New research suggests further potential for reversing age related diseases

Posted on 2018-08-21

How do we define ageing? Many suggest that we can attribute age to simple physics and its principles of entropy; a system moving from order to disorder, an inevitable bodily decline over time into dysfunction. Whilst there exists a myriad of tools to halt the appearance of time, these options often simply mask the issue, not solve the cause. Naturally, it is a human obsession to attempt to slow or reverse age, but despite our efforts, if the universe itself cannot escape the influences of entropy, how can we?

Biologically, ageing can be used as an umbrella term for a collection of cellular changes leading to a decline in physiological function. Though many discuss finding a 'cure' for this process, ageing is not characterised as or by a disease itself, but more so the increased risk of disease and a greater likelihood of susceptibility, caused by numerous factors and changes. Delving down to a genomic level, one may consider the progressive shortening of the telomeres, DNA damage, oxidative stress and increased frequency of cell-cycle errors as key events of the ageing process.

Our current understanding of ageing teaches us that, much like cancer, there will be no generic 'cure' for ageing. Age is a personalised process, multifarious and somewhat unpredictable; with so many causes and processes involved, research must consider these processes individually. Vinel et al. (2018) recently demonstrated this specificity in their article in Nature Medicine, which concluded the possibility of reversing age-associated sarcopenia with apelin. Sarcopenia is the degeneration of skeletal muscle, characterised by the loss of muscle mass, strength and function with age. Apelin is an exerkine: an anti-inflammatory molecule released in response to exercise. This paper shows the reduction of apelin production with age and mice lacking this exerkine or its receptor display significantly impaired muscle function, implying an important role for apelin in muscular maintenance. Restoration of apelin signalling in these mice significantly improved muscle function, with the study concluding a possible role for apelin as both a biomarker for age and a treatment target for sarcopenia.

Targeting another age-related pathology, a new study conducted by Mannick et al. (2018) linked the inhibition of mTORs to the enhancement of the immune system and reduction of infections in the elderly. The mTOR network represents the mechanistic targets of rapamycin: growth regulator kinases present in two complexes which monitor a diverse set of extracellular and intracellular signals in order to coordinate a myriad of cellular responses. Previous studies have linked mTORs to ageing and longevity; inhibition of one multiprotein mTOR complex, TORC1, exhibited an increase in lifespan in all model organisms studied. Mannick et al. used a placebo-controlled, randomised clinical trial to measure the effect of a therapy comprised of one catalytic and one allosteric mTOR inhibitor. The results show that TORC1 inhibitor therapy in the elderly significantly decreased the incidence of infection, improved vaccination responses to influenza and up-regulated antiviral immunity, demonstrated by an up-regulation of antiviral gene expression.

In 2018, science is still challenging theories on age which have been accepted for decades. Whilst logic would support the idea that cumulative damage over time would create a steady decline ultimately resulting in death, new studies suggest that this may not be true for the human process of age. Biodemographers from Italy claim that from analysis of statistical population data, the risk of dying plateaus once the age of 105 is reached, suggesting we have yet to reach the human limit of longevity. However, this research is still in its infancy; this so-called 'morbidity plateau' needs to have larger, more representative samples of the population in the research before it can be generalised into an accepted theory. Ageing does possess huge scope for potential research, with over 30 laboratories worldwide already investigating senescence. Current generations are in amongst the first to experience the socioeconomic effects of an ageing population, thus calling for science to look to not just extend an individual's lifespan, but also to maintain and extend their quality of life. Both Vinel at al. and Mannick et al. provide hope for this concept.

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References-

Article- Science, June 2018: Once you hit this age, ageing appears to stop.

Article- Science, July 2018: TORC1 inhibition enhances immune function and reduces infections in the elderly.

Article- Nature Medicine, July 2018: The exerkine apelin reverses age-associated sarcopenia.

Article- Mol. Bio of the Cell, December 2015- The Cell Biology of Ageing.

Information page- International Osteoporosis Foundation: What is Sarcopenia?