LongevityMap: a database of human genetic variants associated with longevity

Budovsky, Arie; Craig, Thomas; Wang, Jingwei; Tăcutu, Robi; Csordás, Attila; Lourenço, Joana; Fraifeld, Vadim E.; Magalhães, João Pedro de

doi:10.1016/j.tig.2013.08.003

Cited by 94 publications

(76 citation statements)

References 7 publications

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“…16 4,552 methylation markers correlated with age-but not with gene expression changes in peripheral blood Steegenga_aDMRs_meta 16 7,477 age-associated methylation markers identified in multiple studies Heyn_aDMRs 11 3,205 age-associated methylation markers differentially methylated in cord blood of newborns and CD4C T cells of centenarian; 1,219 of them showed hypermethylation with age, 1,986 were found to be hypomethylated with age Age-associated genes (aGENs) Hannum_genes_associated 1 326 genes correlated with age by expression, whole blood, data not related to methylation data Hannum_genes_predictive; 1 Hannum_genes_predictive_pos; Hannum_genes_predictive_neg 55 genes predictive of age based by their expression, whole blood, data not related to methylation data. Twenty-four of these genes showed positive correlation with age by expression, 31 were found to be negatively correlated with age Genes_LongevityMap 47 752 manually curated list of age-associated genes deMagalhaes_genes_all; 33 deMagalhaes_genes_pos; deMagalhaes_genes_neg 73 age-associated genes. 56 genes overexpressed with age; 17 genes underexpressed with age.…”

Section: Resultsmentioning

confidence: 99%

Polycomb repressive complex 2 epigenomic signature defines age-associated hypermethylation and gene expression changes

Dozmorov

2015

Epigenetics

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Although age-associated gene expression and methylation changes have been reported throughout the literature, the unifying epigenomic principles of aging remain poorly understood. Recent explosion in availability and resolution of functional/regulatory genome annotation data (epigenomic data), such as that provided by the ENCODE and Roadmap Epigenomics projects, provides an opportunity for the identification of epigenomic mechanisms potentially altered by age-associated differentially methylated regions (aDMRs) and regulatory signatures in the promoters of ageassociated genes (aGENs). In this study we found that aDMRs and aGENs identified in multiple independent studies share a common Polycomb Repressive Complex 2 signature marked by EZH2, SUZ12, CTCF binding sites, repressive H3K27me3, and activating H3K4me1 histone modification marks, and a "poised promoter" chromatin state. This signature is depleted in RNA Polymerase II-associated transcription factor binding sites, activating H3K79me2, H3K36me3, H3K27ac marks, and an "active promoter" chromatin state. The PRC2 signature was shown to be generally stable across cell types. When considering the directionality of methylation changes, we found the PRC2 signature to be associated with aDMRs hypermethylated with age, while hypomethylated aDMRs were associated with enhancers. In contrast, aGENs were associated with the PRC2 signature independently of the directionality of gene expression changes. In this study we demonstrate that the PRC2 signature is the common epigenomic context of genomic regions associated with hypermethylation and gene expression changes in aging.

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Section: Resultsmentioning

confidence: 99%

Polycomb repressive complex 2 epigenomic signature defines age-associated hypermethylation and gene expression changes

Dozmorov

2015

Epigenetics

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“…In addition to the above-mentioned genes, many other genes can influence lifespan. The possible influence of a gene on lifespan can be found in GenAge, a database with information on over 700 genes (Tacutu et al ., 2012; Budovsky et al ., 2013). The possible relevance of most of these age-related genes on PD cannot be directly checked because there is not a gene bank for PD similar to GenAge (Wirdefeldt et al ., 2011).…”

Section: Genetic Control Of Pd and Agingmentioning

confidence: 99%

Parkinson's disease as a result of aging

et al. 2015

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It is generally considered that Parkinson's disease is induced by specific agents that degenerate a clearly defined population of dopaminergic neurons. Data commented in this review suggest that this assumption is not as clear as is often thought and that aging may be critical for Parkinson's disease. Neurons degenerating in Parkinson's disease also degenerate in normal aging, and the different agents involved in the etiology of this illness are also involved in aging. Senescence is a wider phenomenon affecting cells all over the body, whereas Parkinson's disease seems to be restricted to certain brain centers and cell populations. However, reviewed data suggest that Parkinson's disease may be a local expression of aging on cell populations which, by their characteristics (high number of synaptic terminals and mitochondria, unmyelinated axons, etc.), are highly vulnerable to the agents promoting aging. The development of new knowledge about Parkinson's disease could be accelerated if the research on aging and Parkinson's disease were planned together, and the perspective provided by gerontology gains relevance in this field.

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“…An epigenomic scan revealed 490 differentially methylated regions correlated with chronological age (Bell et al, 2012). As a reference source, LongevityMap has curated genes associated with aging and longevity from genetic studies (Budovsky et al, 2013).…”

Section: Ad Brain Aging and Longevitymentioning

confidence: 99%