Inflammation in neurological and psychiatric diseases

Khansari, Parto S.; Sperlágh, Beáta

doi:10.1007/s10787-012-0124-x

Cited by 53 publications

(25 citation statements)

References 68 publications

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“…Neuroinflammation occurs in a wide range of brain disorders, from neurodegenerative diseases and central nervous system infection to major depressive disorders, autism, and traumatic brain injury (Glass et al, 2010; Khansari and Sperlagh, 2012; Kolb et al, 1999; Vargas et al, 2005; Ziebell and Morganti-Kossmann, 2010). The opioid antagonist, β-FNA crosses the blood-brain barrier (Labuz et al 2007) and is well-tolerated (Egashira et al 2012; Jang and Yoburn 1991; Valle et al 2001).…”

Section: Discussionmentioning

confidence: 99%

The opioid antagonist, β-funaltrexamine, inhibits NF-κB signaling and chemokine expression in human astrocytes and in mice

Davis

Das

Curtis

et al. 2015

European Journal of Pharmacology

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Opioid-immune crosstalk occurs when opioid drugs alter the activity of the immune system. In this study, the opioid antagonist β-funaltrexamine (β-FNA) decreases the expression and release of an inflammatory chemokine, interferon-γ inducible protein-10 (CXCL10) from normal human astrocytes stimulated by interleukin 1β (IL-1β). β-FNA decreased CXCL10 by an unknown action that did not involve the mu opioid receptor (MOR). As IL-1β acts through its receptor to activate NF-κB/MAPK signaling pathways which leads to CXCL10 expression and release, key steps in the IL-1β signaling pathways were examined following β-FNA treatment. IL-1β-induced activation of p38 mitogen-activated protein kinases (p38 MAPK) was inhibited by β-FNA as shown by decreased p38 MAPK phosphorylation in treated cells. β-FNA also decreased the levels of activated subunits of NF-κB (p50 and p65) in treated astrocytes. The impact of β-FNA was also observed in proteins that act to negatively regulate NF-κB signaling. IL-1β upregulated the expression of A20, a ubiquitin (Ub)-editing enzyme that dampens NF-κB signaling by altering ubiquination patterns on IL-1 receptor second messengers, and the increase in A20 was significantly inhibited by β-FNA treatment. Inhibition of the Ub-activating enzyme E1 by the inhibitor PYR41 also decreased CXCL10 release, like β-FNA, and concurrent treatment with both PYR41 and β-FNA inhibited CXCL10 more than did either agent alone. In mice, lipopolysaccharide-induced CXCL10 expression in the brain was inhibited by treatment with β-FNA. These findings suggest that β-FNA exerts an anti-inflammatory action in vitro and in vivo that is MOR-independent and possibly due to the alkylating ability of β-FNA.

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Section: Discussionmentioning

confidence: 99%

The opioid antagonist, β-funaltrexamine, inhibits NF-κB signaling and chemokine expression in human astrocytes and in mice

Davis

Das

Curtis

et al. 2015

European Journal of Pharmacology

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“…23 Compelling evidence suggests that persistent inflammation can also result in neurodegenerative and neuropsychiatric diseases, including depression. 21,24,25 Inflammatory cytokines are observed to cross the blood-brain barrier and interact with a number of pathophysiologic mechanisms associated with depression, including neural plasticity, neurotransmitter metabolism, and regulation of the hypothalamic-pituitary-adrenal (HPA) axis. 26 Furthermore, studies have demonstrated that exogenous infusion of cytokines can lead to depressive-like symptoms and behaviors.…”

Section: Introductionmentioning

confidence: 99%

The association of dietary inflammatory potential with depression and mental well-being among U.S. adults

Bergmans

Malecki

2017

Preventive Medicine

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Current treatment for depression is not considered effective among all cases and, thus far, nutritional protocols are minimal within depression treatment guidelines. Recently, there has been increasing interest in a possible protective and modifiable role of diet in common mental disorders, including depression, due to pro- and anti-inflammatory properties of nutrients. This study aims to investigate whether the Dietary Inflammatory Index (DII), designed to estimate the inflammatory potential of diet, is associated with depression and other measures of mental health. In a representative sample of U.S. adults (>20 years of age, N=11,592), the distribution of DII score is assessed. Multivariate logistic regression models determine the association between DII quintile and depression. Associations of DII quintile with frequent distress and frequent anxiety are also evaluated. In fully adjusted models, higher DII score is associated with over a twofold higher odds of depression (OR (95% CI) = 2.26 (1.60, 3.20) for highest vs. lowest quintile, Type III p-value = <0.0001). DII score is also associated with higher odds of frequent distress (OR (95% CI) = 1.81 (1.20, 2.71) for highest vs. lowest quintile, Type III p-value = 0.0167). This association was not significant for frequent anxiety (Type III p-value = 0.12). Results of this study indicate that dietary inflammatory potential is associated with depression. These results support existing hypotheses that inflammatory pathways play a role in the etiology of depression. Further research examining the underlying biological and cellular mechanisms of depression is warranted.

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“…It is demonstrated that morphological changes are indicators of microglial activation and inflammation surrounding the amyloid plaques [6]. Activation of astrocytes and microglia and releasing of proinflammatory cytokines and chemokines are the main source of the neuroinflammation [7].…”

Section: Introductionmentioning

confidence: 99%

The Evaluation of Neutrophil-Lymphocyte Ratio in Alzheimers Disease

Kuyumcu

Yeşil²,

Öztürk³

et al. 2012

Dement Geriatr Cogn Disord

203

136

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Background/Aim: There is growing consensus in the literature that inflammation plays a significant role in the pathophysiology of Alzheimer’s disease (AD). The blood neutrophil-lymphocyte ratio (NLR) is a new, inexpensive and easily applicable marker of inflammation. The aim of this study was to investigate the association between NLR, as an inflammatory biomarker, and AD. Methods: 241 AD patients and 175 patients with normal cognitive function were evaluated in this study. Results: The mean ± SD NLR of AD patients was significantly higher than that of patients with normal cognitive function (3.21 ± 1.35 vs. 2.07 ± 0.74, p < 0.001, respectively). Receiver operating characteristic curve analysis suggested that the optimum NLR cutoff point for AD was 2.48 with 69.29% sensitivity, 79.43% specificity, 82.30% positive predictive values and 65.30% negative predictive values. Logistic regression analysis showed that elevated NLR (OR: 4.774, 95% CI: 2.821–8.076, p < 0.001) was an independent variable for predicting AD. Conclusion: Elderly people with AD have higher NLR than healthy controls. Elevated NLR levels are usually considered as an inflammatory marker. The results of this study suggested that inflammation plays a role in the pathogenesis of AD.

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Inflammation in neurological and psychiatric diseases

Cited by 53 publications

References 68 publications

The opioid antagonist, β-funaltrexamine, inhibits NF-κB signaling and chemokine expression in human astrocytes and in mice

The opioid antagonist, β-funaltrexamine, inhibits NF-κB signaling and chemokine expression in human astrocytes and in mice

The association of dietary inflammatory potential with depression and mental well-being among U.S. adults

The Evaluation of Neutrophil-Lymphocyte Ratio in Alzheimers Disease

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Inflammation in neurological and psychiatric diseases

Cited by 53 publications

References 68 publications

The opioid antagonist, β-funaltrexamine, inhibits NF-κB signaling and chemokine expression in human astrocytes and in mice

The opioid antagonist, β-funaltrexamine, inhibits NF-κB signaling and chemokine expression in human astrocytes and in mice

The association of dietary inflammatory potential with depression and mental well-being among U.S. adults

The Evaluation of Neutrophil-Lymphocyte Ratio in Alzheimers Disease

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Product

Resources

About

The Evaluation of Neutrophil-Lymphocyte Ratio in Alzheimers Disease