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An NIH study found that women with high levels of two common “forever chemicals” had up to 93% higher rates of an aggressive form of breast cancer. The discovery raises concerns about the potential health effects of persistent chemicals found in everyday products.

Scientists have uncovered a surprising way that fructose, a sugar commonly found in sweetened foods and drinks, may help aggressive ovarian cancer spread. Researchers discovered that cancer cells surviving chemotherapy release fructose that weakens the bonds holding neighboring tumor cells together, making it easier for cancer to spread. High dietary fructose levels and cholesterol-lowering statins also produced concerning effects in preclinical experiments.

A surprising new study suggests that walking, jogging, and even traditional weight training may be less effective at stimulating bone formation than high-intensity sports involving explosive movements and sudden changes in direction. Researchers found that activities such as football and handball increased markers of bone formation by up to 46%, potentially revealing a better way to protect bones against aging and osteoporosis.

A new study found that energy drinks and stimulant supplements were linked to disproportionately frequent reports of serious heart problems, including 11 times more reports of cardiac arrest and 4.5 times more reports of heart attacks. Young adults accounted for nearly half of the cardiovascular reports involving these products, raising concerns about their potential risks despite the study being unable to prove causation.

A surprising study of more than 4,500 older adults found that people who were overweight or obese when diagnosed with dementia had a 16% to 27% lower risk of death than those at a normal weight. Researchers suspect that extra energy and muscle reserves may help patients survive the disease's toll on the body, although the reason for the survival advantage remains unclear.

Ancient manuscripts, including the 1,000-year-old York Gospels, have revealed traces of a deadly sheep virus whose history stretches back more than 3,700 years. Scientists discovered that the virus has remained remarkably unchanged for millennia, turning historic parchment into an unexpected record of ancient disease outbreaks.

Although cerebellum is neuropathologically affected in Alzheimer's disease (AD) and AD-related dementia (ADRD), the cell type-specific genomic and epigenomic changes remain poorly understood. Here, we present single-nucleus multiome (RNA-seq and ATAC-seq) analysis of 103,861 nuclei isolated from both the cerebellum and frontal cortex of diseased individuals and cognitively healthy controls. We identify 431,834 significant peak-to-gene linkages across cell subtypes, revealing cis-regulatory...

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With an aging donor population, ischemic and inflammatory injury during organ procurement and preservation may be associated with senescence-associated programs influencing graft biology. Although donor type-specific injury patterns are known, their role in driving cellular senescence and downstream inflammatory responses remains unclear. We performed smart-3SEQ bulk RNA-sequencing on human liver tissue obtained from donation after brain death (DBD) and donation after circulatory death (DCD)...

Synaptome architecture describes the spatiotemporal distribution of highly diverse excitatory synapses throughout the brain. Whether and how this architecture is impacted by experience and sensory input is unknown. We found that environmental enrichment and monocular visual deprivation drive large-scale reconfiguration of excitatory synapse populations in more than one hundred regions of the mouse brain. Different experiences modify distinct subsets of synapse types and subtypes, with patterns...

Somatic evolution in ageing tissues underlies many cancers^(1,2). However, our quantitative understanding of the rules governing this pre-cancerous evolution remains incomplete. Here we exploit a unique collection of serial blood samples³, collected annually for up to a decade and beginning as early as 15 years before diagnosis of acute myeloid leukaemia, to provide a quantitative description of pre-cancerous evolutionary dynamics. Using deep duplex sequencing and evolutionary theory, we...

Aging is associated with a progressive decline in immune surveillance, yet the mechanisms that constrain this process remain incompletely understood. Here we uncover a lipid-biomechanical mechanism in human natural killer (NK) cells that contributes to age-related immune decline. We show that aging drives a coordinated metabolic and physical state in NK cells, marked by lipid accumulation, increased membrane fluidity, reduced cortical stiffness and defective immune synapse organization,...

Metabolic ageing and associated changes in lipid mobilisation have been heavily studied in humans and model taxa, yet remain poorly understood in farmed animals, with potentially important implications for health and welfare outcomes. Here, we compared three stages of aquaculture production in Atlantic salmon (Salmo salar), the world's most commercially valuable farmed fish. Our sampling captures smoltification, a key life-cycle transition, followed by the metabolic changes occurring during...

CONCLUSION: No substantive difference existed in healthy aging levels between rural-urban older adults, while the associations of individual attributes and social support with healthy aging varied across rural-urban groups. Therefore, differentiated social support systems tailored to local conditions should be established for rural and urban areas to continuously advance equitable healthy aging.

CONCLUSION: U3A students had higher healthy aging and quality of life scores than their peers who were not enrolled in the program, and these differences remained significant after adjustment for sociodemographic and health-related variables. A moderate positive correlation was also found between healthy aging and quality of life. These findings indicate that U3A programs may be considered within the scope of community-based healthy aging initiatives. However, causal inferences cannot be made...

The blood-brain barrier (BBB) has been defined primarily by what it excludes, yet the scale and function of physiological blood-to-brain protein transport remain largely unknown. Using bioorthogonal proteomics, we find that the healthy BBB samples 191 plasma proteins and permits 92 into the brain parenchyma. Enriched for carrier and metabolic functions, these proteins home to distinct brain cell types, such as apolipoprotein A1 (APOA1) to astrocytes and alpha-1 antitrypsin (SERPINA1) to...

Alzheimer's disease (AD), the leading cause of dementia, is increasingly recognized as a metabolic disorder characterized by disrupted insulin and insulin-like growth factor-1 signaling in the brain, a concept now referred to as type 3 diabetes. Central to this perspective is the insulin receptor substrate-1/phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin (IRS-1/PI3K/Akt/mTOR) cascade, which acts as the primary convergence point linking systemic insulin resistance to...

Healthy older adults exhibit both selective impairments in episodic memory - memory for events situated within a specific time and place - and deficits in executive function, reflected by difficulty switching between different tasks and inhibiting task-irrelevant information. Prior work has shown that older adults show diminished mnemonic brain state engagement - recruitment of whole brain activity patterns that selectively support memory encoding and memory retrieval. Our hypothesis is that...

Cellular senescence is a state of irreversible cell-cycle arrest that prevents cancer but promotes aging and inflammation. Conflicting molecular profiles of senescence may arise from contamination by neighboring proliferating cells. Here, we developed SenLect (senescence selection), a genetically encoded system for purifying senescent cells in culture. SenLect expresses mCherry-2A-PuroR under the senescence-activated miR-146a promoter, providing senescent cells a selective advantage over...

Alzheimer's disease (AD), the leading cause of dementia, is increasingly recognized as a metabolic disorder characterized by disrupted insulin and insulin-like growth factor-1 signaling in the brain, a concept now referred to as type 3 diabetes. Central to this perspective is the insulin receptor substrate-1/phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin (IRS-1/PI3K/Akt/mTOR) cascade, which acts as the primary convergence point linking systemic insulin resistance to...