Zombie Cells — and How They Might Reverse Ageing
They’re called zombie cells because they are damaged and refuse to die
By Yash Laddha
Have you ever wondered why we age and develop diseases like Alzheimer’s, arthritis, and cancer as we grow older? The answer lies in a process called cellular senescence, where cells stop dividing but continue to release molecules that can cause age-related problems and diseases. This process creates an endless cycle, as the accumulation of senescent cells leads to the generation of more such cells. This relentless cycle of cellular senescence, marked by arrested cell division and the persistent release of age-inducing molecules, lays the foundation for age-related maladies. The accumulating senescent cells become architects of DNA lesions, mitochondrial dysfunction, and inflammation, culminating in the manifestation of diseases such as Alzheimer’s, arthritis, and cancer.
The Research
Mayo Clinic researchers have conducted a groundbreaking study involving 1,923 adults aged 65 and older, in which they identified a set of diverse proteins secreted by senescent cells that can serve as potent biomarkers of senescence.
The study revealed that these biomarkers have the potential to predict health outcomes in older adults, transcending conventional indicators like age, sex, or chronic disease presence. The research highlighted specific senescent biomarkers whose elevated levels were associated with an increased risk of mortality. These biomarkers could be integrated into clinical practice as powerful tools for identifying individuals at risk of health challenges. The findings of this study hold immense promise for improving the health outcomes of older adults. By identifying specific senescence biomarkers, medical professionals could predict health outcomes in older adults and implement targeted interventions to reduce the risk of age-related diseases.
These biomarkers could be used to create personalized health interventions for older adults based on their biological age and underlying health conditions. Furthermore, the Mayo Clinic researchers’ study of mice suggests that reducing the number of senescent cells could lead to improved health outcomes in older adults. This could be achieved through medical interventions designed to target senescent cells, such as senolytic therapies.
Senolytic drugs stand at the forefront of combating ageing and age-related diseases by selectively removing senescent cells, aiming to restore tissue homeostasis. While pre-clinical results have kindled optimism, the absence of senolytics on the market and constraints in ongoing clinical trials prompt the exploration of more effective alternatives. Investigative efforts encompass repurposed anti-cancer molecules and immune-based clearance, with intermittent senolytic administration holding the potential for minimizing adverse effects.
Directly eliminating senescent cells offers advantages, including the permanent removal of the senescence-associated secretory phenotype (SASP) source and a reduced cancer risk from senescence escape. However, recent research from UC San Francisco urges caution, revealing that not all senescent cells are detrimental “zombies.” Some are integral to young, healthy tissues, aiding in normal repair processes. The careful consideration of senolytics for therapeutic use becomes imperative, recognizing the nuanced roles these cells play in tissue surveillance and the stimulation of nearby stem cells for healing.
Despite the promise of senolytic drugs, a comprehensive understanding of their mechanisms and potential side effects requires further research. The integration of artificial intelligence into senolytic exploration enhances the field, contributing to the discovery of compounds with distinct properties. These collective advancements mark a promising era in ageing research, with the overarching goal of extending both health and longevity through the selective targeting and elimination of senescent cells.
