Age-related hearing loss (ARHL) is the most common sensory deficit in the elderly, leading to the progressive loss of hearing sensitivity and decreased ability to understand speech. About 25% of people over 45 years old, and 60% of those in their 7th decade, have hearing loss that is severe enough to affect communication, causing social isolation and depression.
Despite the impact of ARHL within our society, there are no treatments because we know very little about the underlying causes. Recent research has primarily focused on the role of hair cells and their neurons, but has neglected other key aspects of ageing, such as changes in the intercellular communication among the non-sensory cells, which create a functional syncytium within the cochlea. This intercellular coupling is key to the survival and function of hair cells and their neurons, because it regulates several physiological processes (e.g. Ca2+ homeostasis, purinergic signalling). Moreover, it is responsible for transporting glucose and other nutrients from the blood vessels to the largely avascular sensory epithelium.
Our preliminary data show that the function of these non-sensory cells, the expression of key proteins in their membrane (e.g. connexins, P2X receptors) and genes regulating the expression of these proteins (e.g. Brn4) change with age. Therefore, our overarching hypothesis is that non-sensory cells undergo progressive functional changes with age, and this occurs prior to deterioration of the hair cells and their neurons. Testing this hypothesis is of fundamental biological importance. As we begin to think about therapeutic strategies to combat ARHL, should we target the hair cells/neurons or the non-sensory cells?
Prof Marcotti: w.marcotti@sheffield.ac.uk
University of Sheffield
