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  • Early type 2 diabetes (T2D) risk assessment could help slow or prevent disease onset. Here the authors used blood-based DNA methylation data to develop 10-year risk prediction models for incident T2D. The results show an improvement in performance beyond standard risk factors typically used to predict the risk of T2D onset.

    • Yipeng Cheng
    • Danni A. Gadd
    • Riccardo E. Marioni
  • The authors found that, across tissues and in multiple datasets, aging is accompanied by a length-associated transcriptome imbalance. In most cases, a decrease in the relative abundance of long transcripts was observed and could be reversed by interventions targeting aging.

    • Thomas Stoeger
    • Rogan A. Grant
    • Luis A. Nunes Amaral
    AnalysisOpen Access
  • The authors analyze microbiome profiles from several public repositories to identify the higher-level indices that best reflect the abundance and ranking of disease-associated and health-associated gut microbes and that may help identify targets for therapeutic modulation.

    • Tarini Shankar Ghosh
    • Fergus Shanahan
    • Paul W. O’Toole
    AnalysisOpen Access
  • Transcription factors control cell identity and function in health, disease and aging. Here the authors identify age-associated changes of transcriptional regulatory networks in single cells, revealing cell-type and tissue-type-independent patterns in key pathways, including circadian rhythm, antigen processing, collagen processing and inflammation.

    • Alok K. Maity
    • Xue Hu
    • Andrew E. Teschendorff
  • An economic analysis suggests that targeting aging offers potentially larger economic gains than eradicating individual diseases. Slowing aging to increase life expectancy by 1 year is worth US$38 trillion, and by 10 years, US$367 trillion.

    • Andrew J. Scott
    • Martin Ellison
    • David A. Sinclair
    AnalysisOpen Access
  • Using genetic and demographic data from the UK Biobank, the authors clustered 116 common diseases based on their age-of-onset profiles and found increased genetic similarity within clusters, suggesting common etiologies. Two of the four disease clusters were associated with aging-related genes but differed in functional enrichment and evolutionary profiles.

    • Handan Melike Dönertaş
    • Daniel K. Fabian
    • Janet M. Thornton