Aging is part of the life cycle and, although the effects are not manifest until after adulthood, it actually occurs from birth. The concept of senescence has traditionally been associated with aging. However, an embryo has senescent cells. In that case, what is aging, how can it be measured, and from what point in the life cycle?

Aging is part of the life cycle and, although the effects are not manifest until after adulthood, it actually occurs from birth. The concept of senescence has traditionally been associated with aging. However, an embryo has senescent cells. In that case, what is aging, how can it be measured, and from what point in the life cycle?

Aging is part of the life cycle and, although the effects are not manifest until after adulthood, it actually occurs from birth. The concept of senescence has traditionally been associated with aging. However, an embryo has senescent cells. In that case, what is aging, how can it be measured, and from what point in the life cycle?

Since the publication of The Hallmarks of Aging in 2013, aging research has exploded. The field now has more than 300,000 articles on the biological signals of the effect of time on the body. What would Marty McFly, the legendary character from the Back to the Future saga who traveled with his DeLorean time machine from the ‘80s to the ‘50s, think if he visited 2024 and saw laboratories experimenting with techniques to turn back the biological clocks of cells or increase the lifespan of rejuvenated mice?

Researchers at the Walter and Eliza Hall Institute of Medical Research (WEHI) in Melbourne have discovered new cells that drive the aging process in the thymus that could unlock a way to restore function and prevent immunity from waning as we age. The thymus is the first organ in the body to shrink as people age. As this happens, the T-cell growth areas in the thymus are replaced with fatty tissue, diminishing T-cell production and contributing to a weakened immune system.

Scientists at Harvard Medical School have shown that in mice lacking amyloid beta (Aβ), the fundamental hallmark of Alzheimer's disease (AD), neurons died from the effect of the most harmful mutation of this neurodegenerative disease. They showed that presenilin (PS) could be behind the origin of the disease without the need for Aβ. They maintain that it is time to update theories and redirect efforts.

Researchers in Japan were able to transfer genes from jellyfish into common fruit flies and discovered that the transferred gene suppressed an age-related intestinal issue in the flies. The findings suggest that studying genes specific to animals with high regenerative capability like jellyfish may uncover new mechanisms for rejuvenating stem cell function and extending the healthy lifespan of unrelated organisms.

Researchers in Japan were able to transfer genes from jellyfish into common fruit flies and discovered that the transferred gene suppressed an age-related intestinal issue in the flies. The findings suggest that studying genes specific to animals with high regenerative capability like jellyfish may uncover new mechanisms for rejuvenating stem cell function and extending the healthy lifespan of unrelated organisms.

Increased life expectancy also comes with age-related diseases. But what causes one to age? Although there is no single answer, scientists at Duke-National University of Singapore have shown in mice that interleukin-11 (IL-11) promoted aging. Blocking it improved health and lifespan.