Pathophysiology of Hearing Loss

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Physiology".

Deadline for manuscript submissions: 30 October 2026 | Viewed by 855

Special Issue Editor


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Guest Editor
Department of Otolaryngology and Communicative Sciences, The University of Mississippi Medical Center, Jackson, MS 39216, USA
Interests: hearing loss; auditory; noise; cardiometabolic risk; cochlear impairment; natural cell death

Special Issue Information

Dear Colleagues,

Though it is well established that the cochlea is susceptible to a myriad of potential acquired insults, either from loud noise, natural cell death, inflammation, chemical toxicity, or others, research is showing how obesity-related factors and side-effects of new medications are adding to the list of risks for cochlear hearing loss. This Special Issue will focus on recently identified risks of cochlear hearing loss, including cochlear toxicity from new medications, obesity-related risk factors, and trends in the identification and management of these risks in individuals. We invite submissions to this Special Issue on the following sub-topics: pathophysiology of potential ototoxic effects, new perspectives on mechanisms of cochlear damage from established ototoxins and/or diseases, advances in the identification and treatment of cochlear impairment, and updates on the relationship between cardiovascular and/or cardiometabolic risk and the prevalence and incidence of hearing loss. Additionally, we accept submissions exploring the cochlear effects of COVID-19 infection and immunization.

Prof. Dr. Charles E. Bishop
Guest Editor

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Keywords

  • hearing loss
  • cochlea
  • noise
  • deafness genes
  • cell death
  • hair cells
  • inner ear
  • biotoxicity
  • metabolic risk
  • gene mutation
  • physiology and pathophysiology
  • animal models
  • biomarkers and molecular mechanisms

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Published Papers (2 papers)

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Research

19 pages, 16740 KB  
Article
Immunohistopathology of Cochleovestibular Schwannoma in Human Temporal Bone Specimens
by Jennifer T. O’Malley, Anat O. Stemmer-Rachamimov, Sebahattin Cureoglu, Michael J. McKenna, D. Bradley Welling and Alicia M. Quesnel
Biology 2025, 14(11), 1540; https://doi.org/10.3390/biology14111540 - 3 Nov 2025
Viewed by 156
Abstract
The aim of this study was to investigate the pathology of hearing loss caused by cochleo-vestibular schwannoma. Surgical specimens have demonstrated that a tumor may displace normal nerve fibers of the cochlear nerve to one side (pushing pattern) or the neoplastic cells may [...] Read more.
The aim of this study was to investigate the pathology of hearing loss caused by cochleo-vestibular schwannoma. Surgical specimens have demonstrated that a tumor may displace normal nerve fibers of the cochlear nerve to one side (pushing pattern) or the neoplastic cells may invade the tumor and grow between normal nerve fibers (infiltrating pattern). The goal was to study the relationship of the tumor to the remaining fibers of the cochlear nerve. Nerve fibers within all 28 tumors showed positive anti-neurofilament (NF) labeling. Axons within tumors were sometimes turned orthogonal to their original plane. Onion bulb formations were observed in tumors giving rise to early Antoni B-like regions of degeneration. Positive anti-myelin protein zero (MPZ) labeling was demonstrated. No clear capsule was found between tumor and nerve. There was a comingling of tumor and nerve fibers either with the nerve of origin or with both the nerve of origin and surrounding internal auditory canal nerves. Iba1+ macrophages were prevalent within cochleovestibular schwannomas. Our results suggest that retro cochlear mechanisms of hearing loss go beyond compression of the eighth cranial nerve, involve both myelin and axon degeneration, and suggest an inflammatory component from the earliest stage of the disease. Full article
(This article belongs to the Special Issue Pathophysiology of Hearing Loss)
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15 pages, 2772 KB  
Article
Perinatal Fluoxetine Exposure Has No Major Effect on Myelin-Associated Glycoprotein and Myelin Basic Protein Levels in Auditory Brain Regions
by Joëlle D. Jagersma, Marije Visser, Sonja J. Pyott, Eelke M.S. Snoeren and Jocelien D.A. Olivier
Biology 2025, 14(11), 1482; https://doi.org/10.3390/biology14111482 - 24 Oct 2025
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Abstract
Hearing loss and serotonergic dysfunction both impact social and cognitive behaviors, yet their neurobiological interplay remains poorly understood. This study investigated whether perinatal fluoxetine exposure alters myelination in (auditory) brain regions during development. Female Wistar rats received 10 mg/kg fluoxetine from gestational day [...] Read more.
Hearing loss and serotonergic dysfunction both impact social and cognitive behaviors, yet their neurobiological interplay remains poorly understood. This study investigated whether perinatal fluoxetine exposure alters myelination in (auditory) brain regions during development. Female Wistar rats received 10 mg/kg fluoxetine from gestational day 1 until postnatal day (PND)21. Brain tissue was collected from male offspring at PND21 and PND35. Myelination was assessed via immunohistochemical analysis of Myelin-Associated Glycoprotein (MAG) and Myelin Basic Protein (MBP) in the auditory cortex, inferior colliculus, and corpus callosum. MAG+ cell counts, MBP+ area, and MBP fluorescence intensity were quantified. No major effects of fluoxetine were observed on myelin markers in any brain region or developmental stage. However, changes in myelination emerged between PND21 and PND35. MAG+ cell density declined in the inferior colliculus but remained stable in the auditory cortex. MBP+ area decreased over time in both the corpus callosum and auditory cortex, while MBP fluorescence intensity increased in the corpus callosum. These results suggest that myelination changes between PND21 and PND35 are region- and age-dependent and not altered by fluoxetine. These findings highlight the dynamic nature of postnatal myelination and suggest that serotonergic alterations alone may be insufficient to disrupt structural maturation in auditory regions. Full article
(This article belongs to the Special Issue Pathophysiology of Hearing Loss)
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