{"id":639987,"date":"2026-05-13T05:34:19","date_gmt":"2026-05-13T05:34:19","guid":{"rendered":"https:\/\/www.newsbeep.com\/us\/639987\/"},"modified":"2026-05-13T05:34:19","modified_gmt":"2026-05-13T05:34:19","slug":"new-discovery-challenges-decades-old-theory-of-dna-damage-and-aging","status":"publish","type":"post","link":"https:\/\/www.newsbeep.com\/us\/639987\/","title":{"rendered":"New Discovery Challenges Decades-Old Theory of DNA Damage and Aging"},"content":{"rendered":"

\"B-Cell<\/a>Researchers have identified an overactive immune response as a major contributor to tissue degeneration in severe DNA repair disorders. Their findings suggest that calming this response may restore biological function in ways that challenge long-standing assumptions about aging and cellular damage. Credit: Shutterstock<\/p>\n

Scientists have discovered that the body\u2019s own immune alarms may play a major role in rapid-aging diseases.<\/p>\n

New research suggests that reducing the activity of an overactive immune sensor may help restore tissue function in severe genetic disorders, offering a new perspective on aging and DNA damage.<\/p>\n

The immune system is designed to recognize and eliminate viruses, but this defense mechanism can sometimes turn against the body. When damaged pieces of the body\u2019s own DNA are mistaken for viral material, the immune system can trigger a strong inflammatory response that harms healthy tissue.<\/p>\n

An international research team led by Dr. Marva Bergman and Prof. Itamar Harel at Hebrew University, together with Prof. Yehuda Tzfati, Prof. Ido Ben-Ami (Hebrew University and Sha\u2019are Zedek Medical Center), and Prof. B\u00e9r\u00e9nice Benayoun (University of Southern California), identified this misplaced immune reaction as a major cause of tissue degeneration in severe rapid-aging disorders. By reducing the false immune alarm, the researchers restored function across several biological systems.<\/p>\n

Rethinking the Cause of Cellular Decline<\/p>\n

The study focused on rare DNA damage-repair (DDR) disorders, including Ataxia-Telangiectasia (A-T) and Bloom syndrome. These conditions disrupt the body\u2019s ability to repair routine DNA damage, causing genomic instability, neurodegeneration, increased cancer risk, and premature aging.<\/p>\n

For many years, scientists believed that unrepaired DNA damage itself was mainly responsible for cellular decline. The new findings suggest the body\u2019s reaction to that damage may play an equally important role.<\/p>\n

\"Killifish<\/a>Reversing hallmarks of rapid aging by silencing a cellular alarm system \u2013 single-molecule fluorescent in-situ hybridization (smFISH) in killifish female ovaries, visualizing immature oocytes (ddx4) in red, and for granulosa cells (lhr) in green. Nuclei are visible in blue. Credit: Eitan Moses<\/p>\n

\u201cOur results show that the damage isn\u2019t acting alone,\u201d said Prof. Harel. \u201cIt\u2019s the body\u2019s response to that damage, an exaggerated, chronic inflammatory reaction, that drives much of the degeneration.\u201d<\/p>\n

When cells fail to repair DNA properly, fragments of DNA can escape into the cytosol, the fluid surrounding cellular structures. There, they activate a sensor called cGAS. This system normally detects viral DNA, but it cannot reliably distinguish between foreign DNA and damaged DNA from the body itself. As a result, the immune system launches a prolonged inflammatory response that can damage tissues over time.<\/p>\n

The Double Role of cGAS<\/p>\n

The researchers also discovered that cGAS has another role beyond triggering inflammation. The molecule can enter the cell nucleus and directly interfere with DNA repair. Under normal conditions, cGAS helps protect the body, but when overstimulated, it can contribute to further damage.<\/p>\n

To explore whether controlling this response could slow disease progression, the team used a fast-aging vertebrate model commonly used to study aging-related changes. Lowering cGAS activity significantly improved several disease markers, including neuroinflammation, tissue degeneration, and reduced reproductive capacity.<\/p>\n

\"Marva<\/a>Dr. Marva Bergman (left), and Prof. Itamar Harel Credit: Alon Harel-Katz<\/p>\n

\u201cWe weren\u2019t just slowing decline,\u201d said Dr. Bergman. \u201cWe saw broad restoration of tissue function. It suggests that the body can cope with more DNA damage than we assumed, if the inflammatory response is kept in check.\u201d<\/p>\n

Implications for Aging and Disease Treatment<\/p>\n

The findings could influence future treatment strategies. Instead of trying to repair every DNA lesion, researchers may be able to target the body\u2019s inflammatory response to DNA damage. However, the team noted that cGAS is also important for fighting viral infections, so any future therapy would need to reduce harmful inflammation without weakening immune defenses.<\/p>\n

The research may also have implications beyond rare genetic disorders. Chronic inflammation and genomic instability are common features of many age-related diseases, suggesting the same mechanisms could play a broader role in aging.<\/p>\n

Related studies from the group also examined how biological processes such as reproduction and developmental timing connect to aging and lifespan. Together, the findings support the idea that systems that benefit the body early in life may also contribute to long-term decline later on.<\/p>\n

The researchers emphasized that reversing disease symptoms is not the same as slowing the natural aging process itself. Even so, the study highlights a promising new approach for treating severe degenerative disorders by targeting the body\u2019s own immune signaling pathways.<\/p>\n

Reference: \u201cA dual role for cGAS in shaping cellular and organismal responses to genomic instability\u201d by Marva Bergman, Uri Goshtchevsky, Tehila Atlan, Gwendoline Astre, Ryan Halabi, Hosniyah El Ayoubi, Eitan Moses, Aaron J.J. Lemus, B\u00e9r\u00e9nice A. Benayoun, Yehuda Tzfati, Ido Ben-Ami and Itamar Harel, 14 April 2026, Genes & Development.
DOI: 10.1101\/gad.352760.125<\/a><\/p>\n

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