A new breakthrough in a rare genetic disease which causes children to age rapidly has been discovered using ‘longevity genes’ found in people who live exceptionally long lives—over 100 years old. The research, by the University of Bristol and IRCCS MultiMedica, found these genes which help keep the heart and blood vessels healthy during aging could reverse the damage caused by this life-limiting disease.
This is the first study, published in Signal Transduction and Targeted Therapy, to show that a gene from long-lived people can slow down heart aging in a progeria model. Also known as Hutchinson-Gilford progeria syndrome (HGPS), progeria is a rare, fatal genetic condition of “rapid-aging” in children.
HGPS is caused by a mutation in the LMNA gene, which leads to the production of a toxic protein called progerin. Most affected individuals die in their teens due to heart problems, although a few, like Sammy Basso, the oldest known person with progeria, have lived longer. Sadly, late last year at the age of 28, Sammy passed away.
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.