Immune-related pathways including HLA-DRB113:02 are associated with panic disorder

Shimada-Sugimoto, Mihoko; Otowa, Takeshi; Miyagawa, Taku; Khor, Seik‐Soon; Kashiwase, Koichi; Sugaya, Nagisa; Kawamura, Yoshiya; Umekage, Tadashi; Kojima, Hiroto; Saji, Hiroh; Miyashita, Akinori; Kuwano, Ryozo; Kaiya, Hisanobu; Kasai, Kiyoto; Tanii, Hisashi; Okazaki, Yuji; Tokunaga, Katsushi; Sasaki, Tsukasa

doi:10.1016/j.bbi.2015.01.002

Cited by 17 publications

(18 citation statements)

References 62 publications

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“…35 To identify associated single nucleotide polymorphisms (SNP) with modest effects, we also performed pathway analyses using Japanese PD GWAS data. 41 As a result, we found immune-related pathways and HLA-DRB1*13:02 were significantly associated with PD (P = 2.50 × 10 −4 , OR = 1.5). Erhardt et al conducted GWAS of PD in three German samples (in total, 909 cases vs 915 controls) and reported two associated SNP located in TMEM132D on 12q24.3.…”

Section: Genome-wide Association Studiesmentioning

confidence: 63%

“…A combined meta‐analysis of the two Japanese PD data followed by a replication has been performed (1147 cases vs 2578 controls), with no genome‐wide significance . To identify associated single nucleotide polymorphisms (SNP) with modest effects, we also performed pathway analyses using Japanese PD GWAS data . As a result, we found immune‐related pathways and HLA‐DRB1*13:02 were significantly associated with PD ( P = 2.50 × 10 −4 , OR = 1.5).…”

Section: Molecular Geneticsmentioning

confidence: 99%

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Genetics of anxiety disorders: Genetic epidemiological and molecular studies in humans

Shimada-Sugimoto

Otowa

Hettema

2015

Psychiatry Clin Neurosci

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132

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This review provides a broad overview of the state of research in the genetics of anxiety disorders (AD). Genetic epidemiological studies report a moderate level of familial aggregation (odds ratio: 4–6) and heritability estimates are about 30–50%. Twin studies suggest that the genetic architecture of AD is not isomorphic with their classifications, sharing risk factors with each other. So far, linkage and association studies of AD have produced inconclusive results. Genome‐wide association studies of AD can provide an unbiased survey of common genetic variations across the entire genome. Given the shared causes of AD that transcend our current diagnostic classifications, clustering anxiety phenotypes into broader groups may be a powerful approach to identifying susceptibility locus for AD. Using such a shared genetic risk factor, meta‐analyses of genome‐wide association studies of AD conducted by large consortia are needed. Environmental factors also make a substantial contribution to the cause of AD. Although candidate gene studies of gene by environmental (G × E) interaction have appeared recently, no genome‐wide search for G × E interactions have been performed. Epigenetic modification of DNA appears to have important effects on gene expression mediating environmental influences on disease risk. Given that G × E can be linked to an epigenetic modification, a combination analysis of genome‐wide G × E interaction and methylation could be an alternative method to find risk variants for AD. This genetic research will enable us to utilize more effective strategies for the prevention and treatment of AD in the near future.

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Section: Genome-wide Association Studiesmentioning

confidence: 63%

Section: Molecular Geneticsmentioning

confidence: 99%

Genetics of anxiety disorders: Genetic epidemiological and molecular studies in humans

Shimada-Sugimoto

Otowa

Hettema

2015

Psychiatry Clin Neurosci

Self Cite

132

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“…The uncleaned apoptotic components which recognized by both the innate and the adaptive immune systems can trigger the pathogenesis of SLE. Therefore, the dysregulation of effective genes involved in the clearance of apoptotic components has a fundamental role in SLE [41][42][43][44][45]. Remarkably, we showed upregulation of MACROH2A1, SNRPD3, and Ro60 and downregulation of MACROH2A2, TRIM21…”

Section: Discussionmentioning

confidence: 62%

An integrative Bayesian network approach to highlight key drivers in systemic lupus erythematosus

Maleknia

Salehi

Sharifi‐Zarchi

et al. 2020

Preprint

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Background: To perceive a comprehensive illustration of the systemic lupus erythematosus (SLE), as a complex and multifactorial disease, draw a biological challenge. Dealing with this challenge needs employing sophisticated bioinformatics algorithms to discover the unknown aspects. This study aimed to distinguish key molecular characteristics of SLE pathogenesis, which may serve as effective targets for therapeutic intervention. Methods: In the present study, six gene expression microarray datasets included SLE patients (n=220) and healthy controls (n=135) were collected. We integrated the datasets by cross-platform normalization. Subsequently, through BNrich method, the structures of Bayesian networks (BNs) were extracted from SLE, TCR and BCR signaling pathways and the parameters of BNs were estimated using integrated datasets. Finally, a meta-analysis was performed to distinguish the signaling pathways alterations in the SLE pathogenesis. Results: We identified the most dysregulated genes involved in the clearance mechanism (most inhibition in MACROH2A2 and H4C9, most activation in SNRPD3, MACROH2A1 and RO60). Augmented autoantigens presentation by MHCII (HLA-DQA1, HLA-DOB and HLA-DPB1) and CD80 and CD86 to CD28 biological functions were also observed. The increased expression of FCGR1A, C8G, C7 and C9 genes and decreasing biological functions in edges from C1R and C1S to C2 and from C1R to C4B, all involved in end-organ damage, were detected. On the other hand, many of subnetworks alterations of TCR and BCR reported in previous research (PI3K/AKT, MAPK, AP-1 transcription factor). Conclusions: Overall, the BNrich as a hybridized network construction method, which integrates intergenic relations inferred from signaling pathways and gene expression profiling, can be employed to study complex diseases. Here we applied BNrich and highlighted significant genes and intergenic relationships and systemic alterations in SLE, TCR and BCR signaling pathways.

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“…There is increasingly strong genetic evidence to suggest a direct link between altered immune function and PD [ 127 , 128 ]. However, the strongest clinical evidence of altered immune function in PD patients is provided in a systematic review of 14 studies carried out between 1991 and 2002 [ 129 ].…”

Section: An Incremental Evidence-based Reasoningmentioning

confidence: 99%

Lifestyle Behaviours Add to the Armoury of Treatment Options for Panic Disorder: An Evidence-Based Reasoning

Lambert

2015

IJERPH

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This article presents an evidence-based reasoning, focusing on evidence of an Occupational Therapy input to lifestyle behaviour influences on panic disorder that also provides potentially broader application across other mental health problems (MHP). The article begins from the premise that we are all different. It then follows through a sequence of questions, examining incrementally how MHPs are experienced and classified. It analyses the impact of individual sensitivity at different levels of analysis, from genetic and epigenetic individuality, through neurotransmitter and body system sensitivity. Examples are given demonstrating the evidence base behind the logical sequence of investigation. The paper considers the evidence of how everyday routine lifestyle behaviour impacts on occupational function at all levels, and how these behaviours link to individual sensitivity to influence the level of exposure required to elicit symptomatic responses. Occupational Therapists can help patients by adequately assessing individual sensitivity, and through promoting understanding and a sense of control over their own symptoms. It concludes that present clinical guidelines should be expanded to incorporate knowledge of individual sensitivities to environmental exposures and lifestyle behaviours at an early stage.

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Immune-related pathways including HLA-DRB113:02 are associated with panic disorder

Cited by 17 publications

References 62 publications

Genetics of anxiety disorders: Genetic epidemiological and molecular studies in humans

Genetics of anxiety disorders: Genetic epidemiological and molecular studies in humans

An integrative Bayesian network approach to highlight key drivers in systemic lupus erythematosus

Lifestyle Behaviours Add to the Armoury of Treatment Options for Panic Disorder: An Evidence-Based Reasoning

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