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Scientists have discovered that a potential new drug can reverse severe fatty liver disease in animal models by restoring gut health and blocking harmful substances from reaching the liver. The breakthrough could pave the way for new treatments for liver disease and potentially other serious conditions, including cardiovascular disease.

Scientists have uncovered a surprising cause of age-related cognitive decline involving brain cells previously thought to be entirely beneficial. As these cells become dysfunctional, they can produce abnormal amounts of myelin, disrupting nerve fibers and potentially contributing to worsening memory and thinking skills.

Scientists have discovered a surprising two-way relationship between sleep and growth hormone, revealing how the brain carefully balances physical recovery with wakefulness. The findings could help explain why poor sleep harms metabolism and brain health, potentially opening the door to new treatments for sleep and neurological disorders.

Stanford scientists have developed a revolutionary microscope that reveals the hidden inner workings of living cells in real time, without the fluorescent labels that can interfere with observations. The breakthrough could provide new insights into cancer, infectious diseases, and how drugs interact with cells.

USC scientists have discovered a way to create a potentially renewable supply of genetically engineered immune cells that can attack cancer and strengthen the body's natural defenses. By growing and modifying immature immune cells rather than mature ones, researchers developed a system that can continuously produce tumor-fighting cells inside the body.

Yale scientists have uncovered how the stress hormone cortisol helps the brain turn emotional experiences into stronger, longer-lasting memories. The discovery reveals that stress can reshape communication between brain networks involved in emotion and memory, potentially explaining why certain moments are so difficult to forget.

Flap endonuclease 1 (FEN1), a key enzyme in DNA metabolism, exhibits oncogenic properties in various cancers. However, its functional role and underlying mechanisms in lung adenocarcinoma (LUAD) progression and tumor immunity remain poorly defined. Here, we demonstrate that FEN1 is significantly upregulated in LUAD tissues and serves as an independent prognostic factor for poor survival. Genetic depletion of FEN1 suppressed LUAD cell proliferation by inducing G0/G1 cell cycle arrest and cellular...

Ageing is accompanied by a progressive decline in homeostatic resilience that increases vulnerability to chronic disease, disability and cognitive impairment. Although unhealthy brain ageing can often be prevented by managing the underlying risk factors, the molecular, cellular and physiological mechanisms that connect risk factors to late-life brain dysfunction remain incompletely understood. This review examines the role of the endocannabinoid system in brain ageing. The endocannabinoid system...

The glymphatic system clears cerebral waste, yet strategies to enhance its function remain elusive. Here, we show that 40.68 MHz ultrashort wave (USW) rapidly enhances glymphatic bulk flow in healthy mice within 10 minutes. USW potentiates both glymphatic influx and efflux, concomitant with increased Delta wave neuronal synchronization, as confirmed by local field potentials and electroencephalograms. Chemogenetic silencing confirms that USW-driven glymphatic enhancement depends on neuronal...

Neurodegenerative diseases (NDs) are increasingly recognised in Sub-Saharan Africa (SSA), but the principal scientific challenge is no longer simply to document a presumed hidden burden. It is to determine how much of the observed heterogeneity reflects underlying neurobiology and how much arises from age structure, case ascertainment, culturally sensitive phenotyping and unequal access to neurological diagnosis. This critical narrative review synthesises evidence from 2000 to July 2026 across...

Aging is accompanied by progressive functional decline and morphological defects of cholinergic neurons. Some probiotic bacteria with proficiency for biofilm formation in the gut are being discussed as potentially neuroprotective. Here, we screened Bacillus subtilis (B. subtilis) strains for biofilm production, using an in vitro assay. Thereafter, a transgenic Caenorhabditis elegans (C. elegans) strain with its cholinergic neurons expressing green fluorescent protein (GFP) was fed for up to 15...

S-adenosyl-L-methionine (SAM) is a fundamental methyl donor; however, the physiological role of its byproduct and competitive inhibitor, S-adenosyl-L-homocysteine (SAH), remains unclear. Here, we show that transient reactive oxygen species (ROS) production triggered by SAH during the early logarithmic phase mimics partial SAH hydrolase inhibition, extending the yeast chronological lifespan (CLS) through a hormetic mechanism. This study reveals that the dual nature of ROS in aging is determined...

Electronic textiles represent a transformative platform for integrating technology into daily wear, yet their development has been undermined by a fundamental challenge: the conflicting requirements between mechanical deformation for functionality and structural stability for performance. This challenge is particularly acute in cylindrical fiber electrodes, where inherent nonuniform electric field distribution leads to dendrite formation and poor active material utilization-problems that are...

The role of senescent tumor cells in modulating the immune microenvironment and influencing immunotherapy efficacy remains poorly understood. In this study, we investigate the function of the senescence-associated gene membrane magnesium transporter 1 (MMGT1) in triple-negative breast cancer (TNBC) immunotherapy. MMGT1 is upregulated in TNBC and correlates with poor prognosis. Mammary gland-specific knockout of Mmgt1 significantly impedes tumor growth. Mechanistically, MMGT1 promotes lipid...

Aging is frequently accompanied by profound alterations in the chromatin landscape, leading to widespread changes in transcriptional programs and cellular functions. Forkhead box O (FOXO) proteins, traditionally viewed as downstream effectors of insulin and stress-response signaling, are now emerging as dynamic chromatin regulators that integrate metabolic cues with epigenetic remodeling during aging. In this review, we first outline the major epigenetic and chromatin alterations associated with...

Ageing profoundly impairs vaccine efficacy, leaving older individuals highly susceptible to infectious diseases despite vaccination. Although B cells retain the intrinsic capacity to generate germinal centre (GC) responses in older people, age-associated defects in T cells, dendritic cells and follicular dendritic cells (FDCs) limit the development of high-affinity, class-switched antibody responses. Here, we hypothesised that senescent fibroblasts disrupt B cell activation and expansion, thus...

CONCLUSIONS: In this post-hoc analysis, group allocation was not associated with lower body weight at follow-up. Despite high levels of motivation and confidence regarding weight loss and favorable changes in diet and physical activity in the intervention group, these changes did not translate into measurable weight loss.

Chronic metabolic stress is increasingly recognized as a driver of aging-like tissue dysfunction, but whether it durably reprograms liver regenerative cells, potentially compromising tissue maintenance and repair, remains unknown. Here, we show that high-fat diet (HFD)-induced metabolic stress promotes a persistent senescence-like state in the liver regenerative compartment. In male rats, chronic HFD feeding induced hepatic steatosis together with oxidative stress, inflammatory responses, and...

Vascular endothelial cell (VEC) senescence drives organismal aging and age-related pathologies, yet the intrinsic factors preserving endothelial youthfulness remain poorly defined. Here, we identify MTR4, an evolutionarily conserved RNA helicase and nuclear RNA exosome cofactor, as a novel regulator of VEC senescence. MTR4 protein declines markedly in senescent HUVECs and aged mouse aortas, independent of general cell cycle exit. Mechanistically, senescence-induced upregulation of the E3...