Extracellular matrix proteins matrix metallopeptidase 9 (<scp>MMP</scp>9) and soluble intercellular adhesion molecule 1 (<scp>sICAM</scp>‐1) and correlations with clinical staging in euthymic bipolar disorder

Reininghaus, Eva; Lackner, Nina; Birner, Armin; Bengesser, Susanne; Fellendorf, Frederike T.; Platzer, Martina; Rieger, Alexandra; Queissner, Robert; Kainzbauer, Nora; Reininghaus, Bernd; McIntyre, Roger S.; Mangge, Harald; Zelzer, Sieglinde; Fuchs, Dietmar; Dejonge, Silvia; Müller, Norbert

doi:10.1111/bdi.12380

Cited by 31 publications

(32 citation statements)

References 45 publications

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“…Recently, it has been reconceptualized as a changing disorder with different clinical manifestations over the course of its development from an at-risk or latent stage to a late or end-stage, thus supporting the assumption that it would benefit from a staging model 1 . Clinical manifestations consistent with staging models include cognitive deterioration and functional decline 2,3 , changes in inflammatory and neuroanatomical biomarkers [3][4][5][6][7][8][9] , less response to treatment 10 , and worse self-reported quality of life (QoL) 11 linked to disorder progression.…”

Section: Introductionmentioning

confidence: 93%

A clinical staging model for bipolar disorder: longitudinal approach

et al. 2020

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Bipolar disorder (BD) has been identified as a life-course illness with different clinical manifestations from an at-risk to a late stage, supporting the assumption that it would benefit from a staging model. In a previous study, we used a clustering approach to stratify 224 patients with a diagnosis of BD into five clusters based on clinical characteristics, functioning, cognition, general health, and health-related quality of life. This study was design to test the construct validity of our previously developed k-means clustering model and to confirm its longitudinal validity over a span of 3 years. Of the 224 patients included at baseline who were used to develop our model, 129 (57.6%) reached the 3-year follow-up. All life domains except mental health-related quality of life (QoL) showed significant worsening in stages (p < 0.001), suggesting construct validity. Furthermore, as patients progressed through stages, functional decline (p < 0.001) and more complex treatment patterns (p = 0.002) were observed. As expected, at 3 years, the majority of patients remained at the same stage (49.6%), or progressed (20.9%) or regressed (23.3%) one stage. Furthermore, 85% of patients who stayed euthymic during that period remained at the same stage or regressed to previous stages, supporting its longitudinal validity. For that reason, this study provides evidence of the construct and longitudinal validity of an empirically developed, comprehensive staging model for patients with BD. Thus, it may help clinicians and researchers to better understand the disorder and, at the same time, to design more accurate and personalized treatment plans.

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Section: Introductionmentioning

confidence: 93%

A clinical staging model for bipolar disorder: longitudinal approach

et al. 2020

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“…It is discovered that ECM alterations in the cognitive component was associated with depressive-like behavior [54,55]. And ECM markers such as MMP9 and sICAM1 were also reported to deficit cognitive function in human brain which may result in serious psychiatric disorders such as depressive disorders and bipolar disorders [56]. To our knowledge, there are many possibilities that the alternation of ECM by differentially expression of LTBP1 in brain may link depressive/anxiety disorders and glioblastoma (Fig.…”

Section: Discussionmentioning

confidence: 99%

LTBP1 plays a potential bridge between depressive disorder and glioblastoma

Zhang

Song

et al. 2020

J Transl Med

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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.

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Section: Discussionmentioning

confidence: 99%

LTBP1 plays a potential bridge between depressive disorder and glioblastoma

Zhang

Song³

et al. 2020

Preprint

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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.

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Extracellular matrix proteins matrix metallopeptidase 9 (MMP9) and soluble intercellular adhesion molecule 1 (sICAM‐1) and correlations with clinical staging in euthymic bipolar disorder

Cited by 31 publications

References 45 publications

A clinical staging model for bipolar disorder: longitudinal approach

A clinical staging model for bipolar disorder: longitudinal approach

LTBP1 plays a potential bridge between depressive disorder and glioblastoma

LTBP1 plays a potential bridge between depressive disorder and glioblastoma

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