"[…] this study addresses a critical gap by providing new insights into the role of telomere attrition across different progeroid conditions."
BUFFALO, NY — June 25, 2025 — A new research paper was published in Aging (Aging-US) Volume 17, Issue 5 , on May 28, 2025, titled " Investigating telomere length in progeroid syndromes: implications for aging disorders ."
In this study, led by first author Luma Srour and corresponding authors Yosra Bejaoui and Nady El Hajj, from Hamad Bin Khalifa University , Qatar Foundation , researchers investigated whether shortened telomeres, a marker of cellular aging, are present across various rare genetic disorders that mimic early aging, known as progeroid syndromes. The study found that telomere shortening, also called telomere attrition, is not a shared characteristic of all these disorders. This finding is important because it challenges the belief that telomere loss is a common thread in premature aging and could help refine how these syndromes are studied and treated.
Progeroid syndromes are rare conditions that cause individuals to display symptoms of aging far earlier than expected. While some of these syndromes share signs of typical aging, others arise from very different genetic alterations. Researchers focused on comparing telomere length in individuals with several of these syndromes to better understand how aging develops at the cellular level. Telomeres are protective ends of chromosomes that shorten as cells divide, acting as a biological clock linked to aging and disease.
Using DNA methylation data from blood samples, the team analyzed telomere length in patients with six progeroid syndromes: Werner Syndrome, Hutchinson-Gilford Progeria Syndrome, Berardinelli-Seip Congenital Lipodystrophy type 2, Dyskeratosis Congenita, Cerebroretinal Microangiopathy with Calcifications and Cysts, and Wiedemann-Rautenstrauch Syndrome. They found significant telomere shortening only in classical Werner Syndrome, Berardinelli-Seip Congenital Lipodystrophy type 2, and Dyskeratosis Congenita. Other syndromes, including the widely studied Hutchinson-Gilford Progeria Syndrome, did not show this pattern.
"To investigate whether progeroid syndromes have telomere attrition, we calculated telomere length using the DNAmAge web-based calculator."
The findings suggest that telomere shortening cannot be used as a universal marker for all forms of premature aging. In fact, some syndromes linked to DNA repair problems showed telomere damage, while others with different genetic mutations did not. These results indicate that the underlying biology of each syndrome is crucial in determining whether telomere shortening plays a role. Researchers also compared telomere lengths in people with genetic variants known to protect against age-related diseases. Those with protective genes had longer telomeres than people with progeroid syndromes.
This study challenges assumptions about aging in rare disorders and highlights the need for more personalized approaches in aging research. By identifying which syndromes involve telomere attrition, it opens new avenues for treating or delaying aging-related symptoms. Future research may explore other biological factors behind premature aging and how genetic differences influence the aging process.
Read the full paper: DOI: https://doi.org/10.18632/aging.206255
