The switch will be flicked today to make the world’s largest dementia-related proteomics dataset freely available to researchers, at the same time as members of the consortium which compiled it publish the proteomics signatures of major neurodegenerative diseases that they uncovered in a first trawl of the data.
Hutchinson-Gilford progeria syndrome (HGPS), an extremely rare genetic disorder, arises when a silent point mutation in the gene encoding the nuclear envelope protein lamin A, LMNA, leads to abnormal splicing of LMNA mRNA.
Chugai Pharmaceutical Co. Ltd. and Gero Pte Ltd. have entered into a joint research and license agreement to develop novel therapies for age-related diseases. Chugai will create novel antibody-drug candidates for new drug targets discovered by Gero using its AI target discovery platform.
All kinds of substances circulate through the bloodstream. Some are beneficial, like oxygen or nutrients, and others less so, like waste products, toxins, pathogens and certain trafficking cells. Among these harmful substances are deleterious factors associated with aging, which can prematurely damage different tissues. The big question is what are those factors that mediate such effects, and what can be done to prevent them. The 11th Cardiac Regeneration and Vascular Biology Conference, held on the Island of San Servolo, Venice, from June 30 to July 2, 2025, included presentations, oral sessions and posters addressing the impact of aging on the cardiovascular system.
Researchers at the Buck Institute for Research on Aging have developed an epigenetic clock that could predict an individual’s intrinsic capacity score, a composite score that is a measure of healthy aging. The clock, which has only limited overlap with other epigenetic clocks, could be “a surrogate for aging that can be used for clinical trials,” senior author David Furman told BioWorld. And even more basically, it could help address a basic conundrum: that aging is the major risk factor for most causes of death, but not itself a disease.
A publication based on longitudinal and cross sectional data and led by researchers at the U.S. NIH’s National Institute on Aging published on June 5, 2025, in Science has stated that the impact of taurine supplementation at delaying aging or treating aging-related conditions is context-dependent, and that the circulating levels of taurine are impacted by factors unique to each individual rather than declining with age. To qualify taurine as a true marker of aging, it should change with age across diverse populations over time and ideally supported by longitudinal data.
Researchers have discovered that reduced expression of the free fatty acid receptor 4 (FFAR4) is a biomarker of podocyte injury and aging, as well as a therapeutic target. Podocyte injury leads to progression of glomerular disease and aging, but the underlying mechanisms are poorly understood.
The variety of blood cells decreases with age. Some are lost, while others become dominant, leading to a loss of functional diversity. This, in turn, weakens the immune system in older individuals and increases the risk of developing hematological diseases. Scientists in Barcelona have developed a method based on DNA methylation that works like a barcode. EPI-Clone identifies and traces the origin of blood cells to measure the complexity of these clones in aging humans and mice.
Adult skeletal muscle tolerates a lack of the coenzyme nicotinamide adenine dinucleotide (NAD), according to a study led by scientists at the University of Copenhagen. Their results suggest that adverse effects previously associated with congenital NAD depletion in this tissue may be due to impaired muscle development rather than to a deficiency of this molecule.
“Just simply getting old, from age 50 to 75, increased risk for Alzheimer’s disease by 100-fold, which really dwarfed 10-fold increase in risk, conferred by all known risk factors combined, including APOE genotype, being a female, hypertension, smoking, physical inactivity and diabetes. And this trend stays true for almost all chronic diseases,” Yousin Suh told her audience earlier this week during a talk for the NIH Director’s Wednesday Afternoon Lecture Series.