Communicating in an increasingly noisier world
Our ability to communicate is our tether to the social world. For most people, hearing difficulties begin as an inability to follow conversations in noisy settings. In an increasingly noisier world, the WHO estimates up to a billion people at risk for hearing damage in the coming decades. The goal of our lab is to understand the neural mechanisms underlying various forms of age-related and noise-induced hearing loss, and accelerate the translation of diagnostics and therapies from pre-clinical studies in animal models to early human trials.
The neural basis of speech intelligibility
Difficulties with speech intelligibility may arise at one or more regions of the auditory pathway.
Sensory loss in the hair cells of the cochlea causing changes in hearing thresholds, traditionally considered "hearing loss".
A loss of synapses between the auditory nerve and the inner hair cell, called cochlear synaptopathy or "hidden hearing loss".
Compensatory neural coding by the central auditory pathway
Modulatory effects of attention, prediction and linguistic context by non-sensory regions.
To design the next generation of diagnostics and therapies, we need to understand the interactions between these various key players, and not just study them in isolation. This gestalt approach is the primary motivation of our lab.
We use an entire gamut of techniques spanning humans and animal models. In humans, we combine perceptual tasks with measures of listening effort (pupillometry) to assess behavioral and cognitive aspects of speech comprehension. In animal models we use neuronal recordings from various stages of the auditory pathway combined with immunohistology to inform mechanistic hypotheses. Non-invasive auditory evoked potentials like auditory brainstem responses (ABRs), envelope and frequency following responses (EFRs and FFRs) and cortical evoked potentials (cAEPs) act as the "Rosetta stone", translating the language of the brain between humans and animal models.