Hearing ability deteriorates with age, leading to communication difficulties and a reduced quality of life. Some of these changes are apparent in the audiogram, the standard clinical measure of hearing sensitivity, which describes the sensitivity of the ear to pure tones at different frequencies. However, in addition to the changes that can be detected using standard clinical techniques, it is becoming increasing clear from animal and human studies that a deterioration in auditory function may occur before, or independently from, a significant decline in sensitivity to low-level sounds as measured by the audiogram.
Listeners with clinically normal hearing may experience an age-related decline in their ability to understand speech in noisy environments, an ability that is vital for real-world communication. It has been suggested that this may be due, in part, to a deficit in the ability of nerve fibres to represent the rapid fluctuations in sounds in terms of their synchronised patterns of activation. An age-related deficit in this “temporal coding” has been demonstrated recently in humans using techniques that record the electrical activity of nerve fibres in the auditory brain by attaching electrodes to the scalp. Temporal coding may be important for speech identification per se, but it is thought to be particularly important for segregating speech from interfering sounds. In particular, we rely on fine-grained timing information to separate sounds on the basis of their spatial locations (for example, several people talking at a noisy party).
The neural bases for the age-related decline in temporal coding are unclear, but there are two potential candidates. First, animal studies and post-mortem examinations of human ears suggest that there is a progressive loss in auditory nerve fibres with age, particularly those fibres that represent information at medium-to-high levels. Hence, this loss can occur without a reduced sensitivity to quiet sounds. Second, it is possible that the deficit in temporal coding may be due to a loss of synchrony between nerve fibres. This may occur because age is associated with a patchy degeneration of the fatty sheaths that surround nerve fibres and increase the speed of transmission of nerve impulses.
The proposed research will use a combination of state-of-the-art electrophysiological and listening-test techniques to provide a comprehensive understanding of the neural bases and perceptual consequences of the age-related decline in temporal coding in humans. Our focus will be on listeners with clinically normal hearing, so that we can study these effects in isolation from the effects of dysfunction of the hair cells and other structures in the inner ear that are associated with clinical loss. By testing a large cohort of volunteers across the age range with measures of nerve-fibre function and listening ability with laboratory and “real world” sounds, we will be able to make connections and inferences that are not possible with less ambitious studies. In particular, we will determine whether the age-related temporal coding deficits are due to a loss in nerve fibres, a reduction in nerve fibre transmission speed, or both. We will also be able to determine how the deficit in temporal coding is related to real-world hearing ability on tasks such as speech detection in noise, and musical pitch perception.
The results will provide the basis for a diagnostic test that can identify the neural dysfunction. Early diagnosis of damage, before any deficit is apparent in the audiogram, will allow clinicians to provide personalised healthcare advice, for example, to avoid any situations that will compound the problems, such as exposure to recreational noise. The research will also pave the way for future interventions that may correct for the deficits, for example hearing aids with directional microphones to facilitate speech reception, and drug and stem cell therapies to restore neural function.