The International Center for Hearing & Speech Research was established a decade ago to promote cutting-edge research in the hearing and speech science by linking interests of the National Institute for the Deaf (NTID) at Rochester Institute of Technology (RIT) with those at the University of Rochester School of Medicine and Dentistry (UR), and other universities such as SUNY Buffalo and Syracuse. This is a program of biomedical research focusing on the auditory system as a probe to the central nervous system. Within this context, we focus on age-related hearing loss generally known as presbycusis. Our immediate goal is to characterize and to determine its neural bases. Our ultimate goal is to prevent arrest and/or reverse hearing loss at any age and to investigate generalizations that can be made to other sensory systems such as vision and balance and other brain-related illnesses.

The problem of hearing loss and aging in and of itself is a significant problem for many families. An estimated 28 million persons nationwide suffer from presbycusis. Its main symptom is difficulty-understanding speech, especially in the presence of background noise. Our research to date suggests that underlying neural mechanisms begin to change in middle age (fourth decade) rather than later when the changes noticeably affect speech recognition (often in the sixth decade of life).

During the past eight years Center scientists have contributed substantially to the characterization and understanding of the neural bases of age-related hearing loss. A global finding is that hearing loss associated with aging has a central nervous system component that behaves much like a degenerative disease, e.g., Alzheimer and Parkinson diseases of the central nervous system. Center scientists from the disciplines of audiology, psychoacoustics, neurology (brain imaging) psychology, neurophysiology, neuroanatomy, neurochemistry, cell biology, otolaryngology, auditory evoked potentials and molecular biology are focused in an integrated and thematic approach to the problem. Young adult, middle aged and older adult humans and animal models are studied. The Center earned its third five-year competitive Program Project grant from the National Institutes of Health (NIH) through its National Institute on Aging (NIA). We have moved in an organized manner our study of the system as a whole, to the study of the individual cell, and are now engaged at the molecular level of the auditory system as well.

Research experience on age-related hearing loss has led us to several conclusions, among which are: 1) both central (brain stem and cortex) and peripheral nervous systems (inner ear) undergo change with age, 2) although these alterations most frequently occur together, either can emerge independently of the other, 3) central auditory system changes can be induced by peripheral hearing loss, 4) brain stem signal processing declines have been identified in cells located in the inferior colliculus (mid-brain), 5) a few calcium binding proteins in the mid-brain have been shown to either upregulate or downregulate with age, 6) upregulated calcium binding protein, calretinin, is activity dependent, 7) static temporal processing (gap detection) thresholds decline with age which compromises perception of voice onset consonant/vowel pairs in speech, 8) dynamic intensity discrimination (amplitude modulation) declines with age which compromises ability to perceive consonant-vowel combinations in speech, 9) age changes in how the human brain processes speech in background noise have been revealed in our Positron Emission Tomography (PET) imaging of human brain activity visualized during the performance of sensorimotor tasks, 10) targeted deletion of superoxide dismutase (SOD) in genes that code for the cystosolic copper/zinc isoform of SOD is associated with accelerated age-related hearing loss and increased susceptibility to noise-induced hearing loss, and 11) neurotrophic growth factors hold promise for protecting ear from damage when one is subjected to intense noise conditions or chemotherapeutic compounds used in treatment of cancer.

A specific example of our work involves constructing molecular genetic probes and neural growth promoters to stimulate the preservation and growth of hair cells (auditory nerve endings) and spiral ganglion nerve cells in the mammalian cochlea (inner ear). These were constructed to promote the preservation of receptor cells in cochleae facing traumas such as loud noises, cancer chemotherapeutic compounds, and other common insults leading to age-related hearing loss and deafness. Specifically, genetic splices and promoters are introduced into the inner ears of mice in conjunction with deafening noise exposures or antibiotic administrations to determine if cell damage can be eliminated or significantly reduced. Some experiments involve the upregulation of neurotrophic factors and calcium-regulatory proteins that have been shown in previous studies to be neuroprotective in other brain systems. A unique strength of this project is that behavioral, physiological and anatomical (multidisciplinary translational techniques utilized in our human/mouse aging studies) assessments of medical interventions are available in the Center to assess outcomes of collaborative molecular biology experiments. Results of these age-related investigations also have implications for molecular genetic studies aimed at reversing profound hearing loss in congenitally deaf persons by reducing or eliminating loss of cochlear receptor cells or spiral ganglion nerve cells.

By organizing our efforts in the ways alluded to above we became part of NIH’s “decade of the Brain” as we examined the neuroscience of the auditory system. With new tools and new techniques, we have unprecedented opportunities to approach amelioration of sensory and central nervous system alterations in serious and productive ways.

[Back to Top]