Ferroptosis, a regulated form of cell death driven by iron-dependent lipid peroxidation, is intricately linked to aging and cellular senescence. Understanding and modulating ferroptosis may offer novel ways to address age-related diseases, improve healthspan, and promote longevity by reducing tissue dysfunction and enhancing overall well-being.
Benzyl butyl phthalate (BBP) exposure damages DNA and accelerates ageing
Benzyl butyl phthalate (BBP), a common plasticiser, disrupts reproductive health by increasing DNA damage and oxidative stress. Exposure impairs chromosome stability and gene expression, potentially affecting fertility and ageing. Findings highlight concerns about environmental toxins’ impact on longevity and underscore the need for minimising exposure.
Machine learning designs gene regulators to slow ageing
Machine learning is used to design synthetic gene regulators that precisely target specific cell types, outperforming natural sequences. This could enable highly targeted therapies for ageing-related diseases, improving gene therapy precision and reducing off-target effects, potentially enhancing longevity by addressing cellular dysfunction more effectively.
DVE-1 and longevity regulation beyond mitochondrial stress
DVE-1 supports longevity in C. elegans through multiple pathways beyond its known role in mitochondrial stress response. It regulates lifespan independently of the mitochondrial unfolded protein response, influencing dietary restriction, germline signalling, and sensory perception. Its reduced nuclear presence in long-lived mutants suggests a broader cytosolic function in ageing.
The limits of human longevity in the twenty-first century
Radical human life extension is deemed unlikely this century. Since 1990, improvements in life expectancy have slowed, and reaching age 100 remains rare without breakthroughs in slowing biological ageing. Maximum lifespan is constrained by biological limits and diminishing returns on public health advancements
Genetic variability and the effects of dietary restriction on lifespan
Caloric restriction (20%-40%) and intermittent fasting enhanced lifespan in genetically diverse mice, with stronger effects tied to stricter calorie reduction. Lifespan varied with genetics and stress resilience, revealing healthspan and longevity are not always aligned. Extreme restrictions caused adverse effects, questioning optimal dietary strategies for ageing.
Epigenetic resilience in axolotls unlocks longevity insights
Axolotls exhibit stable DNA methylation beyond early life, suggesting epigenetic resilience linked to negligible senescence. While methylation predicts age during early years, it ceases thereafter, and regeneration events rejuvenate tissues, shedding light on their remarkable longevity and regeneration abilities. This offers molecular insights into ageing stability and tissue renewal.
Mitochondrial DNA insertions in the brain linked to ageing
Mitochondrial DNA fragments integrate into the nuclear genome (Numts), particularly in brain tissue, increasing with age and correlating with earlier mortality. In cultured fibroblasts, new insertions appear every 13 days, accelerating under stress and mitochondrial dysfunction, suggesting potential implications for ageing and longevity.
N6-Methyladenine in mitochondrial DNA and its role in ageing
Mitochondrial DNA progressively accumulates N6-methyladenine (6mA) with age, potentially serving as an ageing biomarker. In long-lived mutants, this methylation rate slows, linking mitochondrial epigenetics to longevity. The findings highlight mitochondrial DNA’s role in ageing and introduce a precise, cost-effective method for measuring 6mA levels.
The unique mechanism of DdrC in enhancing DNA stability
DdrC, a DNA repair protein from Deinococcus radiodurans, recognises and stabilises DNA breaks by binding to both single-stranded and double-stranded lesions. It bridges and compacts DNA through a novel mechanism dependent on structural asymmetry, enhancing repair efficiency and supporting the bacterium’s exceptional resistance to DNA damage.