Chang and Jain develop a genetically encoded reporter to measure polyamines at single-cell resolution in C. elegans. By mapping polyamine control across tissues and development, they uncover organizing principles of in vivo polyamine regulation, including widespread reliance on transport and a central role for the intestine in coordinating systemic homeostasis.
Therapy resistance is a major obstacle to durable clinical responses. While genetic alterations and signalling rewiring are primary drivers of resistance, metabolic adaptation, which is closely intertwined with these processes, enables tumour persistence under therapeutic pressure and directly contributes to resistance. Peroxisomes are metabolic organelles with a role in controlling lipid metabolism, together with redox signalling and homeostasis—processes that intersect with pathways governing cancer behaviour and therapy response. Indeed, peroxisomal functions are remodelled to support metabolic plasticity and redox buffering under therapeutic stress.
In 2025, the European Medicines Agency approved two antibodies for Alzheimer’s disease: lecanemab (LeqembiTM, from Biogen) and donanemab (Kisunla, from Eli Lilly and Co.), both based on immunotherapy (the use of molecules from the immune system to treat diseases). These antibodies, obtained in the laboratory, act against the Aβ peptide, a protein fragment that accumulates in the brains of patients with Alzheimer’s disease. Elimination of this protein by the immune system helps slow the characteristic cognitive decline of the disease.
These two antibodies are the first disease-modifying therapies for Alzheimer’s. They stop and, in some cases, even partially reverse this devastating condition. However, a frequent and characteristic side effect of these drugs is cerebral bleeding, detectable by magnetic resonance imaging. The brain does not have the molecules and cells that make up the systemic immune system, so the entry of antibodies into the brain is not desirable under healthy conditions, although it is necessary for these treatments to be effective.
The incidence of bleeding in clinical trials ranged from 10% to 27% of treated patients, with a particularly high incidence in individuals carrying a specific apolipoprotein allele: APOEε4. In Europe, these treatments can be administered only to people with one or no copy of the APOEε4 allele, a genetic variant associated with a higher risk of Alzheimer’s.
Why do cells age—and why do we lose our energy and vitality as we get older? This question is one of the central challenges of modern biomedicine. The focus is particularly on mitochondria—tiny cellular organelles long known as the cell’s powerhouses but now understood as dynamic control centers that not only produce energy, but also coordinate cellular communication, adaptation, and many of the processes essential for life.
They supply us with the energy that our body needs for movement, growth, and repair processes. But as we age, these powerhouses begin to slow down. It has long been known that their function declines with age. But until now, the mechanisms driving this gradual decline have been poorly understood.
Focus on membrane lipids For a long time, it was assumed that genetic damage within the mitochondria themselves was primarily responsible. A study now published in Nature Communications by an international research team led by Dr. Maria Ermolaeva of the Leibniz Institute on Aging—Fritz Lipmann Institute (FLI) in Jena provides a surprising answer to this question: A key factor appears to be the imbalance in the structure of the mitochondrial network, which is caused by the absence of a major lipid in the membrane composition.
Northwestern Medicine scientists have developed a novel synthetic biomolecular condensate that can degrade intracellular disease-causing proteins, providing a framework for new therapeutic approaches for a wide range of diseases, as detailed in a recent study published in Nature Communications.
Shana Kelley, Ph.D., the Neena B. Schwartz Professor of Chemistry, Biomedical Engineering, and Biochemistry and Molecular Genetics and the president of the Chan Zuckerberg Biohub Chicago, was senior author of the study.
Targeted protein degradation is an emerging therapeutic strategy that harnesses cells’ own degradation machinery to clear disease-causing proteins. However, achieving this degradation process across different cell types has remained a challenge due to subtle variations in protein structure.
An international collaboration of genetic researchers has identified more than 90 genetic regions associated with the risk of Alzheimer’s disease and related dementias. The large-scale meta-analysis reveals new biological insights into the disease, highlighting the important roles of immune processes, beta-amyloid and tau biology, and lipid metabolism.
Alzheimer’s disease is the most common cause of dementia worldwide, and its development is influenced by a complex interplay of genetic and environmental factors. Understanding the genetic architecture of the disease is essential for improving diagnosis, risk prediction, and the development of targeted therapies.
In this study, researchers combined genome-wide association data from nearly a million individuals of European ancestry, including over 128,000 Alzheimer’s disease cases and nearly 850,000 controls.