Jan Bressler
- Epigenetics and DNA Methylation
- Genetic Associations and Epidemiology
- Birth, Development, and Health
- Health, Environment, Cognitive Aging
- Genetics and Neurodevelopmental Disorders
- Cardiovascular Health and Risk Factors
- Genetic Syndromes and Imprinting
- Air Quality and Health Impacts
- Heavy Metal Exposure and Toxicity
- Autism Spectrum Disorder Research
- RNA modifications and cancer
- Bioinformatics and Genomic Networks
- Diet and metabolism studies
- Alzheimer's disease research and treatments
- Immune responses and vaccinations
- Metabolomics and Mass Spectrometry Studies
- Trace Elements in Health
- Child Nutrition and Water Access
- Prenatal Screening and Diagnostics
- Nutrition, Genetics, and Disease
- Child Nutrition and Feeding Issues
- Mitochondrial Function and Pathology
- Aluminum toxicity and tolerance in plants and animals
- Cancer-related gene regulation
- IL-33, ST2, and ILC Pathways
The University of Texas Health Science Center at Houston
2016-2025
Institute for Neurodegenerative Disorders
2024
The University of Texas Health Science Center at San Antonio
2024
Boston University
2018-2023
Brigham and Women's Hospital
2023
Harbor–UCLA Medical Center
2023
Landscape Research Group
2023
Authorised Association Consortium
2023
University of Washington
2018-2022
Erasmus University Rotterdam
2022
Abstract Characterization of the genetic landscape Alzheimer’s disease (AD) and related dementias (ADD) provides a unique opportunity for better understanding associated pathophysiological processes. We performed two-stage genome-wide association study totaling 111,326 clinically diagnosed/‘proxy’ AD cases 677,663 controls. found 75 risk loci, which 42 were new at time analysis. Pathway enrichment analyses confirmed involvement amyloid/tau pathways highlighted microglia implication. Gene...
Obesity is an important component of the pathophysiology chronic diseases. Identifying epigenetic modifications associated with elevated adiposity, including DNA methylation variation, may point to genomic pathways that are dysregulated in numerous conditions. The Illumina 450K Bead Chip array was used assay leukocyte obtained from 2097 African American adults Atherosclerosis Risk Communities (ARIC) study. Mixed-effects regression models were test association beta value concurrent body mass...
The link between DNA methylation, obesity, and adiposity-related diseases in the general population remains uncertain.We conducted an association study of body mass index (BMI) differential methylation for over 400,000 CpGs assayed by microarray whole-blood-derived from 3,743 participants Framingham Heart Study Lothian Birth Cohorts, with independent replication three external cohorts 4,055 participants. We examined variations whole blood gene expression Mendelian randomization analyses to...
Objective To conduct an epigenome-wide analysis of DNA methylation and obesity traits. Methods was quantified in CD4+ T-cells using the Illumina Infinium HumanMethylation450 array 991 participants Genetics Lipid Lowering Drugs Diet Network. Methylation at individual cytosine-phosphate-guanine (CpG) sites as a function body mass index (BMI) waist circumference (WC), adjusting for age, gender, study site, T-cell purity, smoking, family structure, modeled. Results Epigenome-wide significant...
Background: DNA methylation-based patterns of biological aging, known as epigenetic age acceleration, are predictive all-cause mortality, but little is about their association with cardiovascular disease (CVD). Methods: We estimated 2 versions acceleration (Horvath and Hannum) using whole-blood samples from 2543 blacks. Linear Cox proportional hazards regression, respectively, were used to assess the carotid intima–media thickness (cross-sectionally) incident events, including CVD myocardial...
Mitochondrial DNA copy number (mtDNA-CN) has been associated with a variety of aging-related diseases, including all-cause mortality. However, the mechanism by which mtDNA-CN influences disease is not currently understood. One such may be through regulation nuclear gene expression via modification (nDNA) methylation.
Despite existing reports on differential DNA methylation in type 2 diabetes (T2D) and obesity, our understanding of its functional relevance remains limited. Here we show the effect early phases T2D pathology by a blood-based epigenome-wide association study 4808 non-diabetic Europeans discovery phase 11,750 individuals replication. We identify CpGs LETM1, RBM20, IRS2, MAN2A2 1q25.3 region associated with fasting insulin, FCRL6, SLAMF1, APOBEC3H 15q26.1 glucose. In silico cross-omics...
Age-related changes to the genome-wide DNA methylation (DNAm) pattern observed in blood are well-documented. Clonal hematopoiesis of indeterminate potential (CHIP), characterized by age-related acquisition and expansion leukemogenic mutations hematopoietic stem cells (HSCs), is associated with cancer coronary artery disease (CAD). Epigenetic regulators DNMT3A TET2 two most frequently mutated CHIP genes. Here, we present results from an epigenome-wide association study for 582 Cardiovascular...
Prader-Willi syndrome (PWS) is caused by paternal deficiency of human chromosome 15q11–q13. There conflicting evidence from translocations regarding the direct involvement SNRPN in pathogenesis PWS and it not known if phenotypic features result loss expression a single imprinted gene or multiple genes. In an attempt to dissect genotype/phenotype correlations for homologous region mouse 7C, we prepared three mutant genotypes: (i) mice with deletion Snrpn exon 2, which removes portion small,...
Abstract The genetic contribution to autism is often attributed the combined effects of many loci (ten or more). This conclusion based in part on much lower concordance for dizygotic (DZ) than monozygotic (MZ) twins, and consistent with failure find strong evidence linkage genome‐wide studies. We propose that twin data are compatible oligogenic inheritance a major, epigenetic, de novo component etiology. Based maternal but not paternal duplications chromosome 15q cause autism, we attempted...
Single nucleotide polymorphisms (SNPs) in the fat mass and obesity associated (FTO) gene are with body index (BMI) populations of European descent. The FTO rs9939609 variant, first detected a genome-wide association study diabetes, conferred an increased disease risk that was abolished after adjustment for BMI, suggesting may be due to variation adiposity. relationship between four previously identified span 19.6-kb genomic region, therefore evaluated biracial population-based...