Histopathologic Categorization of Presbycusis

Rizk, Habib G.; Linthicum, Fred H.

doi:10.1097/mao.0b013e31821f84ee

Cited by 10 publications

(10 citation statements)

References 2 publications

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“…In mice, degeneration of cochlear synapses in age-related hearing loss preceded both cochlear nerve degeneration and hair cell loss and occurred long before a threshold elevation was measurable (Kujawa and Liberman, 2015 ). In fact, these observations may relate to a report by Crowe et al ( 1993 ) on “dendritic presbycusis” in which human temporal bones presented a normal cochlea but a loss of dendritic processes of the spiral ganglion (Rizk and Linthicum, 2012 ).…”

Section: Cochlear Pathology In Humans and Animal Modelssupporting

confidence: 55%

Age-related hearing impairment and the triad of acquired hearing loss

Yang

Schrepfer

Schacht

2015

Front. Cell. Neurosci.

113

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Understanding underlying pathological mechanisms is prerequisite for a sensible design of protective therapies against hearing loss. The triad of age-related, noise-generated, and drug-induced hearing loss displays intriguing similarities in some cellular responses of cochlear sensory cells such as a potential involvement of reactive oxygen species (ROS) and apoptotic and necrotic cell death. On the other hand, detailed studies have revealed that molecular pathways are considerably complex and, importantly, it has become clear that pharmacological protection successful against one form of hearing loss will not necessarily protect against another. This review will summarize pathological and pathophysiological features of age-related hearing impairment (ARHI) in human and animal models and address selected aspects of the commonality (or lack thereof) of cellular responses in ARHI to drugs and noise.

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Section: Cochlear Pathology In Humans and Animal Modelssupporting

confidence: 55%

Age-related hearing impairment and the triad of acquired hearing loss

Yang

Schrepfer

Schacht

2015

Front. Cell. Neurosci.

113

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“…2 With the exception of hydrops, sensorineural hearing loss caused by presbycusis, maternal-fetal rubella infection, aminoglycosides, and noise exposure disproportionally impact the basal turn with variable losses of spiral ganglion and hair cells reflected in a down-sloping audiogram. 3 The location of melanin and known function as a free radical scavenger may explain some patterns of sensorineural hearing loss and highlights the need for further investigation of melanocyte function in the cochlea. 2 …”

Section: Discussionmentioning

confidence: 99%

Distribution of Melanocytes in the Human Cochlea

Roberts¹,

Linthicum²

2015

Otology &Amp; Neurotology

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“…Total spiral ganglion losses increase to 50% for individuals over 80 [23]. Loss of dendritic afferents is observed in human postmortem samples, consistent with synaptic losses [14, 25]. Nonetheless, spiral ganglion neurons can still persist for decades after the onset of hearing loss, as they are frequently detected in postmortem samples from such patients [26].…”

Section: Introductionmentioning

confidence: 90%

The Role of the Transcription Factor Foxo3 in Hearing Maintenance: Informed Speculation on a New Player in the Cochlea

White

2016

BioMed Research International

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Molecular genetics has proven to be a powerful approach for understanding early-onset hearing loss. Recent work in late-onset hearing loss uses mouse genetics to identify molecular mechanisms that promote the maintenance of hearing. One such gene, Foxo3, is ontologically involved in preserving mitochondrial function. Significant evidence exists to support the idea that mitochondrial dysfunction is correlated with and can be causal for hearing loss. Foxo3 is also ontologically implicated in driving the circadian cycle, which has recently been shown to influence the molecular response to noise damage. In this review, the molecular framework connecting these cellular processes is discussed in relation to the cellular pathologies observed in human specimens of late-onset hearing loss. In bringing these observations together, the possibility arises that distinct molecular mechanisms work in multiple cell types to preserve hearing. This diversity offers great opportunities to understand and manipulate genetic processes for therapeutic gain.

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Histopathologic Categorization of Presbycusis

Cited by 10 publications

References 2 publications

Age-related hearing impairment and the triad of acquired hearing loss

Age-related hearing impairment and the triad of acquired hearing loss

Distribution of Melanocytes in the Human Cochlea

The Role of the Transcription Factor Foxo3 in Hearing Maintenance: Informed Speculation on a New Player in the Cochlea

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