Over the past few decades, there has been a significant increase in average life expectancy globally. In the US, the average life expectancy increased from 70 to 79 years of age between 1960 and 2015, and this is expected to increase further in the coming decades.
Although this highlights the significant positive impact of modern medicine on life expectancy, it has also become clear that an aging population faces significant challenges in terms of physical and mental deterioration that is one of the consequences of increased life span. Moreover, an aging population with multiple health problems presents challenges in daily functioning and translates into increased healthcare-related costs for the healthcare system. Cognitive decline and hearing loss are some of the most common and least understood challenges that come with age.
Understanding the underlying mechanisms to age-related physical and mental deterioration and studying ways to prevent these adverse events has become a major area of research.
Recently, a study was published in PLOS biology that highlighted the potential positive effect of increasing oxygen supply to tissues to counteract the age-related deteriorative changes.
It is understood that there is a gradual decline in the supply of oxygen to tissues as a person ages. This decrease in oxygen triggers an inflammatory and immune response and it is postulated that these changes can be the underlying mechanism for cognitive decline and hearing loss.
Many studies have reported that adenosine signaling is involved in regulating brain function and it is also involved in the cognitive decline associated with aging. Recent studies concluded that the metabolic adaptation of red blood cells to high altitude low oxygen levels results in the increased delivery of oxygen to tissues. This manifests due to elevated adenosine signaling via ADORA2B. And it is also known that adenosine levels decrease as the person ages. In light of the above evidence, researchers conducted studies on mice to determine the role of erythrocyte-associated ADORA2B activation in age-related cognitive decline and hearing loss.
Researchers determined that genetic ablation of erythrocyte ADORA2B resulted in increased inflammatory and immune response and decreased oxygen supply to different areas of the brain of mice. Also, they determined that this genetic ablation results in early cognitive decline and hearing loss. Moreover, they determined that erythrocyte ADORA2B is required to prevent hypoxia-associated cognitive decline and hearing loss and that it has a protective function against mental deterioration and cochlear function deterioration.
These findings suggest that the adverse consequences of aging like cognitive decline and hearing loss can be prevented through this pathway by increasing oxygen supply to tissues.
Researchers suggest that any drug which will activate this pathway will potentially be able to prevent these age-related changes. According to the lead researcher, there is no such drug available yet.
Researchers believe that further research is needed to study these findings specifically if adenosine levels decline with age in mice and if increasing the erythrocyte-associated activation of ADORA2B leads to prevention of cognitive decline and hearing loss. They also plan to study these pathways in humans in the future.
Going forward, it would be interesting to see if these findings are found in studies in humans and if theoretical understandings are reflected in scientific experiments. If results are positive in terms of producing similar changes in humans and impacting the cognitive decline and hearing loss positively, they may present an interesting area to research further and develop pharmaceutical agents to target this pathway and may improve some of the negative effects of aging and allow people to live longer and functioning lives.