Treating Hearing Loss induced Cognitive Behavioral Impairments
The classic focus of hearing loss related research has been on perceptual processing errors along the primary auditory neuraxis. These studies showed that early hearing loss during a sensitive or critical period of development lead to permanent changes in auditory processing. Recent research has shown that subtle non-sensory cognitive impairments accompany the various forms of hearing loss. These impairments can linger even after treatment has produced full recovery of auditory perceptual abilities. These results suggest that brain regions downstream of the primary auditory neuraxis are sensitive to hearing loss. One likely structure, known as the striatum, is one synapse downstream of primary auditory cortex and forms the bridge between perceptual processing, cognition, and behavior.
The cortico-thalamo-striatal circuit is the gateway between perception, cognition, and behavior.
The auditory thalamus and cortex forms a circuit that serves as a gateway between perception, cognition, and decision making. In developing humans, this circuit allows the establishment of language-based foundational knowledge that provides the basis for internal cognitive abilities. Hearing loss can cause permanent changes to this circuit's function.
Even brief developmental hearing loss has permanent consequences for striatal function.
My early work focused on the effect of brief developmental hearing loss during the critical period of auditory development. Here, permanent functional deficits occur in the striatal region, with evidence of recovery in the highly plastic cortex. This suggested that striatal dysfunction could underlie the cognitive decision making impairments that have been reported in children that have recovered from hearing loss (Mowery et. al., 2017).
Current Research: The impact of brief developmental hearing loss on learning, plasticity, and behavior
A residual change to the striatal cells is present during learning in the hearing impaired group. These baseline deficits are briefly compensated for while the animal learns the task before returning to the impaired state. Furthermore, the learning phase for both groups reveals a shared form of learning related plasticity that may offer important clues for understanding why harder tasks amplify cognitive dysfunction (Paraouty and Mowery 2021).
Future Research: Cell targeted treatments for hearing loss induced cellular and synaptic dysfunction
By understanding the underlying physiological deficits that lead to learning impairments we can target these sources of dysfunction. For example, many drugs have specific targets that can be exploited to manipulate receptor function during learning or behavior. In cases where proteins are chronically low or missing, we can add them back into the cells by using targeted AAV that produces the protein of interest. Here, our preliminary work suggests that producing units of a receptor complex prompts the cell to produce the remaining units and build a functional receptor.