At the heart of many scientific endeavors is a desire to improve human life. For the most part, scientific improvement of human life has been through the avenue of understanding diseases. However, aging is also central aspect of human life, and the biochemical changes that occur in the body with advanced aging have long been thought to be a major risk factor for diseases such cardiovascular disease, cancer, dementia, and arthritis.
The specific mechanisms behind aging have yet to be fully elucidated, but a new study published in Journals of Gerontology this past January may bring us one step closer to this understanding. The study shows that the hormone growth differentiation factor 11 (GDF11) involved in aging is genetically controlled. Previous studies have shown that blood levels of GDF11 decrease over time in mammals and that injecting GDF11 later in life in mice can result in the regeneration of muscle.
The January study confirmed that GDF11 levels decrease with age in mice and demonstrated that patterns of GDF11 levels are heritable. Specifically, the researchers collected blood samples from young-adult, middle-aged, and old mice and quantified GDF11 levels through optical density analyses. By categorizing mice by strain, sex, and age, researchers found that GDF11 levels decreased with age, varied across strains, but did not depend on sex. After examining 22 different mouse strains, researchers found a wide range of characteristic GDF11 levels across strains. More generally, however, a positive linear correlation was found between GDF11 levels and the median life span of mice: higher GDF11 levels predict longer life spans.
Using Efficient Mixed-Model Analysis (EMMA) to conduct association mapping across the different mouse strains, single nucleotide polymorphisms (SNPs) – markers of genetic variation within the genome of a species that may be correlated with specific diseases – were identified. The SNPs found were narrowed down to protein-coding regions and ultimately seven genes were isolated as candidate genes involved in GDF11 regulation. One of these genes, Dsp, encodes desmoplakin, a vital component of desmosomes. Desmosomes are structures involved in cell-cell adhesion and are found in muscle and skin cells. Loss-of-function mutations in Dsp are known to cause cardiomyopathy, suggesting a potential link between GDF11 levels, aging, and cardiovascular disease. In future studies, the researchers hope to understand how Dsp and other genes interact with one another to regulate GDF11 levels.
Although the scientific aspects of this new discovery are exciting for the future of understanding the mechanisms behind aging, the ethical implications of controlling aging are troubling. For example, any therapeutic treatment that may relate to increasing human life will likely only be available to the select few who can afford it. As a result, the unequal balance of healthcare resources available to first- and third-world country populations could easily become more skewed. Health care inequity is already a pressing issue of our modern world, but the introduction of an anti-aging treatment could alter the landscape of healthcare and population dynamics irrevocably.
Khush Dhaliwal is a freshman in Morse College. Contact her at email@example.com.
(Featured image from Wikimedia Commons)