Charles Cranston

Understanding the mechanisms leading to age-related hearing loss

About me

I’ve always been fascinated by the ways in which our bodies function, particularly in relation to ageing. I did an integrated master’s degree at Durham University which had a year-long research project looking at skin ageing that made me driven to pursue a career in research. I chose this project as it meant I’d be investigating an area of ageing which is relatively unknown, so that was exciting. I also thought it’d be an excellent learning experience as I’d have two world-leading academics at my disposal and a DTP programme which has plenty opportunities to develop my research skills.  I also really liked the idea of living in Sheffield as it’s a friendly city with some great mountain biking.

My research

Age-related hearing loss (ARHL) is the most common sensory disorder in elderly humans with an estimated 670 million of over-60s worldwide experiencing some degree of hearing loss. ARHL leads to social isolation, anxiety and depression, but the current therapies of hearing aids and implants do not fully help those suffering, although there are some benefits. My project will be looking at the mechanisms that cause ARHL. The current literature suggests that as we age, the mitochondria within the cells of the cochlea (the organ which detects sound) become dysfunctional, leading to high amounts of oxidative stress. However, we don’t know how these high levels of oxidative stress leads to ARHL. I will be working alongside Professor Walter Marcotti, an expert in auditory physiology, and Professor Sherif El-Khamisy, an expert in DNA damage and repair, to investigate the link between oxidative stress and ARHL. Oxidative stress is well known to cause DNA damage, including strand breaks, topoisomerase-1 cleaved complexes (TOP1cc), and R-loops. We will be observing the levels of these damages within the cochlea during ageing and whether there are any changes that occur to their repair pathways. We predict that the aged cochlea will have high amounts of DNA damage and that the repair pathways will become defective. The results we obtain from this project will improve our understanding of ARHL, and in turn could lead to the development of therapeutics that are more successful than those which we currently use.