Methylation pace of aging is a novel measure requiring only a blood sample that clinical-trial and observational studies can use to test if treatments modify how fast participants are aging.

Biological ages have the potential to provide aging-related information beyond chronological age and can be predictive of mortality independently of both chronological age and different types of biological ages.

An integrative study of five biological clocks in somatic and mental health indicate that one's biological age is best reflected by combining aging measures from multiple cellular levels.

Direct reprogramming of smooth muscle cells from HGPS patients revealed that BMP4 is a key contributor of vascular degeneration and might represent a new therapeutic target.

The tyrosine degradation pathway reprogramming connects mitochondrial dysfunction, aging, and production of tyrosine-derived neuromediators that can be targeted with an FDA-approved drug, Tigecycline.

Site-specific DNA methylation analysis at three CG dinucleotides by pyrosequencing provides a reliable measure for epigenetic aging of mice.

Integrating the analysis of molecular data from different sources may improve our understanding of the effects of biological aging.

Mitochondrial-targeted SS-31 peptide ameliorates mitochondrial dysfunction and rescues pre-existing cardiac dysfunction in old mice, supporting the translational potential of mitochondrial protective interventions to treat age-related diseases.

MicroRNA-based direct conversion of human fibroblasts to neurons is applicable to fibroblasts from donors ranging in age from neonatal to centenarian, allowing the generation of neurons that maintain the age-associated signatures of the starting fibroblasts.

A robust mouse multi-tissue age predictor is presented that can be used to assess the DNA methylation age of mouse tissues and test the effects of longevity interventions.