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Why energy fades with age: Missing membrane lipid may destabilize mitochondria

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.

Strategies to boost antibody selectivity in oncology

Antibodies in oncology are being equipped with toxic cargoes and effector functions that can kill cells at very low concentrations. A key challenge is that most targets on cancer cells are also present on at least some healthy cells. Shared targets can result in off-tumor binding and compromise the safety and potential of therapeutic candidates. In this review, we survey strategies that can help direct biologics to cancer sites more selectively. These strategies are becoming increasingly feasible thanks to advances in molecular design and engineering. The objective is to create therapeutics that exploit changes in cancer and leverage the human body infrastructure, enabling therapeutics that discriminate not just self from non-self but diseased from healthy tissue.

The Hidden Impact: Lingering Brain Injury Symptoms Haunt Concussion Patients

Even mild concussion can cause long-lasting effects to the brain, according to researchers at the University of Cambridge. Using data from a Europe-wide study, the team has shown that for almost a half of all people who receive a knock to the head, there are changes in how regions of the brain commu

How cells fight infection from the inside: Newly identified ADX pathway may broaden understanding of immunity

When thinking of the immune system, most people imagine white blood cells putting up a fight against invading germs in the bloodstream. But now, in research published in Molecular Cell, scientists detail a separate but equally important route by which our bodies fight infection—directly inside already infected cells.

In the report, the authors define a previously undescribed method of germ resistance they coin “antibody-directed xenophagy” (ADX), where cells can digest bacteria and viruses that cross the cell membrane, including Salmonella and adenoviruses.

“People have talked about viral xenophagy before as a sort of concept, but if you look in literature, there aren’t any good examples where people have shown this operating to potently block infection,” says Leo James of the MRC Laboratory of Molecular Biology.

Novel synthetic biomolecule degrades disease-related proteins

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.

Alzheimer’s gene map expands to 91 loci, revealing 16 previously unknown risk regions

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.

Autism risk framework tracks genes, maternal factors and environment across 18,000 families

A new statistical framework developed by researchers at the Johns Hopkins Bloomberg School of Public Health, Johns Hopkins University School of Medicine, and Kaiser Permanente Northern California offers improved understanding of how genetics and environment contribute to autism risk.

Large-scale genetic studies have led to the development of genetic risk scores that estimate a person’s predisposition to diseases and health conditions based on their DNA profiles. The new framework allows researchers and clinicians to analyze these scores using family data and characterize the risk of conditions such as autism and other developmental conditions in children based on their own DNA, parental factors, and environmental influences such as maternal diet and lifestyle.

For their study published in Nature Genetics, the researchers analyzed more than 18,000 case-parent trios —autistic children and their parents—across diverse ancestral populations in the Simons Foundation Powering Autism Research for Knowledge consortium and the Genes and Environment Autism Research Study.

Biohybrid microrobots repair spinal cord by combining stem cells with magnetoelectric nanoparticles

Spinal cord injuries can have devastating consequences for those affected. Nerve cells in the spinal cord rarely regenerate naturally, while scarring often prevents the regrowth of nerve fibers. Modern therapies attempt to influence implanted stem cells using electrical stimulation to promote the growth of new nerve cells. This approach has several drawbacks: it requires implanted electrodes, and the transplanted cells do not always survive or integrate properly into the existing tissue.

Researchers in Zurich are pursuing a new approach, which they have published in the journal Nature Materials. This involves combining therapeutic stem cells with magnetoelectric nanoparticles in such a way that the cells can be guided magnetically to the precise site of an injury and stimulate the stem cells to accelerate repair.

To achieve this, the researchers created a biohybrid microrobot, which combines living neural progenitor cells (NPCs) with a technical component in the form of specially engineered nanoparticles.

Experimental Brain ‘Pacemakers’ May Rewire Circuits Linked to Depression

Every year, more than 2 million people in the United States are diagnosed with treatment-resistant depression.

Desperate for solutions, some brave patients are now volunteering to undergo surgery to place experimental ‘pacemakers’ into their brains.

These implanted electrodes are part of a treatment known as deep brain stimulation, which is currently used to address some cases of Parkinson’s disease and epilepsy.

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