Higher CSF interleukin-6 and CSF interleukin-8 in current depression in older women. Results from a population-based sample

Kern, Silke; Skoog, Ingmar; Börjesson‐Hanson, Anne; Blennow, Kaj; Zetterberg, Henrik; Östling, Svante; Kern, Jürgen; Gudmundsson, Pia; Marlow, Thomas; Rosengren, Lars; Wærn, Margda

doi:10.1016/j.bbi.2014.05.006

Cited by 79 publications

(64 citation statements)

References 22 publications

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“…Pomara and colleagues (Pomara et al , 2012) found higher F2-isoprostane CSF levels indicating pro-oxidative stress status in LLD. Kern and colleagues (Kern et al , 2014) found higher CSF levels of IL-6 and IL-8 in older adults with LLD suggesting older adults with LLD present with pro-inflammatory status. In a recent study, we found that despite no significant differences in AD-related biomarkers, older adults with LLD had significantly lower CSF BDNF levels compared to non depressed control subjects (Diniz et al , 2014).…”

Section: Discussionmentioning

confidence: 99%

Plasma and cerebrospinal fluid amyloid-β levels in late-life depression: A systematic review and meta-analysis

Nascimento

Silva

Malloy-Diniz

et al. 2015

Journal of Psychiatric Research

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This study aimed to evaluate differences in plasma and cerebrospinal fluid (CSF) levels of Aβ peptides in older adults with late-life depression compared to non-depressed older controls. We conducted a systematic review and meta-analysis of the literature using PubMed, Web of science and Scopus databases with no search limits for publication dates or languages. Two independent reviewers extracted data and assessed quality. Six hundred references were retrieved, and we included 12 studies in the meta-analysis after eligibility screening. Older adults with late-life depression (LLD) had a higher plasma Aβ40:Aβ42 ratio compared to non-depressed participants (SMD= 1.10, CI95% [0.28; 1.96], p=0.01), and marginally significant reduction of CSF Aβ42 levels (SMD= −1.12, CI95% [−2.47; 0.22], p=0.1). The present results evidence that older adults with depression have significant differences in Aβ metabolism, in the same direction observed in individuals with AD. These differences in the Aβ metabolism may help identify a subgroup of subjects with LLD at higher risk of developing AD.

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Section: Discussionmentioning

confidence: 99%

Plasma and cerebrospinal fluid amyloid-β levels in late-life depression: A systematic review and meta-analysis

Nascimento

Silva

Malloy-Diniz

et al. 2015

Journal of Psychiatric Research

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“…Elevations of IL-6 in the cerebral spinal fluid (CSF) were found in older women with depression (Kern et al., 2014), in patients with either depression or schizophrenia (Sasayama et al., 2013), suicide attempters (Lindqvist et al., 2009) and women experiencing post-partum depression (Boufidou et al., 2009). Interestingly, studies that examined both plasma and CSF levels of IL-6 did not find correlations between the measures, suggesting that peripheral IL-6 levels do not necessarily directly reflect central IL-6 levels (Boufidou et al., 2009 Lindqvist et al., 2009, Sasayama et al., 2013).…”

Section: Central Il-6 Contributes To Stress Sensitivitymentioning

confidence: 99%

Integrating Interleukin-6 into depression diagnosis and treatment

Hodes

Ménard

Russo

2016

Neurobiology of Stress

226

144

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There is growing evidence of a relationship between inflammation and psychiatric illness. In particular, the cytokine Interleukin-6 (IL-6) has been linked to stress-related disorders such as depression and anxiety. Here we discuss evidence from preclinical and clinical studies examining the role of IL-6 in mood disorders. We focus on the functional role of peripheral and central release of IL-6 on the development of stress susceptibility and depression-associated behavior. By examining the contribution of both peripheral and central IL-6 to manifestations of stress-related symptomatology, we hope to broaden the way the field thinks about diagnosing and treating mood disorders.

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“…As described in the introduction, there is considerable evidence to suggest that elevated neuroinflammation occurs in subsets of depressed patients and may be correlated to symptom severity (Sasayama et al., 2013, Kern et al., 2014, Devorak et al., 2015, Setiawan et al., 2015). Animal studies of social defeat stress corroborate these findings by revealing that social stress exposure leads to long lasting increases in not only the number of macrophages and activated microglia in the brain (Stankiewicz et al., 2015), but also exaggerated activation of these cell types, promoting increased expression of pro-inflammatory cytokines such as IL-1β and TNF-α (Wohleb et al., 2011, Wohleb et al., 2012, Wohleb et al., 2014a).…”

Section: Individual Differences In Social Stress-induced Neuroinflammmentioning

confidence: 99%

“…Approximately 10–30% of those suffering from depression exhibit treatment resistance (Al-Harbi, 2012), which has been linked to an increase in circulating cytokines (Maes et al., 1997, Musselman et al., 2001b, Miller et al., 2002, Alesci et al., 2005, Motivala et al., 2005, Raison et al., 2013). Although much of what is known about inflammation and depression has been determined by studying cytokine levels in the plasma, elevated pro-inflammatory cytokines are also reported in the cerebrospinal fluid (CSF) of subpopulations of depressed patients (Sasayama et al., 2013, Kern et al., 2014, Devorak et al., 2015). It has only recently been shown for the first time using positron emission tomography that microglial activation is increased in the brains of depressed patients compared to healthy controls, and was positively correlated with severity of depressive symptoms (Setiawan et al., 2015).…”

Section: Introductionmentioning

confidence: 99%

Neuroinflammation at the interface of depression and cardiovascular disease: Evidence from rodent models of social stress

Finnell

Wood

2016

Neurobiology of Stress

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A large body of evidence has emerged linking stressful experiences, particularly from one's social environment, with psychiatric disorders. However, vast individual differences emerge in susceptibility to developing stress-related pathology which may be due to distinct differences in the inflammatory response to social stress. Furthermore, depression is an independent risk factor for cardiovascular disease, another inflammatory-related disease, and results in increased mortality in depressed patients. This review is focused on discussing evidence for stress exposure resulting in persistent or sensitized inflammation in one individual while this response is lacking in others. Particular focus will be directed towards reviewing the literature underlying the impact that neuroinflammation has on neurotransmitters and neuropeptides that could be involved in the pathogenesis of comorbid depression and cardiovascular disease. Finally, the theme throughout the review will be to explore the notion that stress-induced inflammation is a key player in the high rate of comorbidity between psychosocial disorders and cardiovascular disease.

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Higher CSF interleukin-6 and CSF interleukin-8 in current depression in older women. Results from a population-based sample

Cited by 79 publications

References 22 publications

Plasma and cerebrospinal fluid amyloid-β levels in late-life depression: A systematic review and meta-analysis

Plasma and cerebrospinal fluid amyloid-β levels in late-life depression: A systematic review and meta-analysis

Integrating Interleukin-6 into depression diagnosis and treatment

Neuroinflammation at the interface of depression and cardiovascular disease: Evidence from rodent models of social stress

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