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Sharon G. Kujawa
Researcher at Massachusetts Eye and Ear Infirmary
Publications - 80
Citations - 9629
Sharon G. Kujawa is an academic researcher from Massachusetts Eye and Ear Infirmary. The author has contributed to research in topics: Hearing loss & Hair cell. The author has an hindex of 42, co-authored 77 publications receiving 8176 citations. Previous affiliations of Sharon G. Kujawa include Louisiana State University & Massachusetts Institute of Technology.
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Journal ArticleDOI
Adding Insult to Injury: Cochlear Nerve Degeneration after “Temporary” Noise-Induced Hearing Loss
TL;DR: It is shown that acoustic overexposures causing moderate, but completely reversible, threshold elevation leave cochlear sensory cells intact, but cause acute loss of afferent nerve terminals and delayed degeneration of the co chlear nerve.
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Noise-induced cochlear neuropathy is selective for fibers with low spontaneous rates
Adam C. Furman,Adam C. Furman,Sharon G. Kujawa,Sharon G. Kujawa,M. Charles Liberman,M. Charles Liberman +5 more
TL;DR: Responses from single auditory nerve fibers in guinea pigs exposed to neuropathic noise were recorded, suggesting recovery of hair cell function and a change in population statistics suggesting a selective loss of fibers with low- and medium-spontaneous rates.
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Age-related cochlear synaptopathy: an early-onset contributor to auditory functional decline.
Y. Sergeyenko,K. Lall,K. Lall,M. C. Liberman,M. C. Liberman,Sharon G. Kujawa,Sharon G. Kujawa,Sharon G. Kujawa +7 more
TL;DR: Age-related cochlear synaptic and neural degeneration in CBA/CaJ mice never exposed to high-level noise is characterized and key functional clues to the synaptopathy are available in the neural response; these can be accessed noninvasively, enhancing the possibilities for translation to human clinical characterization.
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Acceleration of Age-Related Hearing Loss by Early Noise Exposure: Evidence of a Misspent Youth
TL;DR: Comparing noise-induced and age-related hearing loss in groups of CBA/CaJ mice exposed identically but at different ages and held with unexposed cohorts for different postexposure times suggests that pathologic but sublethal changes initiated by early noise exposure render the inner ears significantly more vulnerable to aging.
Journal ArticleDOI
Synaptopathy in the noise-exposed and aging cochlea: Primary neural degeneration in acquired sensorineural hearing loss
TL;DR: The research suggests that primary neural degeneration is an important contributor to the perceptual handicap in SNHL, and in cases where the hair cells survive, neurotrophin therapies can elicit neurite outgrowth from spiral ganglion neurons and re-establishment of their peripheral synapses.