Recent studies investigating longevity have revealed very few convincing genetic associations with increased lifespan. This is, in part, due to the complexity of biological aging, as well as the limited power of genome-wide association studies, which assay common single nucleotide polymorphisms (SNPs) and require several thousand subjects to achieve statistical significance. To overcome such barriers, we performed comprehensive DNA sequencing of a panel of 20 genes previously associated with phenotypic aging in a cohort of 200 individuals, half of whom were clinically defined by an "early aging" phenotype, and half of whom were clinically defined by a "late aging" phenotype based on age (65-75 years) and the ability to walk up a flight of stairs or walk for 15 min without resting.
View Article and Find Full Text PDFObjective: To determine the stage of B cell development at which a systemic lupus erythematosus (SLE)-associated DNA methylation signature originates in African American (AA) and European American (EA) subjects, and to assess whether epigenetic defects in B cell development patterns could be predictive of SLE status in individual and mixed immune cell populations.
Methods: B cells from AA patients (n = 31) and EA patients (n = 49) with or without SLE were sorted using fluorescence-activated cell sorting into 5 B cell subsets. DNA methylation, measured at ~460,000 CpG sites, was interrogated in each subset.