Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1262489 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Alzheimer’s disease (AD) is the leading cause of dementia, driven by complex molecular alterations that disrupt neural and glial cell function. However, the precise epigenomic and chromatin regulatory changes underlying AD pathogenesis across different brain regions remain incompletely understood. To address this, we generated a comprehensive single-cell multi-omic atlas of the human AD brain. We profiled 11 AD donors and 9 age-matched healthy donors, spanning three key brain regions implicated in AD pathology: the visual cortex (VC), temporal cortex (TC), and prefrontal cortex (PFC). Using single-nucleus methylome sequencing (snmC-seq3) and joint profiling of chromatin conformation and DNA methylation (snm3C-seq), we obtained extensive datasets enabling integrated analysis of transcriptional regulation, epigenetic remodeling, and 3D genome architecture. This resource allowed us to characterize AD-associated alterations in DNA methylation at promoters, enhancers, and transposable elements, as well as their consequences on transcription factor motif accessibility. At the chromatin level, we identified disease-related changes in higher-order genome organization, including compartments, topologically associating domains (TADs), and loops. By comparing multiple cortical regions, we also uncovered regional heterogeneity within matched cell types, highlighting both shared and region-specific epigenetic signatures of AD. Together, this atlas provides a systematic, multi-region view of single-cell epigenomic landscapes in AD and offers insights into regulatory mechanisms underlying disease progression.
2025-12-04 | GSE308132 | GEO
Project description:We assayed CpG methylation in cerebral cortex of neurologically and psychiatrically normal human postmortem specimens, as well as mouse forebrain specimens. Cross-species human-mouse DNA methylation conservation analysis shows that DNA methylation is not correlated with sequence conservation. Instead, greater DNA methylation conservation is correlated with increasing CpG density. We identified key genomic features that can be targeted for identification of epigenetic loci that may be developmentally and evolutionarily conserved and wherein aberrations in DNA methylation patterns can confer risk for disease. Characterization of evolutionary signatures of DNA methylation in the brain
2011-10-04 | E-GEOD-32647 | biostudies-arrayexpress
Project description:Epigenetic alterations are increasingly recognized as mechanisms for disease-associated changes in genome function and important risk factors for complex diseases. The epigenome differs between cell types and so far has been characterized in few human tissues only. In order to identify disease-associated DNA methylation differences for atopic dermatitis (AD), we investigated DNA from whole blood, T cells, B cells, as well as lesional and non-lesional epidermis from AD patients and healthy controls. To elicit functional links, we examined epidermal mRNA expression profiles. No genome-wide significant DNA methylation differences between AD cases and controls were observed in whole blood, T cells, and B cells, and, in general, intra-individual differences in DNA methylation were larger than interindividual differences. However, striking methylation differences were observed between lesional epidermis from patients and healthy control epidermis for various CpG sites, which partly correlated with altered transcript levels of genes predominantly relevant for epidermal differentiation and innate immune response. Significant DNA methylation differences were discordant in skin and blood samples, suggesting that blood is not an ideal surrogate for skin tissue. Our pilot study provides preliminary evidence for functionally relevant DNA methylation differences associated with AD, particularly in the epidermis, and represents a starting point for future investigations of epigenetic mechanisms in AD.
2014-08-26 | GSE60709 | GEO
Project description:Recent work has identified roles for environmental, genetic and epigenetic factors in AD risk. Motivated by suspected roles for epigenetic modifications in AD, we performed a genome-wide screen of DNA methylation using the Illumina Infinium HumanMethylation450 array platform on bulk tissue samples from the superior temporal gyrus (STG) of AD cases and non-demented controls. We paired a sliding window approach with linear models that account for age, gender, ethnicity, and estimated cellular proportions (neuronal vs. glial), to characterize AD-associated differentially methylated regions (DMRs). Whole DNA was extracted from STG tissue dissections collected from deceased individuals with and without Alzheimers Disease. DNA was bisulfite converted and global DNA methylation levels were assessed using Illumina Infinium HumanMethylation450 BeadChip.
2015-12-18 | E-GEOD-76105 | biostudies-arrayexpress
Project description:Epigenetic alterations are increasingly recognized as mechanisms for disease-associated changes in genome function and important risk factors for complex diseases. The epigenome differs between cell types and so far has been characterized in few human tissues only. In order to identify disease-associated DNA methylation differences for atopic dermatitis (AD), we investigated DNA from whole blood, T cells, B cells, as well as lesional and non-lesional epidermis from AD patients and healthy controls. To elicit functional links, we examined epidermal mRNA expression profiles. No genome-wide significant DNA methylation differences between AD cases and controls were observed in whole blood, T cells, and B cells, and, in general, intra-individual differences in DNA methylation were larger than interindividual differences. However, striking methylation differences were observed between lesional epidermis from patients and healthy control epidermis for various CpG sites, which partly correlated with altered transcript levels of genes predominantly relevant for epidermal differentiation and innate immune response. Significant DNA methylation differences were discordant in skin and blood samples, suggesting that blood is not an ideal surrogate for skin tissue. Our pilot study provides preliminary evidence for functionally relevant DNA methylation differences associated with AD, particularly in the epidermis, and represents a starting point for future investigations of epigenetic mechanisms in AD. Total RNA obtained from 7 patients from non-lesional skin, 12 patients from lesional skin and 14 controls from healthy skin
2014-08-26 | E-GEOD-60709 | biostudies-arrayexpress
Project description:Psoriasis and atopic dermatitis (AD) are characterized by polarized CD4+ T cell responses. During the polarization of naM-CM-/ve CD4+ T cells, DNA methylation plays an important role in the regulation of gene transcription. In this study, we profiled the genome-wide DNA methylation status of naM-CM-/ve CD4+ T cells in patients with psoriasis or AD and healthy controls using a ChIP-seq method. As a result, twenty-six regions in the genome ranging in size from 10 to 70 kb were markedly hypomethylated in patients with psoriasis. These regions were mostly pericentromeric on 10 different chromosomes and overlapped with various strong epigenomic signals, such as histone modifications and transcription factor binding sites, that were observed in the ENCODE project. Gene-centric analysis indicated that the promoter regions of 124 genes on the X chromosome had dramatically elevated methylation levels in patients with psoriasis as compared to those from healthy controls (> 4-fold). Moreover, immune-related genes on the X chromosome had higher hypermethylation than other genes (P < 0.05). These findings imply that methylation changes in naM-CM-/ve CD4+ T cells may affect CD4+ T cell polarization, especially in the pathogenesis of psoriasis. Keywords: Psoriasis, Atopic dermatitis, DNA methylation, naM-CM-/ve CD4+ T cells Sample submission examines DNA methylation from human naive CD4+ T cells in patients with psoriasis and atopic dermatitis. Note: Raw data available only for Sample GSM871288.
2012-03-17 | E-GEOD-35582 | biostudies-arrayexpress
Project description:To test the differences in genome-wide DNA methylation signatures of haploid, diploid and triploid hESCs, we extracted genomic DNA from these cells and performed RRBS.
2023-05-04 | E-MTAB-11478 | biostudies-arrayexpress
Project description:Joint-specific DNA methylation signatures in rheumatoid arthritis [methylation array]
| PRJNA317756 | ENA