The role of inflammation in core features of depression: Insights from paradigms using exogenously-induced inflammation.

In the paper

“For example, only acute inflammatory challenges appear to induce increases in reactivity to the environment, whereas altered reward processing appears to only be observed in studies with high doses of inflammation regardless of their acute or chronic nature.”

In the paper

“This is exemplified by typhoid vaccine studies which can lead to increases in fatigue within 2–3 hours despite eliciting only mild, acute increases in inflammation (Brydon et al., 2008).”

What the sources say

• Not checked yetcites Brydon et al., 2008 source

In the paper

“Further, IFN-α and typhoid studies have documented links between increases in inflammation and subjective cognitive complaints (Brydon et al., 2009; Capuron et al., 2002; Harrison et al., 2009).”

What the sources say

• Not checked yetcites Brydon et al., 2009 source
• Not checked yetcites Capuron et al., 2002 source
• Not checked yetcites Harrison et al., 2009 source

In the paper

“Similar results have been observed in endotoxin studies, which document elevations in fatigue and other sickness symptoms that peak 2 hours post injection (Eisenberger et al., 2010; Moieni et al., 2015).”

What the sources say

• Not checked yetcites Eisenberger et al., 2010
• Not checked yetcites Moieni et al., 2015 source

In the paper

“However, results from both endotoxin and IFN-α studies were fairly consistent in showing no effects across a range of tasks assessing different aspects of executive function.”

In the paper

“Finally, we found very little evidence that cognitive control, as assessed by validated neuropsychological measures of executive function, was affected by exogenously-induced inflammation in either the endotoxin or the IFN-α model.”

In the paper

“Overall, there is strong and consistent evidence that inflammation leads to changes in somatic symptoms of depression across paradigms.”

In the paper

“That being said, there is no published evidence for or against the role of INF-α in reactivity to negative information, and little behavioral evidence on the role of mild inflammatory challenges in reward processing.”

In the paper

“For example, only acute inflammatory challenges appear to induce increases in reactivity to the environment, whereas altered reward processing appears to only be observed in studies with high doses of inflammation regardless of their acute or chronic nature.”

In the paper

“Indeed, these studies found that major depression was more likely to develop in individuals with pre-existing, subclinical cognitive disturbance (pessimistic thoughts) prior to the initiation of treatment (Capuron et al., 2004).”

What the sources say

• Not checked yetcites Capuron et al., 2004

In the paper

“Further, the cognitive/affective symptoms were more responsive to paroxetine than symptoms of fatigue (Capuron et al., 2002).”

What the sources say

• Not checked yetcites Capuron et al., 2002 source

In the paper

“That being said, there is no published evidence for or against the role of INF-α in reactivity to negative information, and little behavioral evidence on the role of mild inflammatory challenges in reward processing.”

In the paper

“In addition, Eisenberger et al. (2010b) found that feelings of social disconnection following endotoxin persisted for two hours after depressed mood had recovered.”

• Also stated in: § A Network Perspective · plain

  “Further, see Figure 1 of Eisenberger et al., (2010b) which illustrates that feelings of social disconnection following endotoxin persist for two hours after depressed mood has recovered.”

What the sources say

• Not checked yetcites Eisenberger et al., 2010b

In the paper

“However, the majority of studies reviewed here did not control for depressed mood in their models, and therefore more careful testing of these associations is warranted to understand the independence or interdependence of depressed mood on these putative endophenotypes.”

In the paper

“Thus, it is likely that a better understanding of Major Depressive Disorder and its effective treatment will emerge by focusing on the role of inflammation in the onset and maintenance of more homogenous core features that are disrupted among depressed patients (Craske, 2012; Gottesman and Gould, 2003; Hasler et al., 2004).”

What the sources say

• Not checked yetcites Craske, 2012 source
• Not checked yetcites Gottesman and Gould, 2003 source
• Not checked yetcites Hasler et al., 2004 source

In the paper

“However, prolonged inflammatory signaling, such as when the inflammatory response is maintained by ongoing psychosocial stress, can have detrimental effects that include risk for depression and other psychiatric diseases (Dantzer et al., 2008; Miller et al., 2009; Miller and Raison, 2016; Slavich and Irwin, 2014).”

What the sources say

• Not checked yetcites Dantzer et al., 2008 source
• Not checked yetcites Miller et al., 2009 source
• Not checked yetcites Miller and Raison, 2016 source

In the paper

“However, inflammatory cytokines such as TNF-α and IL-1ß interfere with the ability of glial cells to do this by altering their Ca2+ channels. The effect of inflammatory cytokines on calcium ion channels also leads to reverse efflux, which means that instead of glial cells taking in glutamate and detoxifying it, glutamate is released back into the extracellular space (Malarkey and Parpura, 2008).”

What the sources say

• Not checked yetcites Malarkey and Parpura, 2008

In the paper

“For example, inflammatory cytokines can alter neuroplasticity by decreasing expression of the brain-derived neuroprotective hormone BDNF (Calabrese et al., 2014).”

What the sources say

• Not checked yetcites Calabrese et al., 2014 source

In the paper

“Indeed, single injections of high doses of LPS (5 mg/kg) lead to degeneration in dopaminergic system in the brain, particularly in the substantia nigra and the striatum (Qin et al., 2007; Reinert et al., 2014).”

What the sources say

• Not checked yetcites Qin et al., 2007 source
• Not checked yetcites Reinert et al., 2014 source

In the paper

“Inflammation can impact almost all aspects of glutamate neurotransmission (See Haroon and Miller, 2017 for review).”

What the sources say

• Not checked yetcites Haroon and Miller, 2017 source

In the paper

“There is a wealth of experimental research in rodents demonstrating that decreases in dopamine release and binding to the dopamine receptor is closely linked with deficits in reward-motivated behavior in depression (Nestler and Carlezon, 2006).”

What the sources say

• Not checked yetcites Nestler and Carlezon, 2006 source

In the paper

“In preclinical models, activation of inflammation using LPS increases the activity of IDO thereby allocating more tryptophan metabolism toward the kynurenine pathway rather than serotonin synthesis (Zunszain et al., 2012), ultimately resulting in serotonin deficiency (See Dantzer et al., 2011; Nikkheslat et al., 2018; O’Farrell and Harkin, 2017 for a review of research on the kynurenine pathway).”

What the sources say

• Not checked yetcites Zunszain et al., 2012 source
• Not checked yetcites Dantzer et al., 2011 source
• Not checked yetcites Nikkheslat et al., 2018

In the paper

“Following the summary of the kynurenine pathway in the previous paragraph, QUIN and glutamate released by activated microglia operate synergistically to promote excitotoxicity (Dantzer and Walker, 2014).”

What the sources say

• Not checked yetcites Dantzer and Walker, 2014

In the paper

“In preclinical models, LPS-induced depressive behavior is mediated by IDO activation (O’Connor et al., 2009).”

What the sources say

• Not checked yetcites O’Connor et al., 2009 source

In the paper

“A wealth of evidence has implicated inflammation in the development of depression.”

• Also stated in: § Introduction · plain

  “Substantial evidence across various populations and study designs has implicated inflammation in the etiology of depression (Dantzer et al., 2008; Irwin, 2002; Miller et al., 2009; Raison et al., 2006).”

What the sources say

• Not checked yetcites Dantzer et al., 2008 source
• Not checked yetcites Irwin, 2002 source
• Not checked yetcites Miller et al., 2009 source

In the paper

“Inflammatory cytokines may indirectly upregulate glucocorticoids in the body by interfering with the functional capacity of the glucocorticoid receptor (Pace, Hu, & Miller, 2007; Raison & Miller, 2003), resulting in continued synthesis of corticotropin releasing hormone (CRH) and sustained activation of the HPA-axis which has long been implicated in the pathogenesis of depression (Lopez-Duran et a”

What the sources say

• Not checked yetcites Pace, Hu, & Miller, 2007
• Not checked yetcites Raison & Miller, 2003
• Not checked yetcites Lopez-Duran et al., 2009 source

In the paper

“Inflammation can also lead to changes in dopaminergic systems, with relevance for depression (See Felger, 2017 for review).”

What the sources say

• Not checked yetcites Felger, 2017 source

In the paper

“In addition to effects on dopamine, inflammation can influence the serotonin system through alterations in tryptophan metabolism.”

In the paper

“Research conducted over the last several decades has elucidated the mechanisms by which peripheral inflammation can access the brain to influence neural processes relevant for depression, including neuroplasticity, neurotransmitter systems, and neuroendocrine function (see Banks and Erickson, 2010; Haroon et al., 2012 for comprehensive reviews on this topic).”

What the sources say

• Not checked yetcites Banks and Erickson, 2010
• Not checked yetcites Haroon et al., 2012 source

In the paper

“Depressed individuals also display exaggerated physiological responses to laboratory stress tasks, including norepinephrine and epinephrine (Weinstein et al., 2010).”

What the sources say

• Not checked yetcites Weinstein et al., 2010

In the paper

“Yet, one limitation of this model is its use exclusively in the context of chronic disease (hepatitis C, cancer).”

In the paper

“Additionally, IFN-α treatment results in moderate to robust increases in inflammatory markers that are sustained over weeks, depending on the disease being treated and associated dosing schedule.”

In the paper

“Inflammation may exaggerate affective and physiological reactivity to stressors, thus contributing to reactivity to negative stimuli as seen in depression.”

In the paper

“In this study, vaccine-induced negative mood was associated with enhanced sACC activation to emotional information (Harrison et al., 2009).”

What the sources say

• Not checked yetcites Harrison et al., 2009 source

In the paper

“Similarly, recent data from a study of twin pairs—which holds constant shared genetic and early environmental factors—showed that the twin with higher CRP concentrations at baseline was more likely to develop depression five years later (Huang et al., 2017).”

What the sources say

• Not checked yetcites Huang et al., 2017 source

In the paper

“Additionally, the effects of endotoxin on mood and anxiety appear to manifest in a dose-dependent manner, with higher doses associated with degradations in mood and increases in anxiety (Grigoleit et al., 2011).”

What the sources say

• Not checked yetcites Grigoleit et al., 2011 source

In the paper

“Individuals with depression exhibit increased reactivity to negative information (Gotlib and Joormann, 2010).”

What the sources say

• Not checked yetcites Gotlib and Joormann, 2010

In the paper

“Among individuals with depression, processing of negative information is associated with stronger and longer lasting activation of the amygdala (Beevers et al., 2010; Drevets, 2001; Fu et al., 2004; Siegle et al., 2002; Stuhrmann et al., 2013), a region responsible for interpreting the emotional quality and salience of a given stimulus (Fu et al., 2004).”

What the sources say

• Not checked yetcites Beevers et al., 2010 source
• Not checked yetcites Drevets, 2001 source
• Not checked yetcites Fu et al., 2004

In the paper

“Reactivity to negative information may be sustained due to deficits in left dlPFC inhibitory control over the amygdala (Disner et al., 2011; Drevets, 2001); depressed individuals tend to exhibit anatomical and functional abnormalities in the dlPFC, such as reduced gray matter volume, lower resting-state activity, and decreased activation to emotional stimuli (Gotlib and Hamilton, 2008).”

What the sources say

• Not checked yetcites Disner et al., 2011 source
• Not checked yetcites Drevets, 2001 source

In the paper

“Thus, IFN-α studies model the effects of exposure to chronic inflammation at mild or moderate levels, depending on the indication and associated dosing regimen.”

In the paper

“IFN-α treatment causes symptoms sufficient for a major depression diagnosis in up to 50% of patients (Musselman et al., 2001).”

What the sources say

• Not checked yetcites Musselman et al., 2001 source

In the paper

“A strength of these studies is that the mild increases elicited by typhoid vaccination are comparable to the elevations in inflammation seen in some individuals with depression (Dowlati et al., 2010; Raison and Miller, 2011).”

What the sources say

• Not checked yetcites Dowlati et al., 2010
• Not checked yetcites Raison and Miller, 2011 source

In the paper

“Another study similarly found that endotoxin led to exaggerated amygdala responses to threatening stimuli, particularly socially threatening stimuli (e.g., fear faces versus guns) (Inagaki et al., 2012).”

What the sources say

• Not checked yetcites Inagaki et al., 2012 source

In the paper

“Results from such studies have shown that typhoid vaccination can lead to symptoms relevant to depression, including negative mood, fatigue, and confusion (Harrison et al., 2009; Wright et al., 2005).”

What the sources say

• Not checked yetcites Harrison et al., 2009 source
• Not checked yetcites Wright et al., 2005 source

In the paper

“However, when this circuitry is chronically activated, the chronic expression of behavioral symptoms (including negative mood, fatigue, confusion, and feelings of social disconnection) may culminate into clinically significant depression (Miller et al., 2013).”

What the sources say

• Not checked yetcites Miller et al., 2013

In the paper

“Thus, typhoid vaccine studies model the effects of mild, acute increases in inflammation.”

In the paper

“Overall, the existing literature, though limited in size, supports an effect of inflammation on exaggerated affective and neural reactivity to stressors.”

In the paper

“In summary, preclinical models have elegantly outlined the mechanisms through which inflammation can access the brain to influence neural processes relevant for depression, providing strong mechanistic support for this association.”

In the paper

“Moreover, the exaggerated amygdala response to socially threatening images was associated with increased feelings of social disconnection (Inagaki et al., 2012); thus, inflammation may upregulate amygdala reactivity to social threats, resulting in the experience of social disconnection and withdrawal.”

What the sources say

• Not checked yetcites Inagaki et al., 2012 source

In the paper

“Together, these experimental models have been instrumental in providing causal evidence for an association between inflammation and depression.”

In the paper

“The emerging picture is that proinflammatory cytokines can signal the brain to effectively alter the functioning of threat-related neural circuitry leading to amplified neural responses to stressful information.”

In the paper

“Thus, the endotoxin model can inform our understanding of the acute effects of exposure to high levels of inflammation.”

In the paper

“Endotoxin results in a robust but short-term inflammatory response that ranges from 40 to 190 pg/mL (up to a 38000% increase) two hours after injection depending on the bacterial strain and dose (Andreasen et al., 2008; Grigoleit et al., 2011).”

What the sources say

• Not checked yetcites Andreasen et al., 2008 source
• Not checked yetcites Grigoleit et al., 2011 source

In the paper

“Markers of inflammation are elevated in depressed individuals (Dowlati et al., 2010; Haapakoski et al., 2015; Howren et al., 2009) and predict increases in depressive symptoms in longitudinal studies (Gimeno et al., 2009; Valkanova et al., 2013; van den Biggelaar et al., 2007; Wium-Andersen et al., 2013).”

What the sources say

• Not checked yetcites Gimeno et al., 2009 source
• Not checked yetcites Valkanova et al., 2013 source
• Not checked yetcites van den Biggelaar et al., 2007 source

In the paper

“Some of the earliest evidence of a link between inflammation and depression came from clinical observations of patients with Hepatitis C or cancer, who commonly develop clinically significant depressive symptoms after the initiation of IFN-α therapy (Capuron and Miller, 2004; Raison et al., 2005).”

What the sources say

• Not checked yetcites Capuron and Miller, 2004
• Not checked yetcites Raison et al., 2005 source

In the paper

“Markers of inflammation are elevated in depressed individuals (Dowlati et al., 2010; Haapakoski et al., 2015; Howren et al., 2009) and predict increases in depressive symptoms in longitudinal studies (Gimeno et al., 2009; Valkanova et al., 2013; van den Biggelaar et al., 2007; Wium-Andersen et al., 2013).”

What the sources say

• Not checked yetcites Dowlati et al., 2010
• Not checked yetcites Haapakoski et al., 2015 source
• Not checked yetcites Howren et al., 2009 source

In the paper

“There is a growing body of evidence in humans that inflammation plays a role in the pathogenesis of depression.”

In the paper

“led to blunted substantia nigra reactivity to novel stimuli (Harrison et al., 2015)”

What the sources say

• Not checked yetcites Harrison et al., 2015 source

In the paper

“Among individuals with depression, NAc and PFC activation has been shown to dissipate more quickly following the presentation of positive stimuli, compared to healthy controls (Epstein et al., 2006; Heller et al., 2009).”

What the sources say

• Not checked yetcites Epstein et al., 2006 source
• Not checked yetcites Heller et al., 2009 source

In the paper

“Evidence that inflammation leads to changes in objective measures of cognitive control is decidedly more mixed.”

In the paper

“There is less evidence supporting an effect of inflammation on cognitive control as assessed by standard neuropsychological measures.”

In the paper

“These changes may occur through the effect of proinflammatory cytokines on dopaminergic functioning in the ventral striatum (Capuron et al., 2012), as outlined in section 1.2.”

What the sources say

• Not checked yetcites Capuron et al., 2012 source

In the paper

“Patients exhibited increased uptake and decreased turnover of 18F-dopa in the same ventral striatal regions shown to be effected by IFN-α in the previously mentioned fMRI study (Capuron et al., 2012).”

What the sources say

• Not checked yetcites Capuron et al., 2012 source

In the paper

“Typhoid vaccination (vs. placebo) had no effect on hippocampal activation to novelty”

What the sources say

• Not checked yetcites Harrison et al., 2015 source

In the paper

“In one report, endotoxin (vs. placebo) led to attenuated activation of the left ventral striatum to anticipation of monetary reward (Eisenberger et al., 2010a).”

What the sources say

• Not checked yetcites Eisenberger et al., 2010a

In the paper

“From this work, we have begun to understand the neurobiological mechanisms of the effects of inflammation on reward processing, which may involve alterations in corticostriatal neural circuitry (including the ventral striatum) via modulation of dopamine availability and release (Felger and Treadway, 2016).”

What the sources say

• Not checked yetcites Felger and Treadway, 2016

In the paper

“Additionally, depressed individuals or those with trait-like anhedonia display attenuated reactivity of the NAc to pleasurable stimuli (Harvey et al., 2007; Keedwell et al., 2005), monetary rewards (Pizzagalli et al., 2009; Wacker et al., 2009), and positive words (Epstein et al., 2006).”

What the sources say

• Not checked yetcites Harvey et al., 2007 source
• Not checked yetcites Keedwell et al., 2005 source
• Not checked yetcites Pizzagalli et al., 2009 source

In the paper

“Thus, inflammatory cytokines may influence reward processing by specifically targeting the ventral striatum via dopaminergic functioning.”

In the paper

“For example, after 4–6 weeks of IFN-α therapy, patients with hepatitis C showed significantly attenuated ventral striatal activity (as measured by fMRI) to receipt of monetary rewards in a gambling task when compared with hepatitis C patients not receiving IFN-α (Capuron et al., 2012).”

What the sources say

• Not checked yetcites Capuron et al., 2012 source

In the paper

“Importantly, these alterations in reward processing precede and potentially contribute to the etiology of depression in at-risk groups (Gotlib et al., 2010), and number of prospective studies have shown that self-reported anhedonia (less frequent and intense positive affect) is a strong predictor of subsequent increases in depression severity (Morris et al., 2009).”

What the sources say

• Not checked yetcites Morris et al., 2009 source

In the paper

“Further, blunted ventral striatum activity to anticipated reward mediated the relationship between endotoxin exposure and increases in observer-rated (but not self-reported) depressed mood (Eisenberger et al., 2010a).”

What the sources say

• Not checked yetcites Eisenberger et al., 2010a

In the paper

“In particular, IFN-α treatment has been associated with self-reported cognitive deficits, such as concentration difficulties (Capuron et al., 2002).”

What the sources say

• Not checked yetcites Capuron et al., 2002 source

In the paper

“The hippocampus and substantia nigra (a basal ganglia structure) are central to novelty detection and reward evaluation of novelty (Bunzeck and Düzel, 2006; Lisman and Grace, 2005).”

What the sources say

• Not checked yetcites Bunzeck and Düzel, 2006 source
• Not checked yetcites Lisman and Grace, 2005 source

In the paper

“inflammation can lead to heightened ventral striatal reactivity to social rewards, specifically positive social feedback (Muscatell et al., 2016) and viewing images of close others (Inagaki et al., 2015)”

What the sources say

• Not checked yetcites Muscatell et al., 2016 source
• Not checked yetcites Inagaki et al., 2015 source

In the paper

“There is some evidence that inflammation may elicit changes in the subjective experience of cognitive control.”

In the paper

“Typhoid vaccination increases subjective ratings of mental confusion and impaired concentration (Brydon et al., 2009; Harrison et al., 2009).”

What the sources say

• Not checked yetcites Brydon et al., 2009 source
• Not checked yetcites Harrison et al., 2009 source

In the paper

“Evidence from IFN- α, endotoxin, and typhoid research supports an effect of induced inflammation on aspects of reward.”

In the paper

“Leukemia patients receiving IFN-α treatment showed deficits on the TMT part B (Pavol et al., 1995)”

What the sources say

• Not checked yetcites Pavol et al., 1995 source

In the paper

“there was no significant effect of low-dose endotoxin on n-back task performance”

What the sources say

• Not checked yetcites Grigoleit et al., 2011 source

In the paper

“These, perhaps unexpected, findings may reflect that inflammation facilitates some adaptive behaviors during acute illness or infection, such as drawing an individual closer to potential caretakers and conserving energy by selectively pursuing rewards that are highly likely and valuable (Eisenberger et al., 2016; Lasselin et al., 2016b)”

What the sources say

• Not checked yetcites Eisenberger et al., 2016
• Not checked yetcites Lasselin et al., 2016b

In the paper

“Depressed individuals display attenuated subjective and neural reactivity to positive stimuli, including diminished emotional and affective responses to pleasant stimuli compared with non-depressed controls (Dunn et al., 2004; Sloan et al., 2001, 1997).”

What the sources say

• Not checked yetcites Dunn et al., 2004 source
• Not checked yetcites Sloan et al., 2001 source
• Not checked yetcites Sloan et al., 1997 source

In the paper

“Reduced ventral striatal activation was in turn significantly associated with more severe symptoms of anhedonia, depressed mood, and fatigue (Capuron et al., 2012).”

What the sources say

• Not checked yetcites Capuron et al., 2012 source

In the paper

“hepatitis C patients who received 6 months of IFN-α performed significantly worse on the TMT part B when compared with hepatitis C patients who did not undergo IFN-α treatment (Hilsabeck et al., 2005)”

What the sources say

• Not checked yetcites Hilsabeck et al., 2005 source

In the paper

“In addition to reduced reactivity to reward, there is also evidence that individuals with depression have reduced capacity to sustain positive affect following a reward.”

In the paper

“In summary, all three models of induced inflammation has demonstrated effects on neural responses to reward.”

In the paper

“endotoxin led to increased motivation for monetary rewards using a behavioral measure of reward motivation, the Effort Expenditure for Rewards Task (EEfRT), but only when the probability of winning was high (Lasselin et al., 2016b)”

What the sources say

• Not checked yetcites Lasselin et al., 2016b

In the paper

“Thus, inflammatory signaling may reduce basal ganglia (specifically substantia nigra) responsivity to novel stimuli”

In the paper

“Studies across the endotoxin, typhoid vaccination, and IFN-α paradigms have consistently shown that exogenous stimulation of proinflammatory cytokines leads to reports of increased fatigue (Brydon et al., 2008; Capuron et al., 2002; Dowell et al., 2016; Eisenberger et al., 2010a; Grigoleit et al., 2011; Harrison et al., 2009; Moieni et al., 2015) and decreases in ratings of vigor (Dowell et al., 2”

What the sources say

• Not checked yetcites Dowell et al., 2016 source
• Not checked yetcites Wright et al., 2005 source

In the paper

“Studies across the endotoxin, typhoid vaccination, and IFN-α paradigms have consistently shown that exogenous stimulation of proinflammatory cytokines leads to reports of increased fatigue (Brydon et al., 2008; Capuron et al., 2002; Dowell et al., 2016; Eisenberger et al., 2010a; Grigoleit et al., 2011; Harrison et al., 2009; Moieni et al., 2015) and decreases in ratings of vigor (Dowell et al., 2”

What the sources say

• Not checked yetcites Brydon et al., 2008 source
• Not checked yetcites Capuron et al., 2002 source
• Not checked yetcites Dowell et al., 2016 source

In the paper

“Similarly, two studies among hepatitis C patients (Amodio et al., 2005; Fontana et al., 2007) and one study among melanoma patients (Caraceni et al., 1998) receiving IFN-α therapy found no effect of treatment on digit span performance.”

What the sources say

• Not checked yetcites Amodio et al., 2005 source
• Not checked yetcites Fontana et al., 2007 source
• Not checked yetcites Caraceni et al., 1998 source

In the paper

“At the neural level, fatigue is associated with alterations in dopamine and associated frontostriatal regions (Dobryakova et al., 2015).”

What the sources say

• Not checked yetcites Dobryakova et al., 2015 source

In the paper

“In addition, no significant effects of inflammation on visuospatial working memory were observed following either acute endotoxin (Grigoleit et al., 2010) nor following IFN-α therapy (Caraceni et al., 1998).”

What the sources say

• Not checked yetcites Grigoleit et al., 2010 source
• Not checked yetcites Caraceni et al., 1998 source

In the paper

“Indeed, increased fatigue may be the most consistently reported symptom across these paradigms.”

In the paper

“In summary, detrimental effects of inflammation have not been consistently observed for updating, inhibition, working memory, or planning ability, and in some cases facilitation effects have been observed in these domains.”

In the paper

“Studies using typhoid vaccination to elicit modest increases in inflammation have shown that increases in mood disturbance are driven by increases in items assessing fatigue (as well as confusion), rather than increases in depressed mood (Brydon et al., 2009, 2008; Harrison et al., 2009).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Brydon et al., 2009, 2008
• Not checked yetcites Harrison et al., 2009 source

In the paper

“IFN-α therapy led to reports of fatigue in a sample of patients with malignant melanoma that were positively correlated with increased glucose metabolism in the basal ganglia (the left putamen and left NAc) (Capuron et al., 2007).”

What the sources say

• Not checked yetcites Capuron et al., 2007 source

In the paper

“In another sample of hepatitis C patients, IFN-α treatment elicited increases in fatigue that began 4 hours after patients’ initial IFN-α injection, and continued to persist throughout the 6-month treatment period, peaking between 4–12 weeks (Dowell et al., 2016).”

What the sources say

• Not checked yetcites Dowell et al., 2016 source

In the paper

“In another sample of hepatitis C patients, IFN-α treatment elicited increases in fatigue that began 4 hours after patients’ initial IFN-α injection, and continued to persist throughout the 6-month treatment period, peaking between 4–12 weeks (Dowell et al., 2016).”

What the sources say

• Not checked yetcites Dowell et al., 2016 source

In the paper

“Up to 74% of individual differences in somatic symptoms are explained by genetic factors in twin studies (Kato et al., 2009; Kendler et al., 1992), which supports the co-occurrence of these somatic symptoms as a depression endophenotype.”

In the paper

“Various studies have examined the effect of inflammation on working memory, and have failed to support a role of inflammation in this aspect of executive functioning.”

In the paper

“Stroop performance was not impaired after endotoxin administration at either a low dose (0.4 ng/mL) (Grigoleit et al., 2010) or high dose (2.0 ng/mL) (van den Boogaard et al., 2010).”

What the sources say

• Not checked yetcites Grigoleit et al., 2010 source
• Not checked yetcites van den Boogaard et al., 2010 source

In the paper

“IFN-α therapy led to reports of fatigue in a sample of patients with malignant melanoma that were positively correlated with increased glucose metabolism in the basal ganglia (the left putamen and left NAc) (Capuron et al., 2007).”

What the sources say

• Not checked yetcites Capuron et al., 2007 source

In the paper

“This study used IFN-α (plus ribavirin) as an inflammatory stimulus and measured planning ability with the Stockings of Cambridge task, and no effect of inflammation on planning ability was observed (Majer et al., 2008).”

What the sources say

• Not checked yetcites Majer et al., 2008 source

In the paper

“Similarly, several studies found no effect of IFN-α treatment on verbal fluency (Amodio et al., 2005; Fontana et al., 2007; Pavol et al., 1995)”

What the sources say

• Not checked yetcites Amodio et al., 2005 source
• Not checked yetcites Fontana et al., 2007 source
• Not checked yetcites Pavol et al., 1995 source

In the paper

“There is some evidence that inflammation impairs shifting ability and verbal fluency, yet even in these domains there are more studies reporting null findings than not.”

In the paper

“Brydon et al. (2008) examined Stroop performance after typhoid vaccination, and found that individuals with higher vaccine-induced IL-6 levels had significantly slower reaction times across both incongruent and congruent trials.”

What the sources say

• Not checked yetcites Brydon et al., 2008 source

In the paper

“studies examining effects of both moderate- (0.8 ng/kg) (Reichenberg et al., 2001) and very low-dose (0.2 ng/kg) (Krabbe et al., 2005) endotoxin have failed to find significant effects on performance on the Trail Making Test part B”

What the sources say

• Not checked yetcites Reichenberg et al., 2001 source
• Not checked yetcites Krabbe et al., 2005

In the paper

“The evidence is mixed with regard to the effect of inflammation on verbal fluency.”

In the paper

“Thus, the currently available data provide little evidence that inflammation impairs verbal or visuospatial working memory.”

In the paper

“In summary, detrimental effects of inflammation have not been consistently observed for updating, inhibition, working memory, or planning ability, and in some cases facilitation effects have been observed in these domains.”

In the paper

“A number of studies have examined the effect of inflammation on inhibitory control, as assessed with the color-word Stroop task; most have found no effect.”