Lifestyle and biological factors influence the relationship between mental health and low-grade inflammation

Gialluisi, Alessandro; Bonaccio, Marialaura; Castelnuovo, Augusto Di; Costanzo, Simona; Curtis, Amalia De; Sarchiapone, Marco; Cerletti, Chiara; Donati, M. B.; Gaetano, Giovanni de; Iacoviello, Licia; Investigators, Moli-sani Study

doi:10.1016/j.bbi.2019.04.041

Cited by 50 publications

(37 citation statements)

References 86 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This association was quite robust across varying p-value thresholds (P T ranging from 0.001 to 1.0; Figure 1). Overall, the evidence reported here suggests PDW as a new potential biomarker for Parkinson's disease and is consistent with previous studies reporting positive associations between PDW and depression risk and/or symptoms, both at the epidemiological level (17,24) and at the genetic level (16). Indeed, depression represents one of the main non-motor symptoms of PD, often presenting in its prodromal phase (25), and shows progressive patterns of microglial activation like other neurodegenerative disorders (26).…”

Section: Resultssupporting

confidence: 91%

“…They reported non-significant genetic correlations with both Plt and MPV in the largest PD case-control GWAS metaanalysis carried out so far (involving ∼ 56,300 PD cases and ∼ 1.4 million controls) (15). Of note, in spite of the previous implication of PDW in neurodegenerative disorders (4,(9)(10)(11) and, more recently, in comorbid disorders like major depression (16,17), this parameter has never been investigated with reference to PD risk at the genetic level.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Assessing Genetic Overlap Between Platelet Parameters and Neurodegenerative Disorders

et al. 2020

View full text Add to dashboard Cite

Neurodegenerative disorders such as Parkinson's disease (PD) and Alzheimer's disease (AD) suffer from the lack of risk-predictive circulating biomarkers, and clinical diagnosis occurs only when symptoms are evident. Among potential biomarkers, platelet parameters have been associated with both disorders. However, these associations have been scarcely investigated at the genetic level. Here, we tested genome-wide coheritability based on common genetic variants between platelet parameters and PD/AD risk, through Linkage Disequilibrium Score Regression. This revealed a significant genetic correlation between platelet distribution width (PDW), an index of platelet size variability, and PD risk (r g [SE] = 0.080 [0.034]; p = 0.019), which was confirmed by a summarysummary polygenic score analysis, where PDW explained a small but significant proportion PD risk (<1%). AD risk showed no significant correlations, although a negative trend was observed with PDW (rg [SE] =-0.088 [0.053]; p=0.096), in line with previous epidemiological reports. These findings suggest the existence of limited shared genetic bases between PDW and PD and warrant further investigations to clarify the genes involved in this relation. Additionally, they suggest that the association between platelet parameters and AD risk is more environmental in nature, prompting an investigation into which factors may influence these traits.

show abstract

Section: Resultssupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Assessing Genetic Overlap Between Platelet Parameters and Neurodegenerative Disorders

et al. 2020

View full text Add to dashboard Cite

show abstract

“…However, they were notably weakened by adjustment for obesity, in line with previous evidence that body mass index (BMI) attenuates the association between systemic inflammation and somatic depressive symptoms (Case & Stewart, 2014;Chamberlain et al, 2019;Duivis et al, 2013;Krogh et al, 2014;White et al, 2017), in particular appetite (Lamers et al, 2018). For this symptom, the link with fat mass may be particularly complex, in view of the likely bidirectional relationship between depressive symptoms and systemic inflammation (Gialluisi et al, 2019). In this context, the fat mass may act (a) as a confounder of the relationship, influencing independently circulating inflammation and appetite; (b) as a mediator of the effect of appetite on inflammation; or (c) as an ancestral exposure influencing inflammation and, in turn, appetite, or vice versa (explained in Figure 2).…”

Section: Discussionsupporting

confidence: 80%

“…Then we repeated the logistic model for the four component biomarkers of INFLA-score, namely Plt, CRP, WBC, and GLR. In this case, a further correction for four independent markers tested was applied (α = 2.1 × 10 −3 ), since MatSpD did not detect any reduction in the number of latent variables (Gialluisi et al, 2019).…”

Section: Statistical Analysesmentioning

confidence: 99%

Associations between systemic inflammation and somatic depressive symptoms: Findings from the Moli‐sani study

Gialluisi

Castelnuovo

Bracone

et al. 2020

Depression and Anxiety

View full text Add to dashboard Cite

Background The link between systemic inflammation and depression has been deeply investigated, but relatively few studies explored symptom‐specific associations, mostly focusing on common inflammatory biomarkers like C‐reactive protein (CRP) levels. Methods We investigated associations of low‐grade inflammation with depressive symptoms assessed through a reduced version of Patient Health Questionnaire 9 (PHQ‐9) in a large population‐based cohort of adult Italians (N = 13 301). We built logistic regressions between each depressive symptom and composite index of systemic inflammation based on four circulating biomarkers, namely CRP, Plt, WBC, and GLR (INFLA)‐score, a composite blood‐based inflammation index, and with its component biomarkers, namely CRP, platelets count (Plt), white blood cells count (WBC), and granulocyte‐to‐lymphocyte ratio (GLR). Results We observed a strong association of the altered appetite/eating symptom with standardized INFLA‐score (OR [95% CI] = 1.19 [1.12‐1.26]; corrected p = 3.0 × 10−7), CRP (1.28 [1.20‐1.36]; p = 1.9 × 10−13), and WBC (1.13 [1.06‐1.20]; p = 2.3 × 10−3), and of tiredness/low energy with GLR (1.11 [1.05‐1.17]; p = 9.4 × 10−3). These associations remained stable within nondepressed participants (PHQ‐9 < 10), and after adjustment for the use of antidepressants, main chronic conditions, and lifestyle factors; while they were notably attenuated within depressed participants (PHQ‐9 ≥ 10) and—for altered appetite only—by adjustment for obesity. Conclusions This study provides a robust replication of the association previously reported between CRP and altered appetite in a large US population cohort, and supports a link between systemic inflammation, altered appetite, and tiredness. Moreover, it extends this evidence to inflammatory markers other than CRP and suggests new targets for the treatment of atypical depression.

show abstract

“…It has been reported that mental disorders, especially depression and anxiety disorders, could affect the in ammation level [16], cytokines [17] and chemokines [18], neurotransmitter metabolism [19,20], neuroendocrine function [21], and so forth, which are also recognized as possible causes for the development and heterogeneity of GBM [22]. And research have also discovered that compared with other form of cancers, glioblastoma could be concomitant with depression/anxiety [23,24].…”

mentioning

confidence: 99%

LTBP1 plays a potential bridge between depressive disorder and glioblastoma

Zhang

Song³

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Glioblastoma multiforme (GBM) is the most malignant tumor in human brain. Diagnosis and treatment of GBM may lead to psychological disorders such as depressive and anxiety disorders. There was no research focusing on the correlation between depressive/anxiety disorder and the outcome of GBM. Thus, the aim of this study was to investigate the possibility of depressive/anxiety disorder correlated with the outcome of GBM patients, as well as the overlapped mechanism bridge which could link depressive/anxiety disorders and GBM.Methods: Patient Health Questionnaire (PHQ-9) and Generalized Anxiety Disorder (GAD-7) were used to investigate the psychological condition of GBM patients in our department. To further explore the potential mechanism, bioinformatic methods were used to screen out genes that could be indicators of outcome in GBM, followed by gene ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, and protein-protein interaction (PPI) analysis. Further, cellular experiments were conducted to evaluate the proliferation, migration capacity of primary GBM cells from the patients.Results: It was revealed that patients with higher PHQ-9 and GAD-7 scores had significantly worse prognosis than their lower-scored counterparts. Bioinformatic mining revealed that LTBP1 could be a potential genetic mechanism in both depressive/anxiety disorder and GBM. Primary GBM cells with different expression level of LTBP1 should significantly different proliferation and migration capacity. GO, KEGG analysis confirmed that extracellular matrix (ECM) was the most enriched function of LTBP1. PPI network showed the interaction of proteins altered by LTBP1. Hub genes COL1A2, COL5A1 and COL10A1, as well as mesenchymal marker CD44 and Vimentin were statistically higher expressed in LTBP1 high group; while proneural marker E-cadherin was significantly higher expressed in low LTBP1 group.Conclusion: There is closely correlation between depressive/anxiety disorders and GBM. LTBP1 could be a potential bridge linking the two diseases through the regulation of ECM.

show abstract

Lifestyle and biological factors influence the relationship between mental health and low-grade inflammation

Cited by 50 publications

References 86 publications

Assessing Genetic Overlap Between Platelet Parameters and Neurodegenerative Disorders

Assessing Genetic Overlap Between Platelet Parameters and Neurodegenerative Disorders

Associations between systemic inflammation and somatic depressive symptoms: Findings from the Moli‐sani study

LTBP1 plays a potential bridge between depressive disorder and glioblastoma

Contact Info

Product

Resources

About