New insights into accelerated aging in young sickle cell patients

A new research paper was published in Aging (listed by MEDLINE/PubMed as “Aging (Albany NY)” and “Aging-US” by Web of Science) Volume 16, Issue 21 on November 14, 2024, entitled, “Adolescents and young adults with sickle cell disease exhibit accelerated aging with elevated T-cell p16INK4a expression.”

Researchers Samuel R. Wilson, Natalia Mitin, Vanessa L. Ayer Miller, Andrew B. Smitherman, and Marcus A. Carden, from the University of North Carolina at Chapel Hill,  Sapere Bio, Campbell University, and Cogent Biosciences have discovered that young people with sickle cell disease (SCD) exhibit signs of accelerated biological aging compared to those without the disease. By measuring levels of p16INK4a, a key marker of cellular aging, the team found significantly higher levels in individuals with SCD. Remarkably, some participants showed biological aging equivalent to an additional 43 years. These findings suggest that SCD may drive faster aging in the body, offering new insights into the disease’s long-term impact.

Sickle cell disease (SCD) is a genetic condition primarily affecting individuals of African or Mediterranean descent. While treatments have advanced, people with SCD often face significant health challenges, including complications that mimic the effects of aging.

Cellular aging, or senescence, occurs when cells stop dividing yet continue to send harmful signals that damage surrounding tissues. Researchers believe this process happens at an accelerated rate in people with SCD, underscoring the importance of finding ways to slow it down and mitigate its impact.

The study compared p16INK4a levels in 18 adolescents and young adults with SCD to 27 healthy people of the same age. The results showed that even the youngest participant with SCD had higher levels of this aging marker than anyone in the non-SCD group. 

“Our youngest participant, a 15-year-old with SCD, had a higher p16 expression than all the comparators, underscoring the early rise of p16 expression in this population.“

The researchers believe this faster aging could be caused by the chronic inflammation, lack of oxygen, and stress on the body associated with SCD. Along with managing the symptoms of the disease, SCD patients also face a higher risk of aging-related problems like organ damage and physical decline much earlier in life.

The findings suggest that measuring p16INK4a levels could help clinicians identify patients at risk for these problems earlier and offer targeted care. The study also opens the door to new treatments, such as drugs that aim to remove old, damaged cells. These therapies could potentially slow down the aging process.

Further research is essential to confirm these findings and to gain a deeper understanding of how to support SCD patients effectively. Larger, long-term studies could investigate whether therapies targeting cell aging can help prevent complications and improve the quality of life for individuals with SCD.

In conclusion, this study marks an important step in understanding how SCD accelerates aging and offers new ways to improve the lives of those living with the condition.