Researchers in Northern Ireland examined whether exposure to fine particulate matter (PM2.5) and nitrogen dioxide (NO₂) increases the risk of Parkinson’s disease. While no overall link was found after adjusting for confounders, younger adults under 50 showed a modest association with PM2.5, raising questions about age-related susceptibility and diagnostic misclassification.
Scientists have discovered a method to induce human endothelial cells from a small biopsy sample to multiply in the laboratory, producing more than enough cells to replace damaged blood vessels or nourish organs for transplantation, according to a preclinical study by Weill Cornell Medicine investigators.
Endothelial cells form the inner lining of blood vessels and regulate blood flow, inflammation and healing. Traditional approaches for growing these cells in the lab have yielded only limited numbers before they lose their ability to function. The new method involves treating adult endothelial cells with a small molecule that triggers the hibernating cells to wake up and divide hundreds of times without signs of aging, mutation or loss of function.
The findings, published Oct. 14 in Nature Cardiovascular Research, may provide a reliable way to generate an enormous number of a patient’s own endothelial cells, enabling vascular grafts for heart disease, diabetes treatments and organ transplants and strategies to target abnormal tumor blood vessels.
Medical drugs are expensive to make and can have an adverse effect on the environment. Researchers Stefano Cucurachi and Justin Lian have developed a framework to help the health care system assess the economic and environmental sustainability of medical compounds. The research is published in the Proceedings of the National Academy of Sciences.
With a growing and aging population, and more people living with chronic disease, health care costs are rising and the pharmaceutical industry is expanding fast. Patients and health care professionals are also beginning to wonder about the environmental impact of medicines. But information on this is lacking.
“Some sources claim 10% of all pharmaceuticals have an environmental risk, but only the smallest fraction has ever been assessed,” says Cucurachi, Associate Professor of industrial ecology.
Liz Parrish, founder and CEO of BioViva, delivers a compelling keynote on the revolutionary potential of gene therapy for human longevity and rejuvenation.
As one of the boldest voices in the longevity field and the first person to undergo experimental gene therapy for aging, Parrish shares her insights into how genetic interventions are ready to extend human healthspan.
Parrish challenges the status quo of medical research and advocates for faster translations of scientific advances, arguing that delayed access is costing millions of lives.
Our skin protects us from everyday mechanical stresses, like friction, cuts, and impacts. A key part of this function—standing as a bulwark against the outside world—is the skin’s amazing ability to regenerate and heal. But where does this healing ability begin?
In a new study published in Nature Communications, an interdisciplinary team led by the laboratories of Kaelyn Sumigray, Ph.D., and Stefania Nicoli, Ph.D., discovered that, during the earliest stages of embryonic development, skin stem cells contribute to forming a protective skin layer that accelerates healing as the embryo grows.
Their findings reveal one of the earliest steps in how skin stem cells learn to repair tissue—knowledge that could help engineer improved skin grafts for transplantation.
Cellular senescence occurs in response to endogenous or exogenous stresses and is characterized by stable cell cycle arrest, alterations in nuclear morphology and secretion of proinflammatory factors, referred to as the senescence-associated secretory phenotype (SASP). An increase of senescent cells is associated with the development of several types of cancer and aging-related diseases. Therefore, senolytic agents that selectively remove senescent cells may offer opportunities for developing new therapeutic strategies against such cancers and aging-related diseases. This review outlines senescence inducers and the general characteristics of senescent cells. We also discuss the involvement of senescent cells in certain cancers and diseases. Finally, we describe a series of senolytic agents and their utilization in therapeutic strategies.
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Naked mole-rats are one of nature’s most extraordinary creatures. These burrowing rodents can live for up to 37 years, around ten times longer than relatives of a similar size. But what is the secret to their extreme longevity? How are they able to delay the decay and decline that befalls other rodents? The answer, at least in part, is due to a switch in a common protein that boosts DNA repair, according to new research published in the journal Science.
One of the main causes of aging in all animals, including humans, is the accumulation of damaged DNA, our genetic instruction manual. When this damage is not fixed, it leads to defective cells, damaged proteins and eventually a breakdown in the body’s functions.
To understand how the naked mole-rat is so resistant to DNA damage, a study led by researchers at Tongji University in China focused on a common protein called cGAS (cyclic GMP-AMP synthase). In most mammals, cGAS interferes with DNA repair, but the researchers suspected it may have evolved a different function in the long-living rats.
Research led by Vladimír Sládek sheds new light on how bones age, questioning long-standing assumptions that sedentary lifestyles are the primary cause of weakening bone strength in modern humans.
The study analyzed 1,881 adult humeri, femora, and tibiae from European Holocene populations to examine how bone strength and structure change with age. Surprisingly, researchers found that patterns of diaphyseal (shaft) aging were consistent across both Early and Late Holocene adults—despite significant differences in physical activity levels between the two groups. The research is published in the journal Science Advances.
“Our findings suggest that lifestyle differences may not fully explain age-related declines in bone strength,” said Dr. Sládek. “Instead, the biology of bone growth and aging itself plays a critical role.”
Efficient DNA repair might make possible the longevity of naked mole-rats. However, whether they have distinctive mechanisms to optimize functions of DNA repair suppressors is unclear. We find that naked mole-rat cyclic guanosine monophosphate–adenosine monophosphate synthase (cGAS) lacks the suppressive function of human or mouse homologs in homologous recombination repair through the alteration of four amino acids during evolution. The changes enable cGAS to retain chromatin longer upon DNA damage by weakening TRIM41-mediated ubiquitination and interaction with the segregase P97. Prolonged chromatin binding of cGAS enhanced the interaction between repair factors FANCI and RAD50 to facilitate RAD50 recruitment to damage sites, thereby potentiating homologous recombination repair.