Myelin‐associated oligodendrocyte basic protein rs616147 polymorphism as a risk factor for Parkinson's disease

Siokas, Vasileios; Aloizou, Athina‐Maria; Liampas, Ioannis; Bakirtzis, Christos; Tsouris, Zisis; Σγάντζος, Μάρκος; Liakos, Panagiotis; Bogdanos, Dimitrios P.; Hadjigeorgiou, Georgios M.; Dardiotis, Efthimios

doi:10.1111/ane.13538

Cited by 18 publications

(11 citation statements)

References 45 publications

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“…We recruited consecutive AD patients admitted to the Neurology Department (outpatient and inpatient clinics) of the General University Hospital of Larissa, a tertiary referral institution located in Central Greece. This current study includes the sample from previously published articles [47][48][49][50][51]. Briefly, all patients diagnosed with probable AD (G30 according to the International Classification of Diseases, 10th Revision) by a senior neurologist, based on the National Institute of Neurological and Communicative Disorders and Stroke/Alzheimer Disease and Related Disorders Association (NINCDS/ADRDA) criteria [52].…”

Section: Study Populationmentioning

confidence: 99%

Analysis of ADORA2A rs5760423 and CYP1A2 rs762551 Genetic Variants in Patients with Alzheimer’s Disease

Siokas

Mouliou

Liampas

et al. 2022

IJMS

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Various studies have been conducted, exploring the genetic susceptibility of Alzheimer’s disease (AD). Adenosine receptor subtype A2a (ADORA2A) and cytochrome P450 1A2 (CYP1A2) are implicated in pathways such as oxidative stress and caffeine metabolism, which are associated with AD. The aim of this study was to explore for any potential association between the ADORA2A rs5760423 and the CYP1A2 rs762551 genetic variants and AD. A case–control study was performed with a total of 654 subjects (327 healthy controls and 327 patients with AD). Five genetic models were assumed. We also examined the allele–allele combination of both variants. The value of 0.05 was considered as the statistical significance threshold. A statistically significant association was found between ADORA2A rs5760423 and AD, as the “T” allele was associated with increased AD risk in recessive (OR = 1.51 (1.03–2.21)) and log-additive (OR = 1.30 (1.04–1.62)) genetic modes. In the codominant model, the TT genotype was more prevalent compared to the GG genotype (OR = 1.71 (1.09–2.66)). The statistical significance was maintained after adjustment for sex. No association between CYP1A2 rs762551 or allele–allele combination and AD was detected. We provide preliminary indication for a possible association between the ADORA2A rs5760423 genetic polymorphism and AD.

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Section: Study Populationmentioning

confidence: 99%

Analysis of ADORA2A rs5760423 and CYP1A2 rs762551 Genetic Variants in Patients with Alzheimer’s Disease

Siokas

Mouliou

Liampas

et al. 2022

IJMS

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“…VIP (vasoactive intestinal peptide) [336], CD40 [337], CCL2 [338], DKK2 [339], ACE (angiotensin I converting enzyme) [340], KCNN4 [341], A2M [342], CDKN2A [343], MYD88 [344], TLR6 [345], ANXA1 [346], SPHK1 [347], CACNA1A [348], SLITRK2 [349], IL33 [350], CAT (catalase) [351], GPR78 [352], ANG (angiogenin) [353], GDF15 [354] and ADH1B [355] might be a potential therapeutic targets for neurodegenerative diseases treatment. At present, abnormal expression of VIP (vasoactive intestinal peptide) [356], HFE (homeostatic iron regulator) [357], CCL2 [358], HLA-DRA [359], TFF3 [360], NOS1 [361], NPPC (natriuretic peptide C) [362], ACE (angiotensin I converting enzyme) [363], GSDMD (gasdermin D) [364], A2M [365], PLXNA4 [366], CD44 [367], CASP1 [364], DRD3 [368], UNC5C [369], CAV1 [370], SPHK1 [371], CD163 [372], RPH3A [373], HGF (hepatocyte growth factor) [374], CCKBR (cholecystokinin B receptor) [375], TNFSF9 [376], MEG3 [377], GPR78 [378], NEUROG2 [379], ANG (angiogenin) [380], GDF15 [381], UNC5A [382], SLC1A2 [383], DRD2 [384], GPR143 [385], RASGRP1 [386] and MOBP (myelin associated oligodendrocyte basic protein) [387] have been found in a Parkinson’s disease. VIP (vasoactive intestinal peptide) [388], CD40 [389], WT1 [390], HFE (homeostatic iron regulator) [391], TAC1 [392], AQP5 [393], WNT2B [394], RUNX1 [395], NOS1 [396], DKK2 [339], ADAM12 [397], ABCG2 [398], NINJ2 [399], ACE (angiotensin I converting enzyme) [400], PRKCB (protein kinase C beta) [401], A2M […”

Section: Discussionmentioning

confidence: 99%

Screening of the Key Genes and Signaling Pathways for Schizophrenia Using Bioinformatics and Next Generation Sequencing Data Analysis

Vastrad,

Vastrad

2023

Preprint

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Schizophrenia is thought to be the most prevalent chronic psychiatric disorder. Numerous proteins have been identified that are associated with the occurrence and development of schizophrenia. This study aimed to identify potential core genes and pathways involved in schizophrenia, through exhaustive bioinformatic and next generation sequencing (NGS) data analyses using GSE20966 NGS data of neural progenitor cells and neurons obtained from healthy controls and patients with schizophrenia. The NGS data were downloaded from the Gene Expression Omnibus database. NGS data was processed by the DESeq2 package in R software and the differentially expressed genes (DEGs) were identified. Gene Ontology (GO) enrichment analysis and REACTOME pathway enrichment analysis were carried out to identify potential biological functions and pathways of the DEGs. Protein-protein interaction (PPI) network, module, miRNA-hub gene regulatory network and TF-hub gene regulatory network analysis were performed to identify the hub genes, miRNA and TFs. Potential hub genes were analyzed using receiver operating characteristic (ROC) curves in the R package (pROC). In this investigation, an overall 955 DEGs were identified: 478 genes were remarkably up regulated and 477 genes were distinctly down regulated. These genes were enriched for GO terms and pathways mainly involved in the multicellular organismal process, GPCR ligand binding, regulation of cellular process and amine ligand-binding receptors. MYC, FN1, CDKN2A, EEF1G, CAV1, ONECUT1, SYK, MAPK13, TFAP2A and BTK were considered the potential hub genes. miRNA-hub gene regulatory network and TF-hub gene regulatory network were constructed successfully. On the whole, the findings of this investigation enhance our understanding of the potential molecular mechanisms of schizophrenia and provide potential targets for further investigation.

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“…The association of MOBP with other neurodegenerative diseases is well-established. To date, autoreactivity against MOBP has been detected among individuals with MS [13,15] and MOBP immunoreactivity has been detected in the core of Lewy Bodies (LBs) among patients with Parkinson' s disease and dementia with LBs [37,38]. MOBP SNPs have been associated with Apolipoprotein-E e4 positive AD [14], FTD (and the severity of white matter degeneration [16,39]), PSP [17,[40][41][42][43][44], Corticobasal Degeneration [43,44], while decreased expression of MOBP was revealed in familial Globular Glial Tauopathy [45] and differential DNA methylation of MOBP was shown in Multiple System Atrophy [46].…”

Section: Discussionmentioning

confidence: 99%

MOBP rs616147 Polymorphism and Risk of Amyotrophic Lateral Sclerosis in a Greek Population: A Case-Control Study

et al. 2021

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Background and Objectives: To date, only one study has investigated the association between the rs616147 polymorphism of the Myelin-associated Oligodendrocyte Basic Protein (MOBP) locus and Amyotrophic Lateral Sclerosis (ALS). Materials and Methods: A case-control study was performed. Patients with definite sporadic ALS were prospectively and consecutively recruited from the inpatient and outpatient clinics of the Neurology Department of the General University Hospital of Larissa, Central Greece. Community based, age and sex matched healthy individuals with a free personal and family history constituted the control group. Results: A total of 155 patients with definite sporadic ALS and an equal number of healthy controls were genotyped. The power of our sample size was slightly above 80% and MOBP rs616147 was determined to be in Hardy-Weinberg Equilibrium among healthy participants (p = 1.00). According to the univariate analysis, there was no significant relationship between rs616147 and ALS [log-additive OR = 0.85 (0.61, 1.19), over-dominant OR = 0.73 (0.46, 1.15), recessive OR = 1.02 (0.50, 2.09), dominant OR = 0.74 (0.47, 1.16), co-dominant OR1 = 0.71 (0.44, 1.14) and co-dominant OR2 = 0.88 (0.42, 1.84). Additionally, the effect of rs616147 on the age of ALS onset was determined insignificant using both unadjusted and adjusted (sex, site of onset) cox-proportional models. Finally, rs616147 was not related to the site of ALS onset. Conclusions: Our study is the first to report the absence of an association between MOBP rs616147 and ALS among individuals of Greek ancestry. Additional, larger nationwide and multi-ethnic studies are warranted to shed light on the connection between rs616147 and ALS.

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Myelin‐associated oligodendrocyte basic protein rs616147 polymorphism as a risk factor for Parkinson's disease

Cited by 18 publications

References 45 publications

Analysis of ADORA2A rs5760423 and CYP1A2 rs762551 Genetic Variants in Patients with Alzheimer’s Disease

Analysis of ADORA2A rs5760423 and CYP1A2 rs762551 Genetic Variants in Patients with Alzheimer’s Disease

Screening of the Key Genes and Signaling Pathways for Schizophrenia Using Bioinformatics and Next Generation Sequencing Data Analysis

MOBP rs616147 Polymorphism and Risk of Amyotrophic Lateral Sclerosis in a Greek Population: A Case-Control Study

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