Aging is a pre-programmed process of the organism

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A groundbreaking study conducted by Rockefeller University in New York has challenged long-standing views of the aging process. According to the new findings, aging is not chaotic molecular degradation, but rather a gradual, pre-programmed transformation of the body’s cellular system. In humans, this process likely begins before the age of 30.

Cell biologist Junyue Cao and her team studied 21 million cells from 14 organs of mice at five different stages of life, examining the expression of up to 20,000 genes in each cell. The study showed that aging does not affect all cells in the body equally. Only about 25% of cells undergo substantial changes, while the rest remain relatively stable throughout life.

The scientists found that aging is not a linear process, but is divided into distinct phases (with approximate human-age equivalents):

  • Early stage (20s to 30s): The body begins to lose certain fat and muscle cells, as well as cells responsible for repairing brain tissue.
  • Middle stage (30s to 40s–50s): There is a sharp decline in cells responsible for maintaining tissues, including cells that protect blood vessels, kidneys, and the intestines.
  • Late stage (50s and beyond): The loss of cells is replaced by their uncontrolled proliferation. Stress-affected, so-called “selfish” immune cells emerge, which over time contribute to inflammation, heart disease, arthritis, and cancer in the body.

For decades, aging was thought to result from the gradual accumulation of damage to DNA and proteins. However, the new study suggests that the process is governed by a specific genomic program. The authors compare it to the shedding of leaves from a tree in autumn: just as changes in light signal a tree to shed its leaves, molecular signals in the body activate specific stages of aging. The scientists have already identified up to 280,000 genomic regions that become activated or silenced in specific cells during this process.

The finding opens up entirely new possibilities for developing anti-aging therapies. Pharmacologists may now be able to focus not on general molecular damage, but directly on the vulnerable cells and genetic code that regulate the aging program. However, as the authors note, because the body’s regenerative capacity begins to decline well before middle age, preventive interventions may need to start at an early stage.

QuantaMagazine

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