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Three genetic modifiers may alter inherited Alzheimer’s onset and progression

Autosomal dominant Alzheimer’s disease (ADAD) is a genetically inherited form of Alzheimer’s disease that accounts for only about 1% of Alzheimer’s disease cases. However, because individuals with the gene mutations are extremely likely to develop Alzheimer’s disease at an early age, and because the mutation is highly heritable, ADAD is widely studied by Alzheimer’s disease researchers.

A new study by WashU Medicine researchers and collaborators, published in The Lancet Neurology, identified variants in three other genes that seem to change how Alzheimer’s disease presents in people with ADAD mutations. Pinpointing these and other genetic factors that affect Alzheimer’s disease development and progression may allow investigators to provide more effective genetic counseling for families, design clinical trials and develop new treatments to prevent or slow Alzheimer’s disease in the larger population.

Previous studies had already identified three key genes—amyloid precursor protein (APP), presenilin 1 (PSEN1) and presenilin 2 (PSEN2)—that are associated with ADAD, as well as 279 variants in those genes that lead to Alzheimer’s disease. What remains unclear, however, is what leads to differences in disease onset and progression among individuals who have a disease-causing variant. For instance, even if a person carries an APP, PSEN1 or PSEN2 mutation and is therefore very likely to develop early-onset Alzheimer’s, there is variability in when symptoms of cognitive decline might begin, even among individuals who have the same disease-causing mutation.

Creating a healthspan digital twin: A new era for humanity to better living — Jul 30

Zahi A. Fayad, PhD, is the Lucy G. Moses Professor of Medical Imaging and Bioengineering at the Icahn School of Medicine at Mount Sinai, where he also serves as Vice Chair for Research in Radiology and holds professorships in Medicine (Cardiology) and AI & Human Health. He is the founding Director of the BioMedical Engineering and Imaging Institute (BMEII), home to one of the nation’s top NIH-funded radiology programs (#2 in 2025 per Blue Ridge rankings). Dr. Fayad also co-leads Mount Sinai’s system-wide Healthspan initiative, coordinating research, clinical, and digital infrastructure to advance precision prevention across the enterprise.

Dr. Fayad is Principal Investigator on multiple major grants, including five NIH-funded projects (3 R01s, 2 P01s) supported by the National Heart, Lung, and Blood Institute, NIAID, and NIDA. A leader in biomedical engineering, his interdisciplinary work integrates advanced imaging, AI, and nanomedicine to drive precision medicine, with research interests focused on how lifestyle stressors — chronic stress, diet, exercise, and sleep — affect long-term cardiovascular and whole-person health.

A Clarivate Highly Cited Researcher since 2018 (~190,000 citations; h-index 142), Dr. Fayad’s seminal contributions include MRI vessel wall imaging (leading to Carotid Plaque-RADS), FDG PET imaging of vascular inflammation, and defining the link between amygdala activity, systemic inflammation, and cardiovascular risk. His research on HDL-based nanoparticles for immune modulation is progressing toward clinical translation for cancer, autoimmune diseases, and transplant rejection — work he is advancing commercially as co-founder of Trained Therapeutix Discovery (TTxD), an early-stage biotech company. He is also a recipient of the Jean Paul II Award for Medicine and Research.

His current projects span cardiovascular, neuroimmune, and transplant-focused research, including stress-induced immune dysregulation; mitral valve prolapse and arrhythmia risk; cocaine use–related carotid atherosclerosis and cognitive impairment; cardiac sarcoidosis therapy monitoring; and immune tracking in organ rejection using nanobiologics — together shifting care upstream toward risk prediction and intervention before clinical events.

He also leads the Mount Sinai DigiTwin Project, an AI-driven platform designed to personalize health optimization by integrating imaging, multi-omics, and real-time physiologic data — initially focused on cardiovascular health and now expanding to whole-person healthspan modeling. Dr. Fayad and colleagues at Mount Sinai are finalists in the $80m XPRIZE Healthspan competition, where they are evaluating a multimodal strategy to meaningfully extend human healthspan.

Rogue DNA can move from cell to cell and change how they function

“We were looking at this in a two-dimensional culture, but in actual human tissue where cells are packed together very tightly, you might anticipate that this would occur even more frequently,” said Gary Gorbsky, OMRF professor and study co-author. “This opens up the possibility of a new process of genetic transfer of information.”

What effect did rogue DNA have on the new cell?

To test whether this new DNA that came from another cell had a functional impact on the new cell, the scientists engineered donor cells with resistance to a specific antibiotic. After combining donor and recipient cells in culture and inducing chromosome damage, they found that recipient cells acquired the same antibiotic resistance – direct evidence that mammalian cells can trade genetic material through simple cell-to-cell contact.

Pregnancy complications linked to long-term risk of peripheral artery disease

Women who experience pregnancy complications such as gestational diabetes, preeclampsia or preterm delivery have a significantly increased long-term risk of developing peripheral artery disease (PAD) later in life, according to a new study published in PLOS Medicine by Casey Crump of the University of Texas, U.S., and colleagues.

PAD, a condition in which narrowed arteries reduce blood flow to the limbs, affects more than 230 million people worldwide and is a strong predictor of future stroke, ischemic heart disease and premature mortality. Adverse pregnancy outcomes have been identified as risk factors for other cardiovascular diseases, but their association with long-term PAD risk had not been well established.

‘Cellular behavioromics’ reveals how immune cells swarm during sepsis

Despite the best efforts of intensive care unit (ICU) staff and physicians and the most advanced life support, Dr. Bryan Yipp, witnesses many deaths in the ICU attributed to sepsis. “Sepsis is the body’s overwhelming immune response to an infection, and sometimes that response can cause death,” says Yipp, a critical care physician and clinician-scientist at the Cumming School of Medicine. “While many cases involve people with long-term illnesses, seemingly healthy people can be at work or home one moment and then, within hours, be admitted to the ICU.”

Earlier this year, 41-year-old NASCAR race champion Kyle Busch died after pneumonia progressed to sepsis. Yipp says a recent discovery in his lab, published in Science, could lead to new treatments for this often-fatal condition.

Researchers expand simulation tool to help design the next generation of photonic and quantum devices

Many modern technologies, from optical communications and artificial intelligence (AI) hardware to advanced sensors and medical imaging, depend on photonic and semiconductor devices that precisely control the interaction between light and electrons. Designing these devices, however, remains a major challenge because existing simulation tools often require researchers to choose between modeling an entire device or capturing the detailed behavior of electrons. Few can do both within the same model.

Researchers from the Singapore University of Technology and Design (SUTD) and National University of Singapore (NUS) have developed a new computational approach that extends the widely used open-source particle-in-cell (PIC) method with condensed-matter physics. The result is a single platform that can simulate a much broader range of light-matter interactions in metals, semiconductors and emerging quantum materials.

Published in Computer Physics Communications, the research, “Particle-in-cell simulations of quantum plasmas,” demonstrates how an established plasma physics tool can be adapted to study condensed-matter systems, opening new possibilities for designing photonic and quantum technologies.

Engineered enzyme erases a stubborn mark of aging by up to 70% in human tissue samples

A biotech company called Revel Pharmaceuticals is looking into ways to reverse aging, and the company’s science team, along with researchers from the company Calico and the University of Colorado, may be a step closer to realizing the so-called fountain of youth. The team recently published their study in Nature Communications detailing how they engineered an enzyme capable of reversing a particular form of age-related damage and demonstrated its competence with test results.

One common sign of aging in the cells of living organisms is a type of protein damage called Nε-carboxymethyl-lysine (CML). CML is part of a group of harmful compounds aptly named “AGEs” (or advanced glycation and lipoxidation end products). Oddly enough, it is also part of the Maillard reaction, known for causing the browning in cooked food that creates rich, savory flavors, complex aromas and golden-brown crusts. In living organisms, CML builds up on long-lived proteins, like those in skin, blood vessels and the eye. This stiffens tissues and can fuel chronic inflammation through an immune-signaling receptor called “RAGE.”

“The engagement of the CML-RAGE axis triggers a signaling cascade that activates NF-κB and stimulates the release of pro-inflammatory cytokines and profibrotic growth factors. In the context of the central nervous system, CML accumulation has been linked to oxidative stress and mitochondrial damage in microglia, further disrupting brain homeostasis during aging,” the authors of the new study explain.

Kindness emerges intuitively in young children before reflection catches up, study finds

While humans are inherently social beings, psychology studies suggest that their social skills are gradually fine-tuned over time and with experience. Understanding when different social skills emerge and how they typically develop could help devise new strategies that encourage people to behave prosocially and cooperate with others around them.

Researchers at London School of Economics, University of Stavanger and University of Milan-Bicocca recently carried out a study exploring how social behaviors emerge and become stable across childhood. Their findings, published in Nature Human Behavior, suggest that while kindness and cooperation are intuitive behaviors in early childhood, they later become deliberate and part of children’s personal disposition.

“Our study was initially motivated by the wish to extend findings of our previous paper in Scientific Reports,” Elena Nava, senior author of the paper, told Medical Xpress.

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