et al., 2010 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
“Immunoenhancement is observed when acute stress is experienced at early stages of immune activation, while immunosuppression may be observed at late stages of the immune response”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 4. Interactions between cytokines and glucocorticoids: what comes first? > 4.1. Effect of duration and timing of stress
What the sources say
- Not checked yetcites Dhabhar, 2009 source
hedgedconditional- 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 states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“mice lacking IL-1 receptor exhibited adrenal hypertrophy and elevated serum corticosterone levels in response to stressors and failed to develop glucocorticoid resistance”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 4. Interactions between cytokines and glucocorticoids: what comes first?
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: unclear — It is unclear why the paper says 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
“it is possible that increased levels of pro-inflammatory cytokines, especially IL-1 and IL-6, may contribute to the pathophysiology of depression inducing, as we will discuss below, glucocorticoid resistance, neurodegeneration, or indeed other yet unknown mechanism”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 3. Inflammation and depression > 3.2. Pro-inflammatory cytokines IL-1beta and IL-6
hedgedconditional- 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
“glucocorticoids potentiate both the peripheral and central pro-inflammatory response to a peripheral immune challenge if they are administered prior to the challenge. Contrarily, when glucocorticoids are administered after the peripheral immune challenge, they suppress the pro-inflammatory response measured as IL-1beta and IL-6.”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 4. Interactions between cytokines and glucocorticoids: what comes first? > 4.1. Effect of duration and timing of stress
What the sources say
- Not checked yetcites Frank et al. (2010) 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
“An interesting recent study supports the idea that chronic stress is accompanied by GR resistance and activation of pro-inflammatory pathways”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 4. Interactions between cytokines and glucocorticoids: what comes first?
What the sources say
- Not checked yetcites Miller et al., 2008 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
“Multiple inflammatory cytokines, oxygen radical damage, tryptophan catabolites (see below) and neurodegenerative biomarkers have all been established in patients with MD and corroborated by animal models of depression”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 5. Neurodegeneration
What the sources say
- Not checked yetcites Maes et al., 2009 source
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
“Glucocorticoid resistance can underlie the HPA axis disturbances and this might be caused by cytokines.”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 4. Interactions between cytokines and glucocorticoids: what comes first?
hedgedconditional- 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.
- Rests on an assumption: Communication occurs between the endocrine, immune, and central nervous systems, so activation of inflammatory responses can affect neuroendocrine processes and vice versa.
In the paper
“mice subjected to chronic mild stress (CMS) showed increased IL-1beta levels in the hippocampus and in parallel a development of changes in behaviour resembling depressive symptoms, such as decreased sucrose preference and reduced social exploration. In contrast, mice with deletion of the IL-1 receptor did not display such behavioural changes”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 3. Inflammation and depression > 3.2. Pro-inflammatory cytokines IL-1beta and IL-6
What the sources say
- Not checked yetcites Goshen et al., 2008 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
“The selective and persistent loss of hippocampal volume could be induced by neurodegeneration, leading to hippocampal neuronal death, and also by decreased neurogenesis”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 5. Neurodegeneration
What the sources say
- Not checked yetcites Sapolsky, 2004 source
hedgedconditional- 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
“an acute injection of IL-1beta increases sickness and levels of plasma corticosterone, while these effects are attenuated after subchronic treatment”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 4. Interactions between cytokines and glucocorticoids: what comes first? > 4.1. Effect of duration and timing of stress
What the sources say
- Not checked yetcites Anisman et al., 2008a
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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“the study of MD patients done by Müller et al. (2001) did not found any proof of patterns of reactive astrogliosis, synaptic density or synaptic reorganization”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 5. Neurodegeneration
What the sources say
- Not checked yetcites Müller et al. (2001) source
plain- 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
“neuroimaging studies have consistently shown reduced size of hippocampal volume in MD as reported by meta-analysis studies of patients with recurrent depression”
- Also stated in: § 5. Neurodegeneration · plain
“and with longer duration of illness”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 5. Neurodegeneration
What the sources say
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.
- Also stated in: § 5. Neurodegeneration · plain
None of the sources cited for this claim have been checked yet.
In the paper
“depressed patients with increased inflammatory biomarkers are more likely to be resistant to antidepressant therapy, a response to treatment has been associated with decreased inflammatory responses”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 4. Interactions between cytokines and glucocorticoids: what comes first?
What the sources say
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
“the removal of endogenous glucocorticoids abolished the depressive-like effects of CMS, indicating that the blunting of the adrenocortical activation may play a role in their resistance to develop depression”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 4. Interactions between cytokines and glucocorticoids: what comes first?
What the sources say
- Not checked yetcites Goshen et al., 2008 source
hedgedconditional- 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 states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“many of the structural changes and the volume reduction appear to be reversible”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 5. Neurodegeneration
hedged- 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: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
In the paper
“Dexamethasone is used in premature infants to prevent and/or treat bronchopulmonary dysplasia that can adversely affect early neurodevelopment and can probably cause a loss of cerebral volume (Grier and Halliday, 2003).”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 5. Neurodegeneration > 5.2. Neurodegeneration and glucocorticoids
What the sources say
- Not checked yetcites Grier and Halliday, 2003 source
hedgedconditional- 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.
In the paper
“They showed that peripheral administration of LPS in mice activates IDO to induce a depressive-like behavioural syndrome and to increase the brain serotonin turnover.”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 5. Neurodegeneration > 5.1. Neurodegeneration due to imbalances in the kynurenine pathway caused by cytokines
What the sources say
- Not checked yetcites O’Connor et al., 2009
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
“Interestingly, this GR blockade attenuated the hippocampal abnormalities and rescued the diabetic mice from the cognitive deficits (Revsin et al., 2009).”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 5. Neurodegeneration > 5.2. Neurodegeneration and glucocorticoids
What the sources say
- Not checked yetcites Revsin et al., 2009 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
“Therefore, while dexamethasone can exert neurodegenerative effects in the developing brain, it can also increase VEGF levels, which, in contrast, may play a neuroprotective role (Feng et al., 2009).”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 5. Neurodegeneration > 5.2. Neurodegeneration and glucocorticoids
What the sources say
- Not checked yetcites Feng et al., 2009 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
“This ‘glucocorticoid cascade hypothesis’ of stress and hippocampal damage was proposed to be involved in age-related accumulation of hippocampal damage in disorders like Alzheimer’s disease and depression (Sapolsky et al., 1986).”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 5. Neurodegeneration > 5.2. Neurodegeneration and glucocorticoids
What the sources say
- Not checked yetcites Sapolsky et al., 1986 source
plainconditional- 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.
Probably not a substantial claim.
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
“Therefore, we cannot unequivocally accept the simple model that glucocorticoids cause neurodegeneration, but rather that elevated cytokines, in the context of glucocorticoid resistance, are probably the offenders.”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 5. Neurodegeneration > 5.3. Are cytokines or glucocorticoids the culprits? Final remarks
hedgedconditional- 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 states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Chronic inflammation is now considered to play a central role in the pathogenesis of cardiovascular disease, multiple sclerosis, diabetes, cancer and MD.”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 5. Neurodegeneration > 5.3. Are cytokines or glucocorticoids the culprits? Final remarks
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: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In response to LPS, cells produce several cytokines, and glucocorticoids control their expression. In the absence of this negative feedback, some cytokines, in particular tumor necrosis factor alpha (TNF-alpha), become highly toxic and cause a nonselective cell death.”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 5. Neurodegeneration > 5.2. Neurodegeneration and glucocorticoids
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
“At the same time, dexamethasone causes an increase in mRNA and protein levels of vascular endothelial growth factor A (VEGF), which has neurotrophic and neurogenesis enhancing effects.”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 5. Neurodegeneration > 5.2. Neurodegeneration and glucocorticoids
What the sources say
- Not checked yetcites Feng et al., 2009 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
“it has been hypothesized that depression is not a true neurodegenerative disorder (Thompson et al., 2008) or at least it does not involve only a deficit in neurogenesis”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 5. Neurodegeneration
What the sources say
- Not checked yetcites Thompson et al., 2008 source
hedged- Asserted: fails — The authors may not 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 authors may not put it forward as true. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Chronic stressors induce sustained elevations in cortisol, which, over time, cause immune cells to undergo a compensatory downregulation of GR activity.”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 5. Neurodegeneration > 5.3. Are cytokines or glucocorticoids the culprits? Final remarks
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.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Indeed there is clinical evidence that depression is a common antecedent of Alzheimer’s disease and may be an early manifestation of dementia before the cognitive declines become apparent.”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 5. Neurodegeneration > 5.3. Are cytokines or glucocorticoids the culprits? Final remarks
hedgedconditional- 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: unclear — It is unclear why the paper says it holds.
It may state two separate claims as one.
In the paper
“Interestingly, both the anti-inflammatory drug and the IDO antagonist are able to normalize the kynurenine/tryptophan ratio.”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 5. Neurodegeneration > 5.1. Neurodegeneration due to imbalances in the kynurenine pathway caused by cytokines
What the sources say
- Not checked yetcites O’Connor et al., 2009
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
“Contrary to the studies shown above where glucocorticoids exert neurodegenerative effects in the developing brain, a few studies have shown that dexamethasone may also play a neurotrophic and neuroprotective role.”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 5. Neurodegeneration > 5.2. Neurodegeneration and glucocorticoids
hedgedconditional- 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
“kynurenic acid is an N-methyl d-aspartate (NMDA) receptor antagonist, and is generally considered neuroprotective”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 5. Neurodegeneration > 5.1. Neurodegeneration due to imbalances in the kynurenine pathway caused by cytokines
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.
- 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
“This limits the ability of cortisol to further reduce immune responses, even in the presence of high circulating glucocorticoid levels, and as a result there is low-grade inflammation, which is hypothesized to contribute to the infectious, autoimmune, and cardiac diseases, whose risk is linked to stress.”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 5. Neurodegeneration > 5.3. Are cytokines or glucocorticoids the culprits? Final remarks
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.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“An additional useful model to assess the effect of glucocorticoids on neurodegeneration is Type 1 diabetes, a common metabolic disorder characterized by an increased secretion of glucocorticoids and cognitive deficits.”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 5. Neurodegeneration > 5.2. Neurodegeneration and glucocorticoids
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
“3-hydroxykynurenine and quinolinic acid are NMDA receptor agonists, potentially neurotoxic and thus potentially contributing to depression”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 5. Neurodegeneration > 5.1. Neurodegeneration due to imbalances in the kynurenine pathway caused by cytokines
What the sources say
hedgedconditional- 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 states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The development of depressive symptomatology is a frequent side effect of glucocorticoid treatment and one of the symptoms of Cushing’s syndrome.”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 5. Neurodegeneration > 5.2. Neurodegeneration and glucocorticoids
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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Boldrini et al. (2009) showed increased progenitor cells in MD patients treated with antidepressants. More specifically, patients receiving these drugs had more dividing cells in the hippocampus than untreated patients and controls.”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 5. Neurodegeneration
What the sources say
- Not checked yetcites Boldrini et al. (2009) 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.
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
“Due to an inhibitory control of the hippocampus on the HPA axis, damage to this structure is expected to disinhibit the HPA axis, causing increased glucocorticoid levels over time.”
§ Glucocorticoids, cytokines and brain abnormalities in depression > 5. Neurodegeneration > 5.2. Neurodegeneration and glucocorticoids
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.
The paper relies on this without support.
Communication occurs between the endocrine, immune, and central nervous systems, so activation of inflammatory responses can affect neuroendocrine processes and vice versa.
“Since communication occurs between the endocrine, immune and central nervous system, an activation of the inflammatory responses can affect neuroendocrine processes, and vice versa.”
The paper relies on this without support.
Activation of the inflammatory immune system provokes neuroendocrine and neurotransmitter changes similar to those provoked by physical or psychological stressors.
“activation of the inflammatory immune system provokes numerous neuroendocrine and neurotransmitter changes, many of which are similar to those provoked by physical or psychological stressors”
The paper relies on this without support.
Stress can promote inflammatory responses through effects on sympathetic and parasympathetic nervous system pathways.
“stress can promote inflammatory responses through effects on sympathetic and parasympathetic nervous system pathways”
The paper relies on this without support.
Depression is comorbid with many other conditions in which neurodegeneration is present.
“depression is comorbid with many other conditions where neurodegeneration is present”
The paper relies on this without support.
Animal models of chronic stress and inflammation-induced depressive-like behavior are valid models for human depression.
“preclinical studies in which animals are exposed to chronic stress (a paradigm used to mimic what happens in depressed patients where stressful life events represent a precipitating factor for the pathogenesis of depression) have been used to understand the hippocampal shrinkage in depressed patients.”
The paper relies on this without support.
Findings from post-mortem tissue reflect antemortem brain states in depression.
“All these analyses were conducted on post-mortem tissues, where results are indicative of conditions at one time point only”
The paper relies on this without support.
Chronic inflammatory changes are a common feature of depression.
“If chronic inflammatory changes represent a common feature of depression, this could predispose depressed patients to neurodegenerative changes later in life.”
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
“an extensive literature, some from our own group, which shows that antidepressants directly regulate the function of the glucocorticoid receptor (GR).18, 19, 20, 21, 22, 23, 24”
From Antidepressants increase human hippocampal neurogenesis by activating the glucocorticoid receptor (2011) · cites this paper as [20]
Citations
Cites
Cognitive Therapy for Depression
(2012) · PsycEXTRA Dataset · doi:10.1037/e675542012-001 · Cited by 9,678
From inflammation to sickness and depression: when the immune system subjugates the brain
Dantzer, R., O'Connor, J. C., Freund, G. G., Johnson, R. W., & Kelley, K. W. (2008) · Nature Reviews Neuroscience · doi:10.1038/nrn2297 · Cited by 7,395
A Meta-Analysis of Cytokines in Major Depression
Dowlati, Y., Herrmann, N., Swardfager, W., Liu, H., Sham, L., Reim, E. K., & Lanctôt, K. L. (2010) · Biological Psychiatry · doi:10.1016/j.biopsych.2009.09.033 · Cited by 4,729
Cognitive Therapy of Depression
HOLLON, S. D., & BECK, A. T. (1979) · Cognitive-Behavioral Interventions · doi:10.1016/b978-0-12-404480-7.50012-5 · Cited by 4,685
Stress and the brain: from adaptation to disease
de Kloet, E. R., Joëls, M., & Holsboer, F. (2005) · Nature Reviews Neuroscience · doi:10.1038/nrn1683 · Cited by 4,621
Inflammation and Its Discontents: The Role of Cytokines in the Pathophysiology of Major Depression
Miller, A. H., Maletic, V., & Raison, C. L. (2009) · Biological Psychiatry · doi:10.1016/j.biopsych.2008.11.029 · Cited by 3,848
Cytokines sing the blues: inflammation and the pathogenesis of depression
Raison, C. L., Capuron, L., & Miller, A. H. (2006) · Trends in Immunology · doi:10.1016/j.it.2005.11.006 · Cited by 3,009
Mechanisms and Functional Implications of Adult Neurogenesis
Zhao, C., Deng, W., & Gage, F. H. (2008) · Cell · doi:10.1016/j.cell.2008.01.033 · Cited by 3,007
Associations of depression with C-reactive protein, IL-1, and IL-6: a meta-analysis.
Howren, M. B., Lamkin, D. M., & Suls, J. (2009) · Psychosomatic Medicine · doi:10.1097/psy.0b013e3181907c1b · Cited by 2,766
The Neuroendocrinology of Stress and Aging: The Glucocorticoid Cascade Hypothesis
Sapolsky, R. M., Krey, L. C., & McEwen, B. S. (1986) · Science of Aging Knowledge Environment · doi:10.1126/sageke.2002.38.cp21 · Cited by 2,343
Cited by
Sorted by citations
Items 101–200 of 554
Wnt signaling in neuropsychiatric disorders: Ties with adult hippocampal neurogenesis and behavior
Hussaini, S. M. Q., Choi, C., Cho, C. H., Kim, H. J., Jun, H., & Jang, M. (2014) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2014.09.005 · Cited by 88
The Immune System and Electroconvulsive Therapy for Depression
Guloksuz, S., Rutten, B. P. F., Arts, B., van Os, J., & Kenis, G. (2014) · The Journal of ECT · doi:10.1097/yct.0000000000000127 · Cited by 90
Dietary phospholipids: Role in cognitive processes across the lifespan
Schverer, M., O’Mahony, S. M., O’Riordan, K. J., Donoso, F., Roy, B. L., Stanton, C., Dinan, T. G., Schellekens, H., & Cryan, J. F. (2020) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2020.01.012 · Cited by 92
Slavich, G. M., Giletta, M., Helms, S. W., Hastings, P. D., Rudolph, K. D., Nock, M. K., & Prinstein, M. J. (2020) · Depression and Anxiety · doi:10.1002/da.22987 · Cited by 103
Ahmad, M. H., Rizvi, M. M. A., Fatima, M., & Mondal, A. C. (2020) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2020.111093 · Cited by 87
Quines, C. B., Rosa, S. G., da Rocha, J. T., Gai, B. M., Bortolatto, C. F., Duarte, M., & Nogueira, C. W. (2014) · Life Sciences · doi:10.1016/j.lfs.2014.04.032 · Cited by 84
Overtraining Syndrome as a Complex Systems Phenomenon
Armstrong, L. E., Bergeron, M. F., Lee, E. C., Mershon, J. E., & Armstrong, E. M. (2022) · Frontiers in Network Physiology · doi:10.3389/fnetp.2021.794392 · Cited by 118
Effects of Electroconvulsive Therapy on Depression and Its Potential Mechanism
Li, M., Yao, X., Sun, L., Zhao, L., Xu, W., Zhao, H., Zhao, F., Zou, X., Cheng, Z., Li, B., et al. (2020) · Frontiers in Psychology · doi:10.3389/fpsyg.2020.00080 · Cited by 92
Gulyaeva, N. V. (2019) · Biochemistry (Moscow) · doi:10.1134/s0006297919110087 · Cited by 81
Brain glucose metabolism in an animal model of depression
Detka, J., Kurek, A., Kucharczyk, M. W., Głombik, K., Basta‐Kaim, A., Kubera, M., Lasoń, W., & Budziszewska, B. (2015) · Neuroscience · doi:10.1016/j.neuroscience.2015.03.046 · Cited by 86
Maternal depression alters stress and immune biomarkers in mother and child
Ulmer-Yaniv, A., Djalovski, A., Priel, A., Zagoory‐Sharon, O., & Feldman, R. (2018) · Depression and Anxiety · doi:10.1002/da.22818 · Cited by 77
Li, M., Fu, Q., Li, Y., Li, S., Xue, J., & Ma, S. (2014) · Fitoterapia · doi:10.1016/j.fitote.2014.06.007 · Cited by 79
The Neurobiological Pathogenesis of Poststroke Depression
Feng, C., Fang, M., & Liu, X. (2014) · The Scientific World JOURNAL · doi:10.1155/2014/521349 · Cited by 82
Au, B., Smith, K. J., Gariépy, G., & Schmitz, N. (2015) · International Journal of Geriatric Psychiatry · doi:10.1002/gps.4250 · Cited by 79
Biomarker Approaches in Major Depressive Disorder Evaluated in the Context of Current Hypotheses
Jentsch, M., van Buel, E. M., Bosker, F. J., Gladkevich, A. V., Klein, H. C., Voshaar, R. C. O., Ruhé, H. G., Eisel, U. L., & Schoevers, R. A. (2015) · Biomarkers in Medicine · doi:10.2217/bmm.14.114 · Cited by 84
Detka, J., & Głombik, K. (2021) · Pharmacological Reports · doi:10.1007/s43440-021-00274-8 · Cited by 79
Depression and Visual Functioning in Patients With Ocular Inflammatory Disease
Ying, Q., Glaser, T. S., Esterberg, E. J., & Acharya, N. R. (2011) · American Journal of Ophthalmology · doi:10.1016/j.ajo.2011.06.028 · Cited by 78
Pretransplant depression, antidepressant use, and outcomes of orthotopic liver transplantation
Rogal, S. S., Landsittel, D. P., Surman, O. S., Chung, R. T., & Rutherford, A. (2010) · Liver Transplantation · doi:10.1002/lt.22231 · Cited by 76
Effect of combined chronic predictable and unpredictable stress on depression-like symptoms in mice
Qiao, Y., Zhao, J., Li, C., Zhang, M., Wei, L., Zhang, X., Kurskaia, O. V., Bi, H., & Gao, T. (2020) · Annals of Translational Medicine · doi:10.21037/atm-20-5168 · Cited by 80
Pathomechanisms of Vascular Depression in Older Adults
Jellinger, K. A. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms23010308 · Cited by 82
The role of inflammatory cytokines on the aetiopathogenesis of depression
Makhija, K., & Karunakaran, S. (2013) · Australian & New Zealand Journal of Psychiatry · doi:10.1177/0004867413488220 · Cited by 81
Inflammation and Immune Regulation as Potential Drug Targets in Antidepressant Treatment
Schmidt, F. M., Kirkby, K. C., & Lichtblau, N. (2016) · Current Neuropharmacology · doi:10.2174/1570159x14666160115130414 · Cited by 75
Kong, H., Zeng, X., Fan, Y., Yuan, S., Ge, S., Xie, W., Wang, H., & Hu, G. (2014) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.12222 · Cited by 72
Gragnoli, C. (2014) · The Application of Clinical Genetics · doi:10.2147/tacg.s39993 · Cited by 74
Pandemic-related mental health risk among front line personnel
Wright, H. M., Griffin, B. J., Shoji, K., Love, T. M., Langenecker, S. A., Benight, C. C., & Smith, A. J. (2021) · Journal of Psychiatric Research · doi:10.1016/j.jpsychires.2020.10.045 · Cited by 69
Everyday discrimination and subsequent cognitive abilities across five domains.
Zahodne, L. B., Morris, E. P., Sharifian, N., Zaheed, A. B., Kraal, A. Z., & Sol, K. (2020) · Neuropsychology · doi:10.1037/neu0000693 · Cited by 72
Neuroprotective offerings by agmatine
(2019) · doi:10.1016/j.neuro.2019.05.001 · Cited by 72
Effect of caloric restriction on depression
Manchishi, S. M., Cui, R., Zou, X. H., Cheng, Z. Q., & Li, B. J. (2018) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.13418 · Cited by 71
Animal models of fibromyalgia: What is the best choice?
Brum, E. S., Becker, G., Fialho, M. F. P., & Oliveira, S. M. (2022) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2021.107959 · Cited by 71
The role and mechanism of tryptophan – kynurenine metabolic pathway in depression
Gong, X., Chang, R., Zou, J., Tan, S., & Huang, Z. (2022) · Reviews in the Neurosciences · doi:10.1515/revneuro-2022-0047 · Cited by 72
Depression in polycystic ovary syndrome: Focusing on pathogenesis and treatment
Xing, L., Xu, J., Wei, Y., Chen, Y., Zhuang, H., Tang, W., Yu, S., Zhang, J., Yin, G., Wang, R., et al. (2022) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2022.1001484 · Cited by 78
Chang, J. P., Chang, S., Yang, H.-T., Chen, H.-T., Chien, Y.-C., Yang, B., Su, H., & Su, K. (2019) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2019.03.012 · Cited by 68
Animal inflammation-based models of depression and their application to drug discovery
Ma, L., Demin, K. A., Kolesnikova, T. O., Kharsko, S. L., Zhu, X., Yuan, X., Song, C., Мешалкина, Д. А., Leonard, B. E., Tian, L., et al. (2017) · Expert Opinion on Drug Discovery · doi:10.1080/17460441.2017.1362385 · Cited by 71
Sturm, M., Becker, A., Schroeder, A., Bilkei‐Gorzó, A., & Zimmer, A. (2015) · Genes Brain & Behavior · doi:10.1111/gbb.12208 · Cited by 68
Poole, L., & Steptoe, A. (2018) · Journal of Psychosomatic Research · doi:10.1016/j.jpsychores.2018.07.009 · Cited by 69
Crosstalk between endocannabinoid and immune systems: a potential dysregulation in depression?
Boorman, E., Zajkowska, Z., Ahmed, R., Pariante, C. M., & Zunszain, P. A. (2015) · Psychopharmacology · doi:10.1007/s00213-015-4105-9 · Cited by 68
Self-citationLee, S., Kim, H.-B., Hwang, E., Kim, E.-S., Kim, S. S., Jeon, T.-D., Song, M.-C., Lee, J.-S., Chung, M.-C., Maeng, S., et al. (2018) · Experimental Neurobiology · doi:10.5607/en.2018.27.3.189 · Cited by 66
Silverman, M. N., Mukhopadhyay, P., Belyavskaya, E., Tonelli, L. H., Revenis, B. D., Doran, J. H., Ballard, B. E., Tam, J., Pacher, P., & Sternberg, E. M. (2013) · Molecular Psychiatry · doi:10.1038/mp.2012.131 · Cited by 64
Amani, M., Shokouhi, G., & Salari, A. (2018) · Psychopharmacology · doi:10.1007/s00213-018-5137-8 · Cited by 63
Domingues, M., Casaril, A. M., Birmann, P. T., Bampi, S. R., Lourenço, D. D. A., Vieira, B. M., Dapper, L. H., Lenardão, E. J., Sonego, M., Collares, T., et al. (2019) · Behavioural Brain Research · doi:10.1016/j.bbr.2019.03.021 · Cited by 64
Understanding the Connection Between the Gut–Brain Axis and Stress/Anxiety Disorders
Lee, Y.-J., & Kim, Y. (2021) · Current Psychiatry Reports · doi:10.1007/s11920-021-01235-x · Cited by 68
Enhanced antidepressant effects of BDNF-quercetin alginate nanogels for depression therapy
Xu, D. W., Gao, L., Song, X., Dong, Q.-W., Chen, Y., Cui, Y., & Wang, Q. (2023) · Journal of Nanobiotechnology · doi:10.1186/s12951-023-02150-4 · Cited by 70
Effect of meditation on neurophysiological changes in stress mediated depression
Kasala, E. R., Bodduluru, L. N., Maneti, Y., & Thipparaboina, R. (2013) · Complementary Therapies in Clinical Practice · doi:10.1016/j.ctcp.2013.10.001 · Cited by 67
Yi, L., Li, J., Li, H.-C., Su, D.-X., Quan, X.-B., He, X.-C., & Wang, X. (2012) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2012.06.009 · Cited by 66
Agmatine Induces Nrf2 and Protects Against Corticosterone Effects in Hippocampal Neuronal Cell Line
Freitas, A. E., Egea, J., Buendía, I., Navarro, E., Rada, P., Cuadrado, A., Rodrigues, A. L. S., & López, M. G. (2014) · Molecular Neurobiology · doi:10.1007/s12035-014-8827-1 · Cited by 59
Caceres-Cardenas, G., Calderón, R., & Ugarte‐Gil, C. (2022) · Therapeutic Advances in Infectious Disease · doi:10.1177/20499361221095831 · Cited by 80
Horowitz, M. A., Cattaneo, A., Cattane, N., Lopizzo, N., Tojo, L. M., Bakunina, N., Musaelyan, K., Borsini, A., Zunszain, P. A., & Pariante, C. M. (2020) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2020.03.012 · Cited by 61
Self-citationEffects of chronic mild stress on behavioral and neurobiological parameters — Role of glucocorticoid
Chen, J., Wang, Z., Zuo, W., Zhang, S., Chu, S., & Chen, N. (2015) · Hormones and Behavior · doi:10.1016/j.yhbeh.2015.11.006 · Cited by 80
Diagnostic Value of Concentration Profiles of Glucocorticosteroids and Endocannabinoids in Hair
Krumbholz, A., Anielski, P., Reisch, N., Schelling, G., & Thieme, D. (2013) · Therapeutic Drug Monitoring · doi:10.1097/ftd.0b013e3182953e43 · Cited by 57
Anacker, C. (2014) · Current topics in behavioral neurosciences · doi:10.1007/7854_2014_275 · Cited by 63
Self-citationGlucocorticoids and Inflammation: A Double-Headed Sword in Depression?
Horowitz, M. A., Zunszain, P. A., Anacker, C., Musaelyan, K., & Pariante, C. M. (2013) · Modern Trends in Psychiatry · doi:10.1159/000343980 · Cited by 57
Self-citationContribution of neural cell death to depressive phenotypes of streptozotocin-induced diabetic mice
Chen, C., Wang, Y., Zhang, J., Ma, L., Gu, J., & Ho, G. (2014) · Disease Models & Mechanisms · doi:10.1242/dmm.016162 · Cited by 58
Quinete, N., Bertram, J., Reska, M., Lang, J., & Kraus, T. (2014) · Talanta · doi:10.1016/j.talanta.2014.11.034 · Cited by 57
Role of yoga in stress management and implications in major depression disorder
Padmavathi, R., Kumar, A., Dhamodhini, K. S., Vijayakumar, V., Silambanan, S., Kuppusamy, M., & Shah, P. B. (2023) · Journal of Ayurveda and Integrative Medicine · doi:10.1016/j.jaim.2023.100767 · Cited by 90
Kim, S. Y., Jeon, S. W., Shin, D., Oh, K., Shin, Y. C., & Lim, S. (2018) · Psychiatry Research · doi:10.1016/j.psychres.2018.08.076 · Cited by 58
Oxidative and Nitrosative stress in major depressive disorder: a case control study
Somani, A., Singh, A. K., Gupta, B., Nagarkoti, S., Dalal, P. K., & Dikshit, M. (2022) · Brain Sciences · doi:10.3390/brainsci12020144 · Cited by 54
“have also reported elevated levels of glucocorticoids in patients with MDD [71].”
BackgroundOgłodek, E. A., Szota, A. M., Just, M. J., Moś, D., & Araszkiewicz, A. S. (2014) · Pharmacological Reports · doi:10.1016/j.pharep.2014.06.001 · Cited by 54
Pala, A. N., Steca, P., Bagrodia, R., Helpman, L., Colangeli, V., Viale, P., & Wainberg, M. L. (2016) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2016.02.013 · Cited by 56
Elevated Brain Glucose and Glycogen Concentrations in an Animal Model of Depression
Detka, J., Kurek, A., Basta‐Kaim, A., Kubera, M., Lasoń, W., & Budziszewska, B. (2014) · Neuroendocrinology · doi:10.1159/000368607 · Cited by 51
Alboni, S., Benatti, C., Montanari, C., Tascedda, F., & Brunello, N. (2013) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2013.08.046 · Cited by 54
Neuroimmune endocrine effects of antidepressants
Carvalho, L. A. (2012) · Neuropsychiatric Disease and Treatment · doi:10.2147/ndt.s16409 · Cited by 52
Self-citationDietary Polyphenols and Their Effects on Cell Biochemistry and Pathophysiology 2013
Maraldi, T., Vauzour, D., & Angeloni, C. (2014) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2014/576363 · Cited by 55
Li, J., Zhou, Y., Liu, B.-B., Liu, Q. F., Geng, D., Lian-jin, W., & Yi, L. (2013) · Evidence-based Complementary and Alternative Medicine · doi:10.1155/2013/359682 · Cited by 52
Hernández, M. E., Cabrera, D. M., Pérez-Tapia, M., Bojalil, R., Estrada‐García, I., Estrada-Parra, S. A., & Pavón, L. (2013) · Clinical and Developmental Immunology · doi:10.1155/2013/267871 · Cited by 53
C-reactive protein and cold-pressor tolerance in the general population: the Tromsø Study
Schistad, E. I., Stubhaug, A., Furberg, A., Engdahl, B., & Nielsen, C. S. (2017) · Pain · doi:10.1097/j.pain.0000000000000912 · Cited by 53
Wu, X., Wu, J., Xia, S., Li, B., & Dong, J. (2013) · Behavioural Brain Research · doi:10.1016/j.bbr.2013.09.034 · Cited by 52
Dattilo, V., Amato, R., Perrotti, N., & Gennarelli, M. (2020) · Frontiers in Genetics · doi:10.3389/fgene.2020.00826 · Cited by 49
Flavonols in Action: Targeting Oxidative Stress and Neuroinflammation in Major Depressive Disorder
Jembrek, M. J., Oršolić, N., Karlović, D., & Peitl, V. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24086888 · Cited by 58
Wolkow, A., Ferguson, S., Aisbett, B., & Main, L. (2015) · International Journal of Occupational Medicine and Environmental Health · doi:10.13075/ijomeh.1896.00227 · Cited by 50
Targeting GLP-1 receptors to reduce nicotine use disorder: Preclinical and clinical evidence
Herman, R. J., & Schmidt, H. D. (2024) · Physiology & Behavior · doi:10.1016/j.physbeh.2024.114565 · Cited by 54
Yi, L., Li, J., Li, H.-C., Zhou, Y., Su, B.-F., Yang, K., Jiang, M., & Zhang, Y. (2012) · Journal of Ethnopharmacology · doi:10.1016/j.jep.2012.09.016 · Cited by 49
The role of the gut microbiota in schizophrenia: Current and future perspectives
Rodrígues-Amorím, D., Baltanás, T. R., Regueiro, B. J., Spuch, C., Heras, M. E. D. L., Méndez, R. V.-N., Nieto-Araujo, M., Barreiro-Villar, C., Olivares, J. M., & Agís‐Balboa, R. C. (2018) · The World Journal of Biological Psychiatry · doi:10.1080/15622975.2018.1433878 · Cited by 51
Anxiety and depression in rheumatologic diseases: the relevance of diagnosis and management
Torta, R., Pennazio, F., & Ieraci, V. (2014) · Reumatismo · doi:10.4081/reumatismo.2014.769 · Cited by 40
Chemokine profile in women with moderate to severe anxiety and depression during pregnancy
Camacho-Arroyo, I., Flores-Ramos, M., Mancilla-Herrera, I., Cruz, F. M. C., Hernández-Ruiz, J., Diaz, G. P., Labonne, B. F., del Pilar Meza-Rodríguez, M., & Gelman, P. L. (2021) · BMC Pregnancy and Childbirth · doi:10.1186/s12884-021-04225-2 · Cited by 41
Mitić, M., Simic, I., Djordjevic, J., Radojcic, M. B., & Adžić, M. (2013) · Neuropharmacology · doi:10.1016/j.neuropharm.2012.12.012 · Cited by 46
Sun, R., Zhao, Z., Feng, J., Bo, J., Rong, H., Lei, Y., Lu, C., Zhang, X., Hou, B., Sun, Y., et al. (2016) · Molecular Neurobiology · doi:10.1007/s12035-016-9976-1 · Cited by 45
Almeida, J., Duarte, J. O., de Oliveira, L. L., & Crestani, C. C. (2015) · Stress · doi:10.3109/10253890.2015.1038993 · Cited by 45
Cubała, W. J., & Landowski, J. (2013) · Journal of Affective Disorders · doi:10.1016/j.jad.2013.10.004 · Cited by 45
Cortisol, oxytocin, and quality of life in major depressive disorder
Tang, A. L., Thomas, S. J., & Larkin, T. (2019) · Quality of Life Research · doi:10.1007/s11136-019-02236-3 · Cited by 45
Nonhuman Primate Models of Depression: Effects of Early Experience and Stress
Worlein, J. M. (2014) · ILAR Journal · doi:10.1093/ilar/ilu030 · Cited by 45
Developmental mechanisms in the prodrome to psychosis
Walker, E. F., Trotman, H. D., Goulding, S. M., Holtzman, C. W., Ryan, A. T., McDonald, A., Shapiro, D. I., & Brasfield, J. L. (2013) · Development and Psychopathology · doi:10.1017/s0954579413000783 · Cited by 46
Correia, A. S., Cardoso, A., & Vale, N. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22168525 · Cited by 46
Smith, R. S., Alkozei, A., Killgore, W. D. S., & Lane, R. D. (2017) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2017.09.011 · Cited by 39
Bottemanne, H., Gouraud, C., Hulot, J., Blanchard, A., Ranque, B., Lahlou‐Laforêt, K., Limosin, F., Günther, S., Lebeaux, D., & Lemogne, C. (2021) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2021.757685 · Cited by 42
Ancelin, M., Farré, A., Carrière, I., Ritchie, K. A., Chaudieu, I., & Ryan, J. L. (2015) · Translational Psychiatry · doi:10.1038/tp.2014.145 · Cited by 42
Overnight Changes of Immune Parameters and Catecholamines Are Associated With Mood and Stress
Rief, W., Mills, P. J., Ancoli‐Israel, S., Ziegler, M. G., Pung, M. A., & Dimsdale, J. E. (2010) · Psychosomatic Medicine · doi:10.1097/psy.0b013e3181f367e2 · Cited by 40
Toxic stress, inflammation and symptomatology of chronic complications in diabetes
Downs, C. A., & Faulkner, M. S. (2015) · World Journal of Diabetes · doi:10.4239/wjd.v6.i4.554 · Cited by 42
Grygiel‐Górniak, B., Limphaibool, N., & Puszczewicz, M. (2019) · Psychiatry and Clinical Neurosciences · doi:10.1111/pcn.12826 · Cited by 46
Effects of antipsychotics on cortisol, interleukin-6 and hippocampal perfusion in healthy volunteers
Handley, R., Mondelli, V., Zelaya, F., Marques, T., Taylor, H., Reinders, A. A. T. S., Chaddock, C., McQueen, G., Hubbard, K., Papadopoulos, A., et al. (2016) · Schizophrenia Research · doi:10.1016/j.schres.2016.03.039 · Cited by 42
“It is well known that HPA axis can affect regulation of immune system, and vice versa (Zunszain et al., 2011), partly through shared down-stream molecular pathways, such as the NF-κB; it is therefore possible that the effect of haloperidol on cortisol and IL-6 levels depends, at least partly, on shared underlying mole…”
BackgroundNguyen, V., Carey, L. M., Giummarra, L., Faou, P., Cooke, I., Howells, D. W., Tse, T., Macaulay, S. L., Ma, H., Davis, S. M., et al. (2016) · Frontiers in Neurology · doi:10.3389/fneur.2016.00085 · Cited by 41
D'Elia, A. T., Juruena, M. F., Coimbra, B. M., Mello, M. F., & Mello, A. F. (2021) · BMC Psychiatry · doi:10.1186/s12888-021-03170-w · Cited by 44
Lopresti, A. L., Smith, S. J., & Drummond, P. D. (2021) · Nutritional Neuroscience · doi:10.1080/1028415x.2021.1892253 · Cited by 48
Wu‐Chung, E. L., Leal, S. L., Denny, B. T., Cheng, S. L., & Fagundes, C. P. (2021) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2021.12.010 · Cited by 49
Saggu, S., Pless, A., Dew, E., Ware, D., Jiao, K., & Wang, Q. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1543730 · Cited by 45
Mechanistic insights into corticosteroids in multiple sclerosis: War horse or chameleon?☆
Krieger, S. C., Sorrells, S. F., Nickerson, M., & Pace, T. W. W. (2014) · Clinical Neurology and Neurosurgery · doi:10.1016/j.clineuro.2013.12.021 · Cited by 40
Zavvari, F., Nahavandi, A., & Goudarzi, M. (2020) · Journal of Chemical Neuroanatomy · doi:10.1016/j.jchemneu.2019.101711 · Cited by 38
Depressive symptoms are associated with reduced neutrophil function in hip fracture patients
Duggal, N. A., Upton, J., Phillips, A. C., Hampson, P., & Lord, J. M. (2013) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2013.07.004 · Cited by 39
“, 1988), due to altered functioning of the glucocorticoid receptor (Zunszain et al., 2011).”
Association between chronic low back pain and degree of stress: a nationwide cross-sectional study
Choi, S., Nah, S., Jang, H., Moon, J. E., & Han, S. (2021) · Scientific Reports · doi:10.1038/s41598-021-94001-1 · Cited by 53
Twayej, A. J., Al‐Hakeim, H. K., Al-Dujaili, A. H., & Maes, M. H. J. (2019) · The World Journal of Biological Psychiatry · doi:10.1080/15622975.2019.1612090 · Cited by 33
Maffioletti, E., Minelli, A., Tardito, D., & Gennarelli, M. (2020) · Genes · doi:10.3390/genes11091089 · Cited by 36
Metadata
- Authors
- Zunszain, P. A., Anacker, C., Cattaneo, A., Carvalho, L. A., & Pariante, C. M.
- Affiliations
- King's College London (GB)
- Corresponding author
- Zunszain, Patricia A.
- ORCID
- Venue
- Progress in Neuro-Psychopharmacology and Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2011-04
- Volume
- 35
- Issue
- 3
- Pages
- 722-729
- ISSN
- 0278-5846 (ISSN-L)
- PMC
- PMC3513408
- OpenAlex
- W2025129891
- Semantic Scholar
- 76fbf367d3a4a4a1d2c2bfe385e7b6268c49e3b0
- Cited by
- 554
- References
- 124
- Citations by year
- 2026: 18 · 2025: 31 · 2024: 30 · 2023: 30 · 2022: 33 · 2021: 52 · 2020: 39 · 2019: 34 · 2018: 44 · 2017: 31 · 2016: 38 · 2015: 42 · 2014: 40 · 2013: 40 · 2012: 31
- FWCI
- 2.57
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Progress in Neuro-Psychopharmacology and Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Research Portal (King's College London) (submittedVersion)
- Funders
- National Institute for Health and Care Research
- NIHR Sheffield Biomedical Research Centre
- 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, glucocorticoids, cortisol, inflammatory cytokines, hypothalamic-pituitary-adrenal axis, glucocorticoid resistance, neuroinflammation, neurodegeneration, kynurenine pathway, neuroendocrine-immune interaction, depression pathophysiology
- MeSH terms
- Animals, Brain, Depression, Female, Glucocorticoids, Humans, Inflammation, Male, Nerve Degeneration, Cytokines, Neurodegenerative Diseases
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 2026-10-06, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-06 (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 ›
Are you an author, or do you see a problem with this page? Request a review
