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A groundbreaking study published in the journal Trends in Genetics suggests that the process of aging may be less about specific “aging genes” and more about the length of genes themselves. Researchers propose that many changes associated with aging could be attributed to decreased expression of long genes, a phenomenon observed across various animal species, tissues, and individuals with neurodegenerative diseases.
The study, led by molecular biologist Jan Hoeijmakers from multiple institutions including Erasmus University Medical Center and the University of Cologne, challenges the prevailing focus on individual genes associated with aging. Instead, the research emphasizes the impact of gene length on the aging process, highlighting a strong association between the decline in expression of long genes and systemic aging.
The research, conducted by four interdisciplinary research groups from Spain, the Netherlands, Germany, and the United States, converges on the same conclusion: aging may be more of a random physical phenomenon linked to gene length rather than specific gene functions.
Explaining the phenomenon, co-author Ander Izeta from the Biogipuzkoa Health Research Institute draws an analogy to a road trip, suggesting that longer genes have more potential sites that could be damaged, akin to a longer journey increasing the likelihood of mishaps. This accumulation of DNA damage over time, particularly in cells expressing long genes and slow or non-dividing cells, contributes to the aging process.
The study underscores the vulnerability of neural cells, known for expressing particularly long genes, to aging and neurodegeneration. Many genes involved in preventing protein aggregation in Alzheimer’s disease are notably lengthy, linking the decline in long-gene expression to neurodegenerative disorders.
While causative evidence linking the decline in long-gene expression to aging remains to be demonstrated, the study highlights the strong relationship between this phenomenon and well-known hallmarks of aging. Moreover, the researchers speculate that various aging accelerants, such as radiation, smoking, and diet, may exacerbate this length-dependent regulation.
In future studies, the researchers aim to delve deeper into the mechanism and evolutionary implications of this phenomenon and explore its intricate relationship with neurodegeneration. By unraveling the role of gene length in aging, the study opens new avenues for understanding the aging process and developing potential interventions to mitigate its effects.
