Lifeboat Foundation

This lifeform can cheat time. Could it also help us push the boundaries of biology?

How organisms age is a question with broad implications for human health. In mammals, DNA methylation is a biomarker for biological age, which may predict age more accurately than date of birth. However, limitations in mammalian models make it difficult to identify mechanisms underpinning age-related DNA methylation changes. Here, we show that the short-lived model plant Arabidopsis thaliana exhibits a loss of epigenetic integrity during aging, causing heterochromatin DNA methylation decay and the expression of transposable elements. We show that the rate of epigenetic aging can be manipulated by extending or curtailing lifespan, and that shoot apical meristems are protected from this aging process. We demonstrate that a program of transcriptional repression suppresses DNA methylation maintenance pathways during aging, and that mutants of this mechanism display a complete absence of epigenetic decay. This presents a new paradigm in which a gene regulatory program sets the rate of epigenomic information loss during aging.

The authors have declared no competing interest.

Surprising findings on bacterial aging have emerged from a study carried out by a team of researchers led by the biologist Dr. Ulrich Steiner at Freie Universität Berlin. In a new paper published in Science Advances, the team demonstrated that even genetically identical bacterial cells living in the same environment react differently to the aging process and that changes occur at different rates within different regions of the cell.

Abstract. Type H vessels have been proven to couple angiogenesis and osteogenesis. The decline of type H vessels contributes to bone loss in the aging process. Aging is accompanied by the accumulation of advanced oxidation protein products (AOPPs). However, whether AOPP accumulation is involved in age-related decline of type H vessels is unclear. Here, we show that the increase of AOPP levels in plasma and bone were correlated with the decline of type H vessels and loss of bone mass in old mice. Exposure of microvascular endothelial cells to AOPPs significantly inhibited cell proliferation, migration, and tube formation, increased NADPH oxidase activity and excessive reactive oxygen species generation, upregulated the expression of vascular cell adhesion molecule-1 and intercellular cell adhesion molecule-1, and eventually impaired angiogenesis, which was alleviated by redox modulator N-acetylcysteine and NADPH oxidase inhibitor apocynin. Furthermore, reduced AOPP accumulation by NAC treatment was able to alleviate significantly the decline of type H vessels, bone mass loss and deterioration of bone microstructure in old mice. Collectively, these findings suggest that AOPPs accumulation contributes to the decline of type H vessels in the aging process, and illuminate a novel potential mechanism underlying age-related bone loss.

To learn more, a research team led by Drs. Asghar Rezaei and Kenton Kaufman of the Mayo Clinic set out to assess gait, balance, and strength in healthy people over age 50. Their study enrolled 40 participants. Half were between ages 50 and 64. The rest were ages 65 or older. In each group, half of the participants were female, and half were male.

Each participant underwent a series of tests in a motion analysis lab. Reflective markers were attached to specific locations on each participant’s feet, thighs, pelvis, head, and more. To assess gait, a 14-camera motion capture system recorded marker movements as people walked back and forth on an eight-meter-long walkway. Force plates on the floor measured ground reaction forces to detect changes in the center of pressure. Balance tests similarly used force plates to record movements and center of pressure data. The balance tests assessed the body’s sway as people stood on one leg with eyes open and on both legs with eyes open and closed. Grip strength and knee strength were measured by using specialized devices. Results were reported on October 23, 2024, in PLOS ONE.

The researchers found that gait characteristics—including walking speed and stride length—were not significantly affected by age. In contrast, several measures of balance and strength showed significant age-related reductions.

Research shows you can influence your genes to crack the longevity code.

Researchers at Wenzhou Medical University in China have discovered that changes in sleep patterns as we age are associated with lower odds of successful aging.

A team of scientists from the Chinese Academy of Sciences (CAS) and BGI Research has uncovered the intricate mechanisms by which immunoglobulins influence the aging process, a finding that might reshape our understanding of aging.

Changes to actin dynamics during brain aging are not well understood. Here, the authors report that there is an age-related increase in F-actin in Drosophila brain which disables autophagy within the tissue and limits the fly lifespan.