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Researchers look at DNA of lab mice and ultimately reverse ageing process Related: Empowered Aging Scientists have made a new discovery about how to reverse the ageing process through looking at the way in which cells in DNA are organised. In a new study published in Cell, David Sinclair, who is a professor of genetics at Harvard Medical School, and his team described how they looked at a genome, which is called epigenome, in mice to study the ageing process.

Summary: Study uncovers new genetic risk factors for age-related macular degeneration, a leading cause of vision loss in adults.

Source: PLOS

Combining a map of gene regulatory sites with disease-associated loci has uncovered a new genetic risk factor of adult-onset macular degeneration (AMD), according to a new study publishing January 17 in the open-access journal PLOS Biology by Ran Elkon and Ruth Ashery-Padan of Tel Aviv University, Israel, and colleagues.

This American cryonics facility has preserved “patients” in liquid nitrogen-filled tanks until a future date when technology allows them to be thawed.

This video was recorded at the Foresight Vision Weekend 2022 at Château du Feÿ in France.

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Scientists at Harvard Medical School have investigated why we age, and identified a possible way to reverse it. In tests in mice, the team showed that epigenetic “software glitches” drive the symptoms of aging – and a system reboot can reverse them, potentially extending lifespan.

Our genome contains our complete DNA blueprint, which is found in every single cell of our bodies. But it’s not the whole picture – an extra layer of information, known as the epigenome, sits above that and controls which genes are switched on and off in different types of cells. It’s as though every cell in our body is working from the same operating manual (the genome), but the epigenome is like a table of contents that directs different cells to different chapters (genes). After all, lung cells need very different instructions to heart cells.

Environmental and lifestyle factors like diet, exercise and even childhood experiences could change epigenetic expression over our lifetimes. Epigenetic changes have been linked to the rate of biological aging, but whether they drove the symptoms of aging or were a symptom themselves remained unclear.

Chromatin structures and transcriptional networks are known to specify cell identity during development which directs cells into metaphorical valleys in the Waddington landscape. Cells must retain their identity through the preservation of epigenetic information and a state of low Shannon entropy for the maintenance of optimal function. Yeast studies in the 1990s have reported that a loss of epigenetic information compared to genetics can cause aging. Few other studies also confirmed that epigenetic changes are not just a biomarker but a cause of aging in yeasts.

Epigenetic changes associated with aging include changes in DNA methylation (DNAme) patterns, H3K27me3, H3K9me3, and H3K9me3. Many epigenetic changes have been observed to follow a specific pattern. However, the reason for changes in the mammalian epigenome is not yet known. A few clues can be obtained from yeast, where DSB is a significant factor whose repair requires epigenetic regulators Esa1, Gcn5, Rpd3, Hst1, and Sir2. As per the ‘‘RCM’’ hypothesis and ‘Information Theory of Aging’’, aging in eukaryotes occurs due to the loss of epigenetic information and transcriptional networks in response to cellular damage such as a crash injury or a DSB.

A new study in the journal Cell aimed to determine whether epigenetic changes are a cause of mammalian aging.

The maximum lifespan varies more than 100-fold in mammals. This experiment of nature may uncover of the evolutionary forces and molecular features that define longevity. To understand the relationship between gene expression variation and maximum lifespan, we carried out a comparative transcriptomics analysis of liver, kidney, and brain tissues of 106 mammalian species. We found that expression is largely conserved and very limited genes exhibit common expression patterns with longevity in all the three organs analyzed. However, many pathways, e.g., “Insulin signaling pathway”, and “FoxO signaling pathway”, show accumulated correlations with maximum lifespan across mammals. Analyses of selection features further reveal that methionine restriction related genes whose expressions associated with longevity, are under strong selection in long-lived mammals, suggesting that a common approach could be utilized by natural selection and artificial intervention to control lifespan. These results suggest that natural lifespan regulation via gene expression is likely to be driven through polygenic model and indirect selection.

The authors have declared no competing interest.

Uncover the truth behind the human lifespan. From Ancient Rome to modern America, discover the progress we’ve made in extending life expectancy and the flaws in measuring it. Join us as we explore the science of aging, the pursuit of immortality, and the ongoing debate on the limits of human longevity.

Why do cells, and by extension humans, age? The answer may have a lot to do with mitochondria, the organelles that supply cells with energy. Though that idea is not new, direct evidence in human cells had been lacking. Until now.

In a study published Jan. 12 in Communications Biology, a team led by Columbia University researchers has discovered that human cells with impaired mitochondria respond by kicking into higher gear and expending more energy. While this adaptation—called hypermetabolism—enhances the cells’ short-term survival, it comes at a high cost: a dramatic increase in the rate at which the cells age.

“The findings were made in cells from patients with rare mitochondrial diseases, yet they may also have relevance for other conditions that affect mitochondria, including neurodegenerative diseases, inflammatory conditions, and infections,” says principal investigator Martin Picard, PhD, associate professor of behavioral medicine (in psychiatry and neurology) at Columbia University Vagelos College of Physicians and Surgeons.