ByJUDY SIEGEL-ITZKOVICHAUGUST 1, 2026 08:34We all celebrate birthdays as though every part of our body ages at exactly the same pace.But according to new research from the Hebrew University of Jerusalem (HUJI), that supposed axiom is not true. While your calendar says you’re 75, 50, or 25, some of your cells may be biologically much older than others – and those “elderly” cells may help explain why aging and age-related diseases develop.“The achievement shows that the way people think about aging is wrong. With our new understanding about cancer – that aging is surprisingly uneven from one cell to the next – we will be in a much better position to do something about it,” Prof. Howard Cedar, the eminent biochemist who led the team and has won numerous prizes for his pioneering work in a molecular process called DNA methylation, told The Jerusalem Post. This fundamental biochemical process involves a tiny chemical tag – a methyl group (one carbon and three hydrogen atoms) – that is added to DNA, acting like a dimmer switch for genes, turning them “on” or “off” without changing the underlying genetic code.PROF. HOWARD CEDAR (credit: NATI SHOHAT/FLASH90)Cedar, together with Prof. Tommy Kaplan, Dr. Hagit Masika, and other researchers at Jerusalem’s Hadassah University Medical Center, discovered that aging does not occur evenly throughout the body. Instead, individual cells age at different speeds, and they have identified a molecular “aging signature” that reveals which cells are growing old first.This finding may potentially help researchers develop drugs that slow aging itself – not just diseases such as cancer, Alzheimer’s, or heart disease that become more common with age.The study has just been published in the prestigious journal Nature Communications under the title “Cell-to-cell variability and gain of methylation at polycomb CpG islands as a hallmark of aging.” Amazingly, the study has 112 footnotes. One of the first accomplishments of Cedar’s lab was figuring out how genes are regulated during development. Every person inherits his genes from his parents, and since the genetic material is copied in its entirety before every cell division, the full complement of genes is found in every cell of the body.Interestingly, each tissue expresses only a subset of these genes – those that are necessary for its function. To this end, there are molecular mechanisms within the cell that turn genes on and off and, in this way, modulate their activity.The most important mechanism for affecting gene activity is DNA methylation. By modifying a gene with a chemical cap (methyl group), the cell effectively turns off that gene.Cedar and his team have made major discoveries that explain how methylation works, how gene-specific patterns are established, and which factors allow the cell to either add new methyl groups or take away existing ones, thus explaining how genes are turned on and off in a programmed manner during development.They also showed that DNA methylation is abnormal in tumors, and it is this change that is responsible for the pathology of cancer. This observation will help develop new approaches for targeting and thereby preventing the fundamental pathology of cancer.Aging and singular cellsCedar was born in New York. He received his bachelor’s degree in mathematics from the Massachusetts Institute of Technology, and an MD and doctorate in microbiology at New York University, followed by postdoctoral research there and at the US National Institutes of Health.In 1973, he made aliyah with his family and joined the Hebrew University-Hadassah Faculty of Medicine, becoming a full professor in 1981. He is one of the world’s pioneers of DNA methylation biology.Cedar was the first to receive the Israel Cancer Research Fund’s Research Professorship Grant, the highest and most prestigious ICRF grant category, for his ground-breaking research. He was awarded the Israel Prize in Biology (1999), is a member of the Israel Academy of Sciences (2003), and won the Wolf Prize in Medicine (2008), described as Israel’s equivalent to the Nobel Prize.He received the EMET Prize in Life Sciences in 2009, the Canada Gairdner International Award in 2011, and the Louisa Gross Horwitz Prize in 2016. He was elected a member of the US National Academy of Sciences (2022) and became the first recipient of the Hebrew University Lifetime Award in 2024.Every cell contains the same instruction manual – DNA – but different pages are switched on or off by tiny chemical tags. As we age, these tags accumulate in specific places in the genome.The researchers discovered that this process doesn’t occur uniformly. “Think of a classroom of students all born on the same day. Although they’re the same age, some seem much older or younger in maturity. The researchers found that our cells behave similarly – some cells ‘grow old’ much faster than their neighbors,” he explained.“Aging is a mosaic of biologically young and old cells, not a synchronized process. Imagine a city where every house is painted every year. Until now, scientists mostly looked at satellite photographs and concluded that the city ages uniformly.“But Cedar’s group walked down every street and looked at individual houses and discovered that some houses are already crumbling while others remain almost new. That’s a completely different picture of aging.”Until now, most methylation-aging studies treated tissues as statistical averages. This paper argues that aging is highly uneven and individualized cell-by-cell, with a subset of cells accumulating age-associated methylation changes much faster than others.Instead of asking “How old is this tissue?” scientists can now ask: “Which individual cells are aging fastest and can we stop them?” If researchers can understand why some cells age rapidly while neighboring cells remain healthy, they may eventually learn how to slow the process, Cedar concluded.Their discovery is unique because it looks at single cells, not averages across millions of cells; it suggests aging is an active biological program, not simply random wear and tear; it identifies a specific molecular marker that appears across many tissues; and it opens the possibility of targeting cells that age fastest rather than treating aging as an all-or-nothing process.In retrospect, the findings could have already been discovered over 100 years ago. It was then that people began noticing that the “graying” associated with getting older is not really made up of grey hairs. A close look reveals that a few individual hairs are actually white, while the rest of the hairs are still very dark. This is the best proof that aging occurs at the level of single cells.It should be noted that Cedar’s research on DNA methylation also serves as the basis for the new simple early-detection kit (Galleri) developed by Prof. Yuval Dor to test for over 50 types of cancer even before there are any symptoms – when they can be easier to treat. This concept can also be used to detect at least 20 other diseases early on, including diabetes.“When I came to Israel and established my own laboratory at HUJI, I decided to investigate methylation, a small chemical attachment to the DNA, whose function was completely unknown at that time. This turned out to be a fundamental part of the cell’s biology, and it took many decades to understand its full implications,” Cedar said.“People kept asking me why I am wasting my time. Instead, I should be trying to find a cure for cancer. As it turned out, because it is so very basic, methylation lies at the source of many diseases. With our new results, we now know that it is also the key to understanding the body’s aging process.“I hope that one day we’ll be able to slow down the vicissitudes of aging and its accompanying diseases.”Follow us on Google
Some parts of your body age faster than others, Israeli study finds
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