All articles tagged with #aging clocks
In a small 12-week study of rentosertib for idiopathic pulmonary fibrosis, six independent aging clocks all indicated the patients' blood appeared biologically younger, with four-week reductions of about 2.7–3.5 years on some clocks, but the findings are limited by the small sample size and potential disease-improvement effects, so they do not prove anti-aging effects and require larger, longer trials.
A large Nature study across 23 aging clocks in ~500,000 people found a U-shaped link between sleep duration and biological aging: the slowest aging occurred for about 6.4–7.8 hours per night, while both under 6 hours and over 8 hours were linked to faster aging; causality isn’t proven, but the takeaway is to aim for roughly seven hours with consistent sleep habits and good daytime-light exposure.
A small study of rentosertib, an experimental drug for idiopathic pulmonary fibrosis, found biomarkers suggesting participants appeared biologically 3–4 years younger across multiple aging clocks. Researchers caution the result is preliminary, based on 42 patients over 12 weeks, and does not prove actual aging reversal or longer life. Larger, longer trials are needed, including a phase 3 study in China; side effects were generally manageable.
An AI-designed drug from Insilico Medicine, rentosertib, reduced biological aging markers across six aging clocks in a 12‑week study with 42 participants, suggesting AI may modulate aging biology. However, aging clocks are debated, and this is an early-stage finding with many trials and regulatory hurdles still to come.
A Nature Aging study using PathStAR analyzed thousands of tissue images from 970 donors and found that aging is organ-specific and often biphasic: arteries show early aging in the 30s, ovaries in two bursts around 35–40 and 55–60, and nine other tissues exhibit two aging peaks in the 30s and 50s. Hormonal changes and inflammation appear to link these shifts, suggesting interventions targeted to vulnerable organs could slow aging more effectively than a single overall aging clock.
A UK Biobank analysis of about 500,000 adults links sleep duration to systemic aging. Using 23 biological aging clocks, researchers found a U‑shaped pattern where roughly 6.4–7.8 hours of sleep per night corresponded to the lowest aging signals across organs (brain, liver, lungs, immune system, skin, endocrine system, adipose tissue, pancreas). Sleeping less than six hours or more than eight hours was associated with faster aging in several clocks, though the exact optimal range varied by organ and sex. The team calls this framework the Sleep Chart, underscoring sleep as a broad, modifiable factor in aging rather than a universal prescription.
A UK Biobank study using organ-specific aging clocks across 17 organs finds a U-shaped relationship between sleep duration and biological aging: both <6 hours and >8 hours accelerate aging, with the slowest aging in people who sleep 6.4–7.8 hours daily. Sleep affects a coordinated brain–body network, linking short sleep to depression and metabolic/cardiovascular diseases, while long sleep associates with different pathways involving adipose clocks. The research suggests sleep optimization could slow systemic aging and reduce disease risk, including late-life depression.
A large international study using 23 aging clocks across organs and UK Biobank data finds that both too little (<6 hours) and too much (>8 hours) sleep are associated with faster biological aging and higher mortality, with an optimal window roughly 6.4–7.8 hours. Short sleep links to cardiovascular, metabolic, and psychiatric risks, while long sleep clusters with brain-related conditions; the depression pathways differ between the two sleep patterns. The findings come from MRI, blood proteins, and metabolite data, highlighting sleep’s broad impact beyond the brain.
A University College London study of more than 3,500 people used seven aging clocks to measure biological age and found that frequency and variety of arts and cultural activities—such as gallery visits and other cultural engagement—are linked to slower aging, with effects comparable to physical activity; strongest in those 40 and older. While the study shows association, not causation, researchers say integrating the arts into public health could improve health outcomes alongside exercise.
Aging clocks applied to single neuron types in C. elegans reveal neuron-type–specific biological ages, with environmentally exposed ciliated amphid neurons aging fastest and degenerating earlier. Reducing translation slows degeneration in fast-aging neurons, and neuronal aging patterns correlate with human brain aging while anticorrelating with known geroprotective interventions. An in silico CMAP screen identifies potential neuroprotective compounds, notably syringic acid and vanoxerine, while some agents (e.g., WAY-100635, Bay K8644) can be neurotoxic. The study suggests neuron-type aging trajectories can guide protective interventions and risk-factor identification for neurodegeneration across species.