A newly identified protein pathway may link blood-brain barrier deterioration to age-related cognitive decline.
While GLP-1 drugs can curb cardiometabolic dysfunction, reducing the risk of life-limiting and life-threatening diseases that would otherwise shorten health and lifespan, mechanistic evidence that they directly influence the biology of aging remains limited.
Can GLP-1 drugs rewind the epigenetic clock?
UCSD researchers conducted a post hoc analysis of a Phase 2b clinical trial evaluating the use of semaglutide in human immunodeficiency virus (HIV)-associated lipohypertrophy (HALS).
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Most people think aging starts with wrinkles.
Cognitive frailty, characterized by the coexistence of physical frailty and cognitive impairment, has emerged as a major challenge in aging populations and is closely linked to sarcopenia, neurodegeneration, and chronic inflammation. Increasing evidence suggests that the gut microbiota acts as a central regulator of neuromuscular and neurocognitive aging through the integrated gut–brain–muscle axis. This review highlights how microbial dysbiosis, reduced short-chain fatty acid (SCFA) production, systemic endotoxemia, and altered microbial metabolites contribute to mitochondrial dysfunction, neuroinflammation, anabolic resistance, and impaired neuroplasticity.
Why does the immune system become less effective as we age? A new USC study published in BMC Biology offers fresh insights by examining a key immune cell type across tissues: macrophages.
Macrophages act as the body’s cleanup and maintenance crew. Found in nearly every tissue, they help fight infections, remove damaged cells, repair tissues and keep inflammation under control, acting as a first line of defense for the immune system. But like many cells in the body, macrophages change as we get older.
In this new study, researchers analyzed data from macrophages collected from different mouse tissues, including the brain, lungs, liver and other organs. By comparing younger and older animals, they uncovered common patterns of aging shared across many macrophage populations, as well as important differences depending on where the cells come from.
The 13th Aging Research & Drug Discovery (ARDD) Meeting, the world’s largest conference dedicated to longevity biotechnology, will take place from October 1–3, 2026, at the David Rubenstein Treehouse at Harvard University. Marking the high-profile launch of Boston Longevity Week, this landmark event is officially organized by Insilico Medicine, which also anchors the conference as a Tier 1 sponsor alongside Eli Lilly.
As longevity science rapidly transitions from theoretical concepts to multi-billion-dollar therapeutic pipelines, ARDD 2026 stands as the premier global nexus connecting basic science, clinical research, big pharma, and institutional investors. Moving the conference to Boston-the global epicenter of biomedical innovation-reflects the field’s evolution into mainstream medicine.
Building on the massive momentum of previous years-including ARDD 2025 in Copenhagen, where leadership from Eli Lilly and Novo Nordisk discussed the profound longevity potential of GLP-1 receptor agonists in Nature Biotechnology-the 2026 conference solidifies aging research as a core pillar of healthcare. Top-tier pharmaceutical companies are now actively developing commercial programs targeting fibrosis, immunology, CNS, cardiometabolic diseases, anti-muscle wasting, and cellular rejuvenation.
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Michael Levin is a biologist at Tufts University working on novel ways to understand and control complex pattern formation in biological systems.
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Biological Robots: https://arxiv.org/abs/2207.00880
Classical Sorting Algorithms: https://arxiv.org/abs/2401.05375
Aging as a Morphostasis Defect: https://pubmed.ncbi.nlm.nih.gov/38636…
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