In a study in aging mice, the first author has uncovered striking age-related changes in the sugary coating – called the glycocalyx – on cells that form the blood-brain barrier, a structure that protects the brain by filtering out harmful substances while allowing in essential nutrients.
“The glycocalyx is like a forest,” the author explains. “In young, healthy brains, this forest is lush and thriving. But in older brains, it becomes sparse, patchy, and degraded.”
These age-related changes to the glycocalyx weaken the blood-brain barrier, the author found. As the barrier becomes leaky with age, harmful molecules can infiltrate the brain, potentially fueling inflammation, cognitive decline, and neurodegenerative diseases.
The results were striking: In older mice, bottlebrush-shaped, sugar-coated proteins called mucins, a key component of the glycocalyx, were significantly reduced. This thinning of the glycocalyx correlated with increased permeability of the blood-brain barrier and heightened neuroinflammation.
When the team reintroduced those critical mucins in aged mice, restoring a more “youthful” glycocalyx, they improved the integrity of the blood-brain barrier, reduced neuroinflammation, and measurably improved cognitive function.
“Modulating glycans has a major effect on the brain – both negatively in aging, when these sugars are lost, and positively, when they are restored,” the lead says. “This opens an entirely new avenue for treating brain aging and related diseases.”
The ice-giant planet Uranus, which travels around the sun tipped on its side, is a weird and mysterious world. Now, in an unprecedented study spanning two decades, researchers using NASA’s Hubble Space Telescope have uncovered new insights into the planet’s atmospheric composition and dynamics. This was possible only because of Hubble’s sharp resolution, spectral capabilities, and longevity.
The team’s results will help astronomers to better understand how the atmosphere of Uranus works and responds to changing sunlight. These long-term observations provide valuable data for understanding the atmospheric dynamics of this distant ice giant, which can serve as a proxy for studying exoplanets of similar size and composition.
When Voyager 2 flew past Uranus in 1986, it provided a close-up snapshot of the sideways planet. What it saw resembled a bland, blue-green billiard ball. By comparison, Hubble chronicled a 20-year story of seasonal changes from 2002 to 2022. Over that period, a team led by Erich Karkoschka of the University of Arizona, and Larry Sromovsky and Pat Fry from the University of Wisconsin used the same Hubble instrument, STIS (the Space Telescope Imaging Spectrograph), to paint an accurate picture of the atmospheric structure of Uranus.
Although lifespan has long been the focus of ageing research, the need to enhance healthspan — the fraction of life spent in good health — is a more pressing societal need. Caloric restriction improves healthspan across eukaryotes but is unrealistic as a societal intervention. Here, we describe the rewiring of a highly conserved nutrient sensing system to prevent senescence onset and declining fitness in budding yeast even when aged on an unrestricted high glucose diet. We show that AMPK activation can prevent the onset of senescence by activating two pathways that remove excess acetyl coenzyme A from the cytoplasm into the mitochondria — the glyoxylate cycle and the carnitine shuttle. However, AMPK represses fatty acid synthesis from acetyl coenzyme A, which is critical for normal cellular function and growth. AMPK activation therefore has positive and negative effects during ageing. Combining AMPK activation with a point mutation in fatty acid synthesis enzyme Acc1 that prevents inhibition by AMPK (the A2A mutant) allows cells to maintain fitness late in life without reducing the mortality associated with advanced age. Our research shows that ageing in yeast is not intrinsically associated with loss of fitness, and that metabolic re-engineering allows high fitness to be preserved to the end of life.
The authors have declared no competing interest.
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As our bodies grow, cells proliferate to form tissues, and cells frequently have to be repaired or replaced throughout life. But the genome can also become less stable over time, or may pick up mutations that can lead to disease; these and other processes can cause cells to enter a state in which they stop dividing, known as senescence. Senescent cells become more common as we age. There also tends to be more inflammation as we age, but the link between increasing instability in the genome and inflammation is not well understood. Now scientists have reported a direct connection between DNA instability and inflammation in senescent cells. The findings have been reported in Nature Communications.
“In addition to no longer growing and proliferating, the other hallmark of senescent cells is that they have this inflammatory program causing them to secrete inflammatory molecules,” noted senior study author Peter Adams, Ph.D., director and professor of the Cancer Genome and Epigenetics Program at Sanford Burnham Prebys.
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Wenzhou Medical University and collaborating institutions have identified a population of human neural retinal stem-like cells able to regenerate retinal tissue and support visual recovery.
Vision loss caused by retinal degeneration affects millions worldwide. Conditions such as retinitis pigmentosa and age-related macular degeneration involve the irreversible loss of light-sensitive neural cells in the retina. While current treatments may slow progression, they do not replace damaged tissue.
For decades, scientists have explored whether stem cells could be used to regenerate the retina, but the existence of true retinal stem cells in humans has remained uncertain. In fish and amphibians, the outer edge of the retina houses stem cells that regenerate tissue continuously. Whether a comparable system exists in the human eye has been debated for more than two decades.
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