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Burrage, J.

Publications and source records attributed to Burrage, J..

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Best Practices for Pre-Processing Large-Scale ATAC-Seq Data: Why Epidemiological Studies Demand Greater Stringency

Assay for transposase accessible chromatin using sequencing (ATAC-seq) and related techniques provide critical insight into the epigenetic mechanisms that regulate gene expression in health and disease. Accurate identification of biologically meaningful chromatin accessibility signals remains an underexplored analytical challenge. Advances in sequencing technologies have increased both the magnitude and complexity of ATAC-seq datasets, leading to demand for scalable, reproducible and robust computational analysis frameworks. Peak calling, which identifies regions of chromatin accessibility, is a critical step that underpins all downstream quantitative analyses. However, there is a lack of consensus regarding the optimal peak calling strategy. Here, we present a novel bioinformatics pipeline PIPPA (Pipeline for Integrative Peak calling in Population-scale ATAC-seq), for quality control and peak set curation of large-scale ATAC-seq datasets. Using two independent cell-type sorted ATAC-seq datasets, we show that peak calling performance is dataset-dependent and that no single significance threshold performs optimally across all scenarios. We provide practical recommendations for parameters to generate high-confidence chromatin accessibility profiles. Our peak calling approach is applicable for other genome wide epigenomic assays such as ChIP-seq and CUT&Tag. By standardising this process, the PIPPA pipeline enhances epidemiological studies focused in identifying epigenetic dysregulation associated with development and disease.

bioinformatics↗

Cell-type-resolved DNA methylation profiling in the cortex reveals female-specific X chromosome differences in autism

Sex differences are a prominent feature of many neurodevelopmental conditions, particularly autism for which approximately three males are diagnosed for every female. Although epigenetic dysregulation has been implicated in autism, the extent to which autism-associated epigenetic differences vary by sex and neural cell type remains poorly understood. Using fluorescence-activated nuclei sorting (FANS), we isolated neuron-enriched (NeuN+), oligodendrocyte-enriched (SOX10+), microglia-enriched (IRF8+) and astrocyte-enriched (NeuN-/SOX10-/IRF8-) nuclei from post-mortem prefrontal cortex tissue from 24 autistic (70.8% male) and 23 non-autistic (69.6% male) donors, and performed cell-type-resolved epigenome-wide association studies (EWASs) of DNA methylation. We identified cell-type-specific autism-associated differentially methylated positions (DMPs), with microglia harbouring the largest number of associations. Modelling the interaction between sex and diagnosis revealed a striking female-specific signature concentrated on the X chromosome in microglia. At the majority of these sex-by-autism DMPs, autistic females showed lower DNA methylation compared to control females consistent with an altered X chromosome inactivation (XCI) profile. Across the X chromosome, autism-associated DNA methylation differences were significantly larger in females than males and were greater at sites annotated to genes normally subject to XCI than at genes that escape XCI. Together, these data further support the importance of microglia in autism and suggest that altered X chromosome dosage regulation may contribute to sex-dependent molecular mechanisms in autism.

genomics↗

Schizophrenia-associated DNA methylation differences in the cortex are neuron-specific

Schizophrenia is a complex neuropsychiatric disorder in which genetic risk is thought to converge on cell type-specific regulatory mechanisms in the brain. We performed a cell type-resolved epigenome-wide association study (EWAS) of schizophrenia using fluorescence-activated nuclei sorting (FANS) to isolate neuron-enriched (NeuN+), oligodendrocyte-enriched (SOX10+) and other glial-enriched (NeuN-/SOX10-) nuclei populations alongside total prefrontal cortex nuclei fractions from 216 donors (104 schizophrenia cases and 112 controls). We identified 16 differentially methylated positions (DMPs) in neuron-enriched nuclei at experiment-wide significance and more than 400 additional neuronal DMPs at a discovery threshold. In contrast, no significant associations were identified in oligodendrocyte-enriched, glial-enriched or total nuclei fractions, demonstrating that schizophrenia-associated cortical methylomic variation is highly neuron-specific and largely masked in bulk tissue analyses. Neuronal DMPs exhibited a significant bias towards hypomethylation in schizophrenia and were enriched at loci implicated by genetic studies, including CACNA1C, CACNA1G and TRIO. Pathway analyses implicated genes involved in neurodevelopment, cell adhesion, synapse organisation, neurotransmission and synaptic plasticity. Schizophrenia-associated DNA methylation signatures identified in prefrontal cortex neurons showed correlated effects in neuronal nuclei isolated from the hippocampus and striatum, indicating partial conservation of disease-associated epigenetic alterations across brain regions. Together, these findings provide strong evidence for widespread neuron-specific epigenetic dysregulation in schizophrenia and highlight the importance of cell type-resolved approaches for elucidating the molecular mechanisms underlying psychiatric disease.

genomics↗

DNA methylation signatures of mismatch repair-deficient colorectal cancer

BackgroundColorectal cancer (CRC) is a molecularly heterogeneous disease shaped by both genetic and epigenetic alterations. Approximately 15% of CRCs display widespread CpG island hypermethylation, known as the CpG Island Methylator Phenotype (CIMP). CIMP-high (CIMP-H) tumours frequently exhibit MLH1 promoter hypermethylation, leading to mismatch repair deficiency (MMRd) and microsatellite instability (MSI). However, DNA methylation patterns associated with MSI, independent of CIMP and MLH1 silencing, and the influence of clinical variables such as anatomical location and patient age on the CRC methylome remain poorly characterised. MethodsWe performed epigenome-wide DNA methylation profiling of 259 primary CRC tissue samples using the Illumina EPICv2 array, comparing differential methylation between MSI and microsatellite stable (MSS) CRC, adjusting for tumour purity, MLH1 promoter methylation, CIMP status, and anatomical location, to account for known confounders. We further evaluated the independent effects of anatomical location and patient age on global methylation patterns. ResultsEpigenome-wide differential methylation between MSS and MSI CRC was dominated by MLH1 promoter hypermethylation. After adjusting for MLH1 hypermethylation and CIMP status, we identified a distinct set of 656 CpG sites associated with MMRd independent of MLH1 silencing. These included hypermethylation at LRP6, GSK3{beta}, and CDK12, implicating altered WNT signalling and transcriptional regulation pathways. Comparison of MSI subgroups revealed the co-occurrence of MLH1 hypermethylation with promoter hypermethylation at TXNRD1. Anatomical location showed a strong independent effect on methylation patterns, while we observed only modest effects of patient age on the CRC methylome after adjustment for confounders. ConclusionsWe identified a distinct methylation profile distinguishing MSS and MSI CRC, including MLH1-independent markers of MMRd, as well as novel differentially methylated loci within MSI subgroups. We further showed that anatomical location has a strong independent impact on the CRC methylome. Together, these findings refine the molecular characterisation of CRC and highlight potential epigenetic markers that could inform patient stratification and precision oncology.

cancer biology↗

Optimised fluorescence-activated nuclei sorting for epigenomic analysis of cortical cell types

Increased understanding of the functional complexity of the genome has led to growing recognition of the role of non-sequence-based regulatory variation in disorders of the human central nervous system. Most genomic analyses of the brain are limited by the use of bulk tissue, which comprises a heterogeneous mix of different neural cell types with distinct epigenetic profiles, thereby limiting the ability to attribute regulatory changes to specific cell populations. Given the limited availability of human post-mortem tissue resources and the importance of integrating multi-omic data from the same samples, there is a critical need for methods that enable parallel, cell-type-resolved genomic profiling. We present optimised protocols using fluorescence-activated nuclei sorting (FANS) to isolate nuclei from different human and mouse brain cell types for downstream multi-omic analysis. Our approach enables the robust purification of neuronal, oligodendrocyte, microglial and other glial-origin nuclei from both adult and fetal brain tissue. We demonstrate that FANS-isolated nuclei are compatible with a wide range of genomic assays, including profiling of DNA modifications, histone modifications, chromatin accessibility, and gene expression. This protocol maximises the utility of limited post-mortem tissue resources and provides a unified workflow for comprehensive, cell-type-specific interrogation of molecular mechanisms involved in the brain.

genomics↗

Cell-type-specific DNA methylation dynamics in the prenatal and postnatal human cortex

The human cortex undergoes extensive epigenetic remodelling during development, although the precise temporal and cell-type-specific dynamics of DNA methylation remain incompletely understood. In this study, we profiled genome-wide DNA methylation across human cortex tissue from donors aged 6 post-conception weeks (pcw) to 108 years of age. We observed widespread, developmentally regulated, changes in DNA methylation, with pronounced shifts occurring during early- and mid-gestation that were distinct from age-associated modifications in the postnatal cortex. Using fluorescence-activated nuclei sorting (FANS), we optimized a protocol for the isolation of SATB2-positive neuronal nuclei, enabling the identification of cell-type-specific DNA methylation trajectories in developing neuronal and non-neuronal populations. Developmentally dynamic DNA methylation sites were significantly enriched near genes implicated in autism and schizophrenia, supporting a role for epigenetic dysregulation in neurodevelopmental disorders. Our findings underscore the prenatal period as a critical window of epigenomic plasticity in the central nervous system with important implications for understanding the genetic basis of neurodevelopmental phenotypes.

genomics↗

Guidance for the design and analysis of cell-type specific epigenetic epidemiology studies.

Recent studies on the role of epigenetics in disease have focused on DNA methylation profiled in bulk tissues limiting the detection of the cell-type affected by disease related changes. Advances in isolating homogeneous populations of cells now make it possible to identify DNA methylation differences associated with disease in specific cell-types. Critically, these datasets will require a bespoke analytical framework that can characterise whether the difference affects multiple or is specific to a particular cell-type. We take advantage of a large set of DNA methylation profiles (n = 751) obtained from five different purified cell populations isolated from human prefrontal cortex samples and evaluate the effects on study design, data preprocessing and statistical analysis for cell-specific studies, particularly for scenarios where multiple cell types are included. We describe novel quality control metrics that confirm successful isolation of purified cell populations, which when included in standard preprocessing pipelines provide confidence in the dataset. Our power calculations show substantial gains in detecting differentially methylated positions for some purified cell populations compared to bulk tissue analyses, countering concerns regarding the feasibility of generating large enough sample sizes for informative epidemiological studies. In a simulation study, we evaluated different regression models finding that this choice impacts on the robustness of the results. These findings informed our proposed two-stage framework for association analyses. Overall, our results provide guidance for cell-specific EWAS, establishing standards for study design and analysis, while showcasing the potential of cell-specific DNA methylation analyses to reveal links between epigenetic dysregulation and disease.

bioinformatics↗

Developmentally dynamic changes in DNA methylation in the human pancreas

Development of the human pancreas requires the precise temporal control of gene expression via epigenetic mechanisms and the binding of key transcription factors. We quantified genome-wide patterns of DNA methylation in human fetal pancreatic samples from donors aged 6 to 21 post-conception weeks. We found dramatic changes in DNA methylation across pancreas development, with >21% of sites characterized as developmental differentially methylated positions (dDMPs) including many annotated to genes associated with monogenic diabetes. An analysis of DNA methylation in postnatal pancreas tissue showed that the dramatic temporal changes in DNA methylation occurring in the developing pancreas are largely limited to the prenatal period. Significant differences in DNA methylation were observed between males and females at a number of autosomal sites, with a small proportion of sites showing sex-specific DNA methylation trajectories across pancreas development. Pancreas dDMPs were not distributed equally across the genome, and were depleted in regulatory domains characterized by open chromatin and the binding of known pancreatic development transcription factors. Finally, we compared our pancreas dDMPs to previous findings from the human brain, identifying evidence for tissue-specific developmental changes in DNA methylation. To our knowledge, this represents the most extensive exploration of DNA methylation patterns during human fetal pancreas development, confirming the prenatal period as a time of major epigenomic plasticity.

genomics↗

Quantifying the proportion of different cell types in the human cortex using DNA methylation profiles

BackgroundDue to inter-individual variation in the cellular composition of the human cortex, it is essential that covariates that capture these differences are included in epigenome-wide association studies using bulk tissue. As experimentally derived cell counts are often unavailable, computational solutions have been adopted to estimate the proportion of different cell-types using DNA methylation data. Here, we validate and profile the use of an expanded reference DNA methylation dataset incorporating two neuronal- and three glial-cell subtypes for quantifying the cellular composition of the human cortex. ResultsWe tested eight reference panels containing different combinations of neuronal- and glial-cell types and characterized their performance in deconvoluting cell proportions from computationally reconstructed or empirically-derived human cortex DNA methylation data. Our analyses demonstrate that these novel brain deconvolution models produce accurate estimates of cellular proportions from profiles generated on postnatal human cortex samples, they are not appropriate for the use in prenatal cortex or cerebellum tissue samples. Applying our models to an extensive collection of empirical datasets, we show that glial cells are twice as abundant as neuronal cells in the human cortex and identify significant associations between increased Alzheimers disease neuropathology and the proportion of specific cell types including a decrease in NeuNNeg/SOX10Neg nuclei and an increase of NeuNNeg/SOX10Pos nuclei. ConclusionsOur novel deconvolution models produce accurate estimates for cell proportions in the human cortex. These models are available as a resource to the community enabling the control of cellular heterogeneity in epigenetic studies of brain disorders performed on bulk cortex tissue.

genomics↗

Uncertainty quantification of reference based cellular deconvolution algorithms

The majority of epigenetic epidemiology studies to date have generated genome-wide profiles from bulk tissues (e.g. whole blood) however these are vulnerable to confounding from variation in cellular composition. Proxies for cellular composition can be mathematically derived from the bulk tissue profiles using a deconvolution algorithm however, there is no method to assess the validity of these estimates for a dataset where the true cellular proportions are unknown. In this study, we describe, validate and characterise a sample level accuracy metric for derived cellular heterogeneity variables. The CETYGO score captures the deviation between a samples DNAm profile and its expected profile given the estimated cellular proportions and cell type reference profiles.We demonstrate that the CETYGO score consistently distinguishes inaccurate and incomplete deconvolutions when applied to reconstructed whole blood profiles. By applying our novel metric to > 6,300 empirical whole blood profiles, we find that estimating accurate cellular composition is influenced by both technical and biological variation. In particular, we show that when using the standard reference panel for whole blood, less accurate estimates are generated for females, neonates, older individuals and smokers. Our results highlight the utility of a metric to assess the accuracy of cellular deconvolution, and describe how it can enhance studies of DNA methylation that are reliant on statistical proxies for cellular heterogeneity. To facilitate incorporating our methodology into existing pipelines, we have made it freely available as an R package (https://github.com/ds420/CETYGO).

bioinformatics↗

DNA methylation signatures of Alzheimer's disease neuropathology in the cortex are primarily driven by variation in non-neuronal cell-types

Alzheimers disease (AD) is a chronic neurodegenerative disease characterized by the progressive accumulation of amyloid-beta and neurofibrillary tangles of tau in the neocortex. Utilizing extensive neuropathology data from the Brains for Dementia Research (BDR) cohort we performed the most systematic epigenome-wide association study (EWAS) of multiple measures of AD neuropathology yet undertaken, profiling DNA methylation in two cortical regions from 631 donors. We meta-analyzed our results with those from previous studies of DNA methylation in AD cortex (total n = 2,013 donors), identifying 334 cortical differentially methylated positions (DMPs) associated with AD pathology including methylomic variation at novel loci not previously implicated in dementia. We subsequently characterized DNA methylation in purified nuclei populations - enriched for neurons, oligodendrocytes and microglia - exploring the extent to which cortex AD-associated DMPs reflect differences manifest in specific cell populations. We find that the majority of DMPs identified in bulk cortex tissue actually reflect DNA methylation differences occurring in non-neuronal cells, with dramatically increased effect sizes observed in microglia-enriched nuclei populations. Our study highlights the power of utilizing multiple measures of neuropathology to identify epigenetic signatures of AD and the importance of characterizing disease-associated variation in purified neural cell-types.

genetics↗

Novel epigenetic clock for fetal brain development predicts fetal epigenetic age for iPSCs and iPSC-derived neurons.

Induced pluripotent stem cells (iPSCs) and their differentiated neurons (iPSC-neurons) are a widely used cellular model in the research of the central nervous system. However, it is unknown how well they capture age-associated processes, particularly given that pluripotent cells are only present during the earliest stages of mammalian development. Epigenetic clocks utilize coordinated age-associated changes in DNA methylation to make predictions that correlate strongly with chronological age. It has been shown that the induction of pluripotency rejuvenates predicted epigenetic age. As existing clocks are not optimized for the study of brain development, we developed the fetal brain clock (FBC), a bespoke epigenetic clock trained in human prenatal brain samples in order to investigate more precisely the epigenetic age of iPSCs and iPSC-neurons. The FBC was tested in two independent validation cohorts across a total of 194 samples, confirming that the FBC outperforms other established epigenetic clocks in fetal brain cohorts. We applied the FBC to DNA methylation data from iPSCs and iPSC-derived neuronal precursor cells and neurons, finding that these cell types are epigenetically characterized as having an early fetal age. Furthermore, while differentiation from iPSCs to neurons significantly increases epigenetic age, iPSC-neurons are still predicted as being fetal. Together our findings reiterate the need to better understand the limitations of existing epigenetic clocks for answering biological research questions and highlight a limitation of iPSC-neurons as a cellular model of age-related diseases.

neuroscience↗

Assessing the co-variability of DNA methylation across peripheral cells and tissues: implications for the interpretation of findings in epigenetic epidemiology

Summary/AbstractO_ST_ABSBackgroundC_ST_ABSMost epigenome-wide association studies (EWAS) quantify DNA methylation (DNAm) in peripheral tissues such as whole blood to identify positions in the genome where variation is statistically associated with a trait or exposure. As whole blood comprises a mix of cell types, it is unclear whether trait-associated variation is specific to an individual cellular population. MethodsWe collected three peripheral tissues (whole blood, buccal and nasal epithelial cells) from thirty individuals. Whole blood samples were subsequently processed using fluorescence-activated cell sorting (FACS) to purify five constituent cell-types (monocytes, granulocytes, CD4+ T cells, CD8+ T cells, and B cells). DNAm was profiled in all eight sample-types from each individual using the Illumina EPIC array. ResultsWe identified significant differences in both the level and variability of DNAm between different tissues and cell types, and DNAm data-derived estimates of age and smoking were found to differ dramatically across sample types from the same individual. We found that for the majority of loci variation in DNAm in individual blood cell types was only weakly predictive of variance in DNAm measured in whole blood, however, the proportion of variance explained was greater than that explained by either buccal or nasal tissues. Instead we observe that DNAm variation in whole blood is additively influenced by a combination of the major blood cell types. For a subset of sites variable DNAm detected in whole blood can be attributed to variation in a single blood cell type providing potential mechanistic insight. ConclusionsWe identified major differences in DNAm between blood cell types and peripheral tissues, with each sample type being characterized by a unique DNAm signature across multiple loci. Our results suggest that associations between whole blood DNAm and traits or exposures reflect differences in multiple cell types and provide important insights for the interpretation of EWAS performed in whole blood. Key MessagesO_LIWe identified major differences in DNA methylation between blood cell types and peripheral tissues, with each sample type being characterized by a unique DNA methylation signature across multiple loci. C_LIO_LIEstimates of DNAmAge and tobacco smoking from DNA methylation data can be highly variable across different sample types collected from the same individual at the same time. C_LIO_LIWhile individual blood cell types did predict more of the variation in whole blood compared to buccal epithelial and nasal epithelial cells, the percentage of variance explained was still small. C_LIO_LIInstead our data indicate that at the majority of sites, variation in multiple blood cell types additively combines to drive variation in DNA methylation in whole blood. C_LIO_LIThere are subset of sites where variable DNA methylation detected in whole blood can be attributed to variation in a single blood cell type. C_LI

genomics↗

Recalibrating the Epigenetic Clock: Implications for Assessing Biological Age in the Human Cortex

Human DNA-methylation data have been used to develop biomarkers of ageing - referred to epigenetic clocks - that have been widely used to identify differences between chronological age and biological age in health and disease including neurodegeneration, dementia and other brain phenotypes. Existing DNA methylation clocks are highly accurate in blood but are less precise when used in older samples or on brain tissue. We aimed to develop a novel epigenetic clock that performs optimally in human cortex tissue and has the potential to identify phenotypes associated with biological ageing in the brain. We generated an extensive dataset of human cortex DNA methylation data spanning the life-course (n = 1,397, ages = 1 to 104 years). This dataset was split into training and testing samples (training: n = 1,047; testing: n = 350). DNA methylation age estimators were derived using a transformed version of chronological age on DNA methylation at specific sites using elastic net regression, a supervised machine learning method. The cortical clock was subsequently validated in a novel human cortex dataset (n = 1,221, ages = 41 to 104 years) and tested for specificity in a large whole blood dataset (n = 1,175, ages = 28 to 98 years). We identified a set of 347 DNA methylation sites that, in combination optimally predict age in the human cortex. The sum of DNA methylation levels at these sites weighted by their regression coefficients provide the cortical DNA methylation clock age estimate. The novel clock dramatically out-performed previously reported clocks in additional cortical datasets. Our findings suggest that previous associations between predicted DNA methylation age and neurodegenerative phenotypes might represent false positives resulting from clocks not robustly calibrated to the tissue being tested and for phenotypes that become manifest in older ages. The age distribution and tissue type of samples included in training datasets need to be considered when building and applying epigenetic clock algorithms to human epidemiological or disease cohorts.

genomics↗

Large-scale analysis of DNA methylation identifies cellular alterations in blood from psychosis patients and molecular biomarkers of treatment-resistant schizophrenia.

ObjectivePsychosis - a complex and heterogeneous neuropsychiatric condition characterized by hallucinations and delusions - is a common feature of schizophrenia. There is evidence for altered DNA methylation (DNAm) associated with schizophrenia in both brain and peripheral tissues. We aimed to undertake a systematic analysis of variable DNAm associated with psychosis, schizophrenia, and treatment-resistant schizophrenia, also exploring measures of biological ageing, smoking, and blood cell composition derived from DNAm data to identify molecular biomarkers of disease. MethodsWe quantified DNAm across the genome in blood samples from 4,483 participants from seven case-control cohorts including patients with schizophrenia or first-episode psychosis. Measures of biological age, cellular composition and smoking status were derived from DNAm data using established algorithms. DNAm and derived measures were analyzed within each cohort and the results combined by meta-analysis. ResultsPsychosis cases were characterized by significant differences in measures of blood cell proportions and elevated smoking exposure derived from the DNAm data, with the largest differences seen in treatment-resistant schizophrenia patients. DNAm at 95 CpG sites was significantly different between psychosis cases and controls, with 1,048 differentially methylated positions (DMPs) identified between schizophrenia cases and controls. Schizophrenia-associated DMPs colocalize to regions identified in genetic association studies, with genes annotated to these sites enriched for pathways relevant to disease. Finally, a number of the schizophrenia associated differences were only present in the treatment-resistant schizophrenia subgroup. ConclusionsWe show that DNAm data can be leveraged to derive measures of blood cell counts and smoking that are strongly associated with psychosis. Our DNAm meta-analysis identified multiple DMPs associated with both psychosis and a more refined diagnosis of schizophrenia, with evidence for differential methylation associated with treatment-resistant schizophrenia that potentially reflects exposure to clozapine.

genomics↗

Major surgery induces acute changes in DNA methylation associated with activation of the immune response.

BackgroundSurgery is an invasive procedure evoking acute inflammatory and immune responses that are believed to mediate risk for postoperative complications including cognitive dysfunction and delirium. Although the specific mechanisms driving these responses have not been well-characterized, they are hypothesized to involve the epigenetic regulation of gene expression. We quantified genome-wide levels of DNA methylation in purified peripheral blood mononuclear cells (PBMCs) longitudinally collected from 55 elderly patients undergoing three types of major surgery (elective colorectal and hip replacement surgery, and emergency hip fracture surgery), comparing samples collected at baseline to those collected immediately post-operatively and at discharge from hospital.\n\nResultsMajor surgery was associated with acute changes in DNA methylation at sites annotated to immune system genes, paralleling changes in serum-levels of markers including C-reactive protein (CRP) and Interleukin 6 (IL-6) measured in the same individuals. Although many of the observed changes in DNA methylation are consistent across the three types of surgery, there is notable heterogeneity between surgery types at certain loci. The acute changes in DNA methylation induced by surgery are relatively stable in the postoperative period, generally persisting until discharge from hospital.\n\nConclusionsOur results highlight the dramatic alterations in gene regulation induced by invasive surgery, primarily reflecting upregulation of the immune system in response to trauma, wound healing and anaesthesia.

genomics↗

Properties of the epigenetic clock and age acceleration

BackgroundThe methylation status of numerous CpG sites in the human genome varies with age. The Horvath epigenetic clock used a wide variety of published DNA methylation data to produce an age prediction that has been widely used to, predict age in unknown samples, and draw conclusions about speed of ageing in various tissues, environments, and diseases. Despite its utility, there are a number of assumptions in the model that require examination. We explore the characteristics of the model in whole blood and multiple brain regions from older people, who are not well represented in the original training data, and in blood from a cross-sectional population study.\n\nResultsWe find that the model systematically underestimates age in tissues from older people. A decrease in slope of the predicted ages were observed at approximately 60 years, indicating that some loci in the model may change differently with age, and that age acceleration measures will themselves be age-dependent. This is seen most strongly in the cerebellum but is also present in other examined tissues, and is consistently observed in multiple datasets. An apparent association of Alzheimers disease with age acceleration disappears when age is used as a covariate. Association tests in the literature use a variety of methods for calculating age acceleration and often do not use age as a covariate. This is a potential cause of misleading findings.\n\nConclusionsAssociations of phenotypes with age acceleration should be evaluated cautiously, and chronological age should be included as a covariate in all analyses.

genomics↗

Leveraging DNA methylation quantitative trait loci to characterize the relationship between methylomic variation, gene expression and complex traits.

Characterizing the complex relationship between genetic, epigenetic and transcriptomic variation has the potential to increase understanding about the mechanisms underpinning health and disease phenotypes. In this study, we describe the most comprehensive analysis of common genetic variation on DNA methylation (DNAm) to date, using the Illumina EPIC array to profile samples from the UK Household Longitudinal study. We identified 12,689,548 significant DNA methylation quantitative trait loci (mQTL) associations (P < 6.52x10-14) occurring between 2,907,234 genetic variants and 93,268 DNAm sites, including a large number not identified using previous DNAm-profiling methods. We demonstrate the utility of these data for interpreting the functional consequences of common genetic variation associated with > 60 human traits, using Summary data-based Mendelian Randomization (SMR) to identify 1,662 pleiotropic associations between 36 complex traits and 1,246 DNAm sites. We also use SMR to characterize the relationship between DNAm and gene expression, identifying 6,798 pleiotropic associations between 5,420 DNAm sites and the transcription of 1,702 genes. Our mQTL database and SMR results are available via a searchable online database (http://www.epigenomicslab.com/online-data-resources/) as a resource to the research community.

genetics↗