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Bermingham, M. L.

Publications and source records attributed to Bermingham, M. L..

8 recordsLinked to original sources

Loss of SORCS2 is associated with neuronal DNA double-strand breaks

SORCS2 is one of five proteins that constitute the Vps10p-domain receptor family. Members of this family play important roles in cellular processes linked to neuronal survival, differentiation and function. Genetic and functional studies implicate SORCS2 in cognitive function, as well as in neurodegenerative and psychiatric disorders. DNA damage and DNA repair deficits are linked to ageing and neurodegeneration, and transient neuronal DNA double-strand breaks (DSBs) also occur as a result of neuronal activity. Here, we report a novel role for SORCS2 in DSB formation. We show that SorCS2 loss is associated with elevated DSB levels in the mouse dentate gyrus and that knocking out SORCS2 in a human neuronal cell line increased Topoisomerase II{beta}-dependent DSB formation and reduced neuronal viability. Neuronal stimulation had no impact on levels of DNA breaks in vitro, suggesting that the observed differences may not be the result of aberrant neuronal activity in these cells. Our findings are consistent with studies linking the VPS10 receptors and DNA damage to neurodegenerative conditions.

neuroscience↗

Assessment of DNA methylation differences between carriers of APOE ε4 and APOE ε2

BACKGROUNDThe Apolipoprotein E (APOE) {varepsilon}4 allele is the strongest genetic risk factor for late onset Alzheimers disease, while the {varepsilon}2 allele confers protection. Previous studies report differential DNA methylation of APOE between {varepsilon}4 and {varepsilon}2 carriers, but associations with epigenome-wide methylation have not previously been characterised. METHODSUsing the EPIC array, we investigated epigenome-wide differences in whole blood DNA methylation patterns between Alzheimers disease-free APOE {varepsilon}4 (n=2469) and {varepsilon}2 (n=1118) carriers from the two largest single-cohort DNA methylation samples profiled to date. Using a discovery, replication and meta-analysis study design, methylation differences were identified using epigenome-wide association analysis and differentially methylated region (DMR) approaches. Results were explored using pathway and methylation quantitative trait loci (meQTL) analyses. RESULTSWe obtained replicated evidence for DNA methylation differences in a ~169kb region, which encompasses part of APOE and several upstream genes. Meta-analytic approaches identified DNA methylation differences outside of APOE: differentially methylated positions were identified in DHCR24, LDLR and ABCG1 (2.59 x 10-100[≤]P[≤]2.44 x 10-8) and DMRs were identified in SREBF2 and LDLR (1.63 x 10-4[≤]P[≤]3.01 x 10-2). Pathway and meQTL analyses implicated lipid-related processes and high density lipoprotein cholesterol was identified as a partial mediator of the methylation differences in ABCG1 and DHCR24. CONCLUSIONSAPOE {varepsilon}4 vs. {varepsilon}2 carrier status is associated with epigenome-wide methylation differences in the blood. The loci identified are located in trans as well as cis to APOE and implicate genes involved in lipid homeostasis.

genetics↗

DNA methylation in the APOE gene: its link with Alzheimer’s and cardiovascular health

Genetic variation in the apolipoprotein E (APOE) gene is associated with Alzheimers disease (AD) and risk factors for cardiovascular disease (CVD). DNA methylation at APOE has been linked to altered cognition and AD. It is unclear if epigenetic marks could be used for predicting future disease. We assessed blood-based DNA methylation at 13 CpGs in the APOE gene in 5828 participants from the Generation Scotland (GS) cohort. Using linear regression, we examined the relationship between APOE methylation, cognition, cholesterol, and the risks for AD and CVD. DNA methylation at two CpGs was associated with the ratio of total-to-HDL cholesterol, but not with cognition, or the risks of AD or CVD. APOE methylation could be involved in the levels of blood cholesterol, but there is no evidence for the utility of APOE methylation as a biomarker for predicting AD or CVD.

neuroscience↗

Characterisation of an inflammation-related epigenetic score and its association with cognitive ability

Results from large cohort studies investigating the association between inflammation and cognition have been mixed, possibly due to methodological disparities. However, a key issue in research utilising inflammatory biomarkers is their typically phasic responses. C-reactive protein (CRP) is widely used to investigate the association between chronic inflammation and cognition, but its plasma concentrations can markedly deviate in response to acute infection. Recently a large-scale epigenome-wide association study identified DNA methylation correlates of CRP. DNA methylation is thought to be relatively stable in the short term, marking it as a potentially useful signature of exposure. Here, we generate an epigenetic CRP score and investigate its trajectories with age, and associations with cognitive ability, in comparison to serum CRP in two cohorts: a longitudinal study of older adults (the Lothian Birth Cohort 1936, n=889) and a large, cross-sectional cohort (Generation Scotland, n=7,028).\n\nWe identified differing trajectories of serum CRP across the cohorts, with no homogeneous trends seen with age. Conversely, the epigenetic score was consistently found to increase with age, and to do so more rapidly in males compared to females. Higher levels of serum CRP were found to associate with poorer cognition in Lothian Birth Cohort 1936, but not in Generation Scotland. However, a consistent negative association was identified between cognition and the epigenetic score in both cohorts. Furthermore, the epigenetic score accounted for a greater proportion of variance in cognitive ability.\n\nOur results suggest that epigenetic signatures of acute inflammatory markers may provide an enhanced signature of chronic inflammation, allowing for more reliable stratification of individuals, and thus clearer inference of associations with incident health outcomes.

genomics↗

Birth weight predicts psychiatric and physical health, cognitive function, and DNA methylation differences in an adult population

BackgroundThe Developmental Origins of Adult Disease (DOAD) theory predicts that prenatal and early life events shape adult health outcomes. Birth weight is a useful indicator of the foetal experience, and has been associated with multiple adult health outcomes. DNA methylation (DNAm) is one plausible mechanism behind the relationship of birth weight to adult health. MethodsThe Generation Scotland study allows data linkage to historic Scottish birth cohorts, and birth records held through the NHS Information and Statistics Division. Data linkage with these sources yielded a sample of 4, 710 individuals. Health measures were related to birth weight in regression models. An epigenome-wide association study (EWAS) was performed in a subgroup (n=1, 395), relating adult DNAm from whole blood to birth weight, with replication in an independent sample (n=362). Associations between birth weight and epigenetic clocks were also assessed. FindingsHigher birth weight was significantly associated with reduced incidence of depression and osteoarthritis, higher body mass index, and higher general intelligence (absolute standardised effect size range 0{middle dot}04 to 0{middle dot}30, p(FDR)<0{middle dot}05). Meta-analysis of discovery and replication EWAS studies yielded one genome-wide significant CpG site (p=5{middle dot}97x10-9), cg00966482. Significant associations between birth weight and Grim Age (p=0{middle dot}0014) and DNAm-derived telomere length (p=3{middle dot}3x10-4) are also described. InterpretationOur results demonstrate associations between birth weight and adult health outcomes, with particularly striking effects for depression risk. It also provides support for an association between birth weight and DNAm, describing the first significant EWAS site associated with birth weight in an adult sample. FundingWellcome Trust Strategic Award 104036/Z/14/Z Research in ContextO_ST_ABSEvidence before this studyC_ST_ABSThe associations between birth weight and various adult health outcomes have been well established. DNA methylation is a plausible mechanism through which early life experiences may continue to affect health throughout the lifecourse; however, evidence for birth weight associations with DNA methylation in adulthood has not yet been robustly established. This is likely due to small sample sizes of previous samples, as well as the use of poor-quality birth weight data, such as binary low/normal variables or retrospective self-report. Alternatively, work has attempted to describe the persistence into adulthood of DNA methylation at sites identified at birth. Added value of this studyWe investigated genome-wide differential DNA methylation patterns from whole blood using data linkage-derived, continuous birth weight data, in the largest reported adult sample (n=1, 395) with replication (n=362) and meta-analysis. Meta-analysis revealed one epigenome-wide significant CpG site, to our knowledge the first significant EWAS result reported for birth weight in a an adult sample. In addition, we found associations between birth weight and GrimAge and a DNA methylation-derived measure of telomere length, demonstrating accelerated biological ageing in lower birth weight individuals. Together, these results suggest differential methylation exists in adulthood related to birth weight, and this may be relevant to health and mortality. Implications of all the available evidenceAlthough CpG sites differentially methylated with birth weight at parturition may not remain so throughout life, the adult epigenome may still provide information on the impact of birth weight on health outcomes. The adult epigenome, therefore, may represent a useful archive of the foetal experience which results in birth weight variability, and this information may provide clinically useful information in mid-life.

genomics↗

An epigenome-wide association study of sex-specific chronological ageing

IntroductionAdvanced age is associated with cognitive and physical decline, and is a major risk factor for a multitude of disorders including neurodegenerative diseases such as Alzheimers disease. There is also a gap in life-expectancy between males and females. DNA methylation differences have been shown to be associated with both age and sex. Here, we investigate age-by-sex differences in DNA methylation in an unrelated cohort of 2,586 individuals between the ages of 18 and 87 years.\n\nMethodsGenome-wide DNA methylation was measured on the Illumina HumanMethylationEPIC beadchip in a subset of unrelated individuals from the Generation Scotland cohort. Mixed linear model-based analyses were performed to investigate the relationship between DNA methylation and an interaction term between age and sex, as well as chronological age.\n\nResultsAt a genome-wide significance level of P < 3.6 x 10-8, 14 loci were associated with the age-by-sex interaction term, the majority of which were X-linked (n = 12). Seven of these loci were annotated to genes. The site with the greatest difference mapped to GAGE10, an X-linked gene. Here, DNA methylation levels remained stable across the male adult age range (DNA methylation x age r = 0.02), but decreased across female adult age range (DNA methylation x age r = -0.61). The seven age-by-sex-associated genes were enriched among differentially-expressed genes in lung, liver, testis and blood.\n\nConclusionThe majority of differences in age-associated DNA methylation trajectories between sexes are present on the X-chromosome. Several of these differences occur within genes which have implicated in multiple cancers, schizophrenia and systemic lupus erythematosus.

genomics↗

Identification of novel differentially methylated sites with potential as clinical predictors of impaired respiratory function and COPD

BackgroundThe causes of poor respiratory function and COPD are incompletely understood, but it is clear that genes and the environment play a role. As DNA methylation is under both genetic and environmental control, we hypothesised that investigation of differential methylation associated with these phenotypes would permit mechanistic insights, and improve prediction of COPD. We investigated genome-wide differential DNA methylation patterns using the recently released 850K Illumina EPIC array in the largest single population sample to date.\n\nMethodsEpigenome-wide association studies (EWASs) of respiratory function and COPD were performed in peripheral blood samples from the Generation Scotland: Scottish Family Health Study (GS:SFHS) cohort (N=3,791; 274 COPD cases and 2,928 controls). In independent COPD incidence data (N=150), significantly differentially methylated sites (DMSs; p<3.6x10-8) were evaluated for their added predictive power when added to a model including clinical variables, age, sex, height and smoking history using receiver operating characteristic analysis. The Lothian Birth Cohort 1936 (LBC1936) was used to replicate association (N=895) and prediction (N=178) results.\n\nFindingsWe identified 29 respiratory function and/or COPD associated DMSs, which mapped to genes involved in alternative splicing, JAK-STAT signalling, and axon guidance. In prediction analyses, we observed significant improvement in discrimination between COPD cases and controls (p<0.05) in independent GS:SFHS (p=0.014) and LBC1936 (p=0.018) datasets by adding DMSs to a clinical model.\n\nInterpretationIdentification of novel DMSs has provided insight into the molecular mechanisms regulating respiratory function and aided prediction of COPD risk.\n\nFundingWellcome Trust Strategic Award 10436/Z/14/Z.\n\nResearch in contextO_ST_ABSEvidence before this studyC_ST_ABSWe searched for articles in PubMed published in English up to July 25, 2018, with the search terms \"DNA methylation\" and \"respiratory function\", or \"COPD\". We found some evidence for association between differential DNA methylation and both respiratory function and COPD. Of the twelve previous studies identified, eight used peripheral blood samples (sample size [N] range = 100-1,085) and four used lung tissue samples (N range = 24-160). The number of CpG loci analysed range from 27,578 to 485,512. These studies have not identified consistent changes in methylation, most likely due to a combination of factors including small sample sizes, technical issues, phenotypic definitions, and study design. In addition, no previous study has: analysed a sample from a large single cohort; used the recently released Illumina EPIC array (which assesses ~850,000 CpG loci); adjusted methylation data and phenotype for smoking history, or used both prevalent and incident COPD electronic health record data.\n\nAdded value of this studyTo our knowledge, this is the largest single cohort epigenome-wide association study (EWAS) of respiratory function and COPD to date (N=3,791). After applying stringent genome-wide significance criteria (P <3.6x10-8), we found that DNA methylation levels at 29 CpG sites in peripheral blood were associated with respiratory function or COPD. Of these 29, seven were testable in an independent population sample: all seven showed consistent direction of effect between the two samples and three showed replication (p<0.007 [0.05/7 CpG sites tested]). Our results suggest that adjustment of both the phenotypic and the DNA methylation probe data for smoking history, which has not been carried out in previous studies, reduces the confounding effects of smoking, identifies larger numbers of associations, and reduces the heterogeneity of effects across smoking strata. We used gene set enrichment and pathway analyses, together with an approach that combines DNA methylation results with gene expression data to provide evidence for enrichment of differentially methylated sites in genes linked to alternative splicing, and JAK-STAT signalling and axon guidance. Finally, we demonstrated that the inclusion of DNA methylation data improves COPD risk prediction over established clinical variables alone in two independent datasets.\n\nImplications of all the available evidenceThere is now accumulating evidence that DNA methylation in peripheral blood is associated with respiratory function and COPD.\n\nOur study has shown that DNA methylation levels at 29 CpG sites are robustly associated with respiratory function and COPD, provide mechanistic insights, and can improve prediction of COPD risk. Further studies are warranted to improve understanding of the aetiology of COPD and to assess the utility of DNA methylation profiling in the clinical management of this condition.

genomics↗

Epigenetic signatures of starting and stopping smoking

BackgroundMultiple studies have made robust associations between differential DNA methylation and exposure to cigarette smoke. But whether a DNA methylation phenotype is established immediately upon exposure, or only after prolonged exposure is less well-established. Here, we assess DNA methylation patterns in current smokers in response to dose and duration of exposure, along with the effects of smoking cessation on DNA methylation in former smokers.\n\nMethodsDimensionality reduction was applied to DNA methylation data at 90 previously identified smoking-associated CpG sites for over 4,900 individuals in the Generation Scotland cohort. K-means clustering was performed to identify clusters associated with current and never smoker status based on these methylation patterns. Cluster assignments were assessed with respect to duration of exposure in current smokers (years as a smoker), time since smoking cessation in former smokers (years), and dose (cigarettes per day).\n\nResultsTwo clusters were specified, corresponding to never smokers (97.5% of whom were assigned to Cluster 1) and current smokers (81.1% of whom were assigned to Cluster 2). The exposure time point from which >50% of current smokers were assigned to the smoker-enriched cluster varied between 5-9 years in heavier smokers and between 15-19 years in lighter smokers. Low-dose former smokers were more likely to be assigned to the never smoker-enriched cluster from the first year following cessation. In contrast, a period of at least two years was required before the majority of former high-dose smokers were assigned to the never smoker-enriched cluster.\n\nConclusionsOur findings suggest that smoking-associated DNA methylation changes are a result of prolonged exposure to cigarette smoke, and can be reversed following cessation. The length of time in which these signatures are established and recovered is dose dependent. Should DNA methylation-based signatures of smoking status be predictive of smoking-related health outcomes, our findings may provide an additional criterion on which to stratify risk.

genomics↗