New research, including a study from Northwestern Medicine, sheds light on a surprising culprit behind aging: long genes. These four independent studies, published today, all point to a connection between the length of genes and the aging process.

Traditionally, scientists have focused on specific "aging genes" to understand how our bodies deteriorate. This new research suggests a more fundamental mechanism might be at play. The studies observed that as we age, the activity of long genes tends to decline across a wide range of organisms, from worms to humans. This decline is seen in various cell types and tissues, and even in individuals with neurodegenerative diseases.

The reason? Imagine genes as instructions on a long sheet of paper. The longer the instructions, the more likely they are to get damaged during the copying process that happens when cells divide. This damage can prevent the cell from reading and following the instructions, hindering important functions.

"Long genes that become less active with age may be the central cause of aging in our bodies," explains co-author Thomas Stoeger, a researcher at Northwestern Medicine. This finding offers a unifying concept that connects many existing theories on aging and provides a measurable factor to track.

While the exact cause-and-effect relationship needs further investigation, this research opens exciting avenues for future studies. Understanding how to protect long genes or enhance their activity could pave the way for new anti-aging therapies.

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