Telomere Length in Immune Cells Linked to Age-Related Macular Degeneration: New Insights

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Researchers at the VN Orekhovich Institute of Biomedical Chemistry (IBMH), in collaboration with colleagues from the MM Krasnov Institute of Eye Diseases, have explored a compelling link between the development of age-related macular degeneration (AMD) and telomere length — the protective caps at the ends of chromosomes. This work, reported to socialbites.ca with input from the Ministry of Education and Science of the Russian Federation, sheds new light on cellular aging processes that may influence eye health in later life.

AMD is a chronic, progressive condition that chiefly affects older adults. It damages the retina and can blur or distort central vision, making everyday tasks like reading or recognizing faces increasingly difficult. While multiple factors are believed to contribute to AMD, researchers have long suspected that immune system activity plays a significant role. In pursuit of this hypothesis, the IBMH team examined a mixed population of white blood cells — the guardians of the immune system — and then isolated each cell subtype to study telomere length as a marker of cellular aging within those specific populations. Their analysis revealed a striking pattern: telomere length in immune cells, particularly monocytes, showed a strong correlation with the onset and progression of various forms of AMD.

Telomeres are natural nucleotide sequences at chromosome ends that shield genetic information from damage and help maintain cellular stability. When telomeres are longer, chromosomes tend to be more stable and cells function more effectively. Shorter telomeres, on the other hand, are associated with decreased cellular activity and aging. By comparing telomere measurements across immune cell subtypes with the clinical manifestations of AMD, the researchers provided evidence that monocytes may actively contribute to the disease’s pathogenesis. This insight points toward the potential of telomere-based biomarkers to aid in diagnosing and monitoring AMD. The team’s leader, Dmitry Zhdanov, head of the RAND laboratory at IBMH, emphasized that the findings open a pathway for future work aimed at developing diagnostic methods that leverage telomere dynamics in immune cells. (Attribution: IBMH study report)

The research underscores a broader view of AMD as not solely a localized retinal condition but one that may be influenced by systemic immune processes and aging signals circulating in the bloodstream. The identification of monocytes as a key cellular player suggests new angles for therapeutic strategies, including approaches that modulate immune cell aging or telomere maintenance to slow disease progression. Importantly, the study adds to the growing body of evidence that aging markers in immune cells can reflect, and perhaps predict, the trajectory of chronic eye diseases in older adults. The implications for clinical practice lie in the potential development of non-invasive tests that track telomere length in specific white blood cell populations as part of AMD risk assessment and disease monitoring. (Cited: IBMH laboratory findings)

As the researchers outline, further work is needed to translate these cellular observations into practical diagnostic tools and treatment approaches. Additional studies will be focused on validating telomere-related biomarkers in larger patient cohorts, understanding how telomere dynamics in monocytes interface with retinal pathology, and exploring whether interventions that influence telomere length or cellular aging could modify AMD outcomes. The overall aim is to build a more comprehensive picture of AMD that integrates immune aging markers with ocular findings, ultimately improving early detection, risk stratification, and patient care. (Source note: IBMH/MM Krasnov collaboration)

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