Physiological and Neurobiological Bases of Age-Related Hearing Loss: Biotherapeutic Implications

2013 ◽  
Vol 22 (2) ◽  
pp. 299-302 ◽  
Author(s):  
Robert D. Frisina ◽  
D. Robert Frisina
Keyword(s):  
Hearing Loss ◽  
Auditory Processing ◽  
Stria Vascularis ◽  
Positive Influence ◽  
Negative Effects ◽  
Age Related ◽  
Women And Aging ◽  
Auditory Tasks ◽  
And Function ◽  
Age Related Hearing Loss

Purpose The aim of this study was to highlight growing evidence of interactions between hormones and the structure and function of the auditory system. Method Recent studies implicating sex hormones and other natural hormones in the modulation of hearing status in age-related hearing loss were reviewed. Results Progesterone, a sex hormone, has been shown to have negative effects on the hearing of older women and aging mice, whereas, in contrast, estrogen was found in some cases to have a positive influence. Aldosterone, used in studies of animal models of autoimmune hearing loss, slowed the progression of hearing loss. Follow-up studies in humans revealed that auditory measures varied as serum aldosterone levels shifted within the normal range, in otherwise healthy older subjects. This was true for simple as well as complex auditory tasks (i.e., sound spatial processing), suggesting benefits of aldosterone to postperipheral auditory processing as well. In addition, evidence suggests that this functional hearing improvement occurred in association with anatomical improvements to the stria vascularis—an important site of anatomical change in presbycusis. Conclusions Audiology is now at the point where the search for biomedical interventions to modulate or prevent age-related hearing loss can move forward. Such interventions would require multidisciplinary collaborative initiatives by researchers in such areas as drug development, anatomy, auditory physiological and perceptual testing, and drug microdelivery systems.

scholarly journals A Review on Recent Advancement on Age-Related Hearing Loss: The Applications of Nanotechnology, Drug Pharmacology, and Biotechnology

Pharmaceutics ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 1041
Author(s):  
Jacqueline Chester ◽  
Edan Johnston ◽  
Daniel Walker ◽  
Melissa Jones ◽  
Corina Mihaela Ionescu ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Bile Acid ◽  
Hearing Aids ◽  
Stria Vascularis ◽  
Cellular Damage ◽  
Relevant Evidence ◽  
Neuronal Signalling ◽  
Age Related ◽  
Recent Advancement ◽  
Age Related Hearing Loss

Aging is considered a contributing factor to many diseases such as cardiovascular disease, Alzheimer’s disease, and hearing loss. Age-related hearing loss, also termed presbycusis, is one of the most common sensory impairments worldwide, affecting one in five people over 50 years of age, and this prevalence is growing annually. Associations have emerged between presbycusis and detrimental health outcomes, including social isolation and mental health. It remains largely untreatable apart from hearing aids, and with no globally established prevention strategies in the clinical setting. Hence, this review aims to explore the pathophysiology of presbycusis and potential therapies, based on a recent advancement in bile acid-based bio-nanotechnologies. A comprehensive online search was carried out using the following keywords: presbycusis, drugs, hearing loss, bile acids, nanotechnology, and more than 150 publications were considered directly relevant. Evidence of the multifaceted oxidative stress and chronic inflammation involvement in cellular damage and apoptosis that is associated with a loss of hair cells, damaged and inflamed stria vascularis, and neuronal signalling loss and apoptosis continues to emerge. New robust and effective therapies require drug delivery deeper into the various layers of the cochlea. Bile acid-based nanotechnology has gained wide interest in its permeation-enhancing ability and potential for numerous applications in treating presbycusis.

scholarly journals Role of Oxidative Stress in the Senescence Pattern of Auditory Cells in Age-Related Hearing Loss

Antioxidants ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1497
Author(s):  
Luz del Mar Rivas-Chacón ◽  
Sofía Martínez-Rodríguez ◽  
Raquel Madrid-García ◽  
Joaquín Yanes-Díaz ◽  
Juan Ignacio Riestra-Ayora ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hearing Loss ◽  
Molecular Mechanisms ◽  
Morphological Changes ◽  
Cell Damage ◽  
Stria Vascularis ◽  
Organ Of Corti ◽  
Age Related ◽  
Age Related Hearing Loss

Age-related hearing loss (ARHL) is an increasing and gradual sensorineural hearing dysfunction. Oxidative stress is an essential factor in developing ARHL; additionally, premature senescence of auditory cells induced by oxidative stress can produce hearing loss. Hydrogen peroxide (H2O2) represents a method commonly used to generate cellular senescence in vitro. The objective of the present paper is to study H2O2-induced senescence patterns in three auditory cell lines (House Ear Institute-Organ of Corti 1, HEI-OC1; organ of Corti, OC-k3, and stria vascularis, SV-k1 cells) to elucidate the intrinsic mechanisms responsible for ARHL. The auditory cells were exposed to H2O2 at different concentrations and times. The results obtained show different responses of the hearing cells concerning cell growth, β-galactosidase activity, morphological changes, mitochondrial activation, levels of oxidative stress, and other markers of cell damage (Forkhead box O3a, FoxO3a, and 8-oxoguanine, 8-oxoG). Comparison between the responses of these auditory cells to H2O2 is a helpful method to evaluate the molecular mechanisms responsible for these auditory cells’ senescence. Furthermore, this in vitro model could help develop anti-senescent therapeutic strategies for the treatment of AHRL.

scholarly journals Roles of Key Ion Channels and Transport Proteins in Age-Related Hearing Loss

2021 ◽  
Vol 22 (11) ◽  
pp. 6158
Author(s):  
Parveen Bazard ◽  
Robert D. Frisina ◽  
Alejandro A. Acosta ◽  
Sneha Dasgupta ◽  
Mark A. Bauer ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Ion Channels ◽  
Auditory System ◽  
Auditory Processing ◽  
Mechanical Energy ◽  
Transport Proteins ◽  
Oval Window ◽  
Cochlear Hair Cells ◽  
Age Related ◽  
Age Related Hearing Loss

The auditory system is a fascinating sensory organ that overall, converts sound signals to electrical signals of the nervous system. Initially, sound energy is converted to mechanical energy via amplification processes in the middle ear, followed by transduction of mechanical movements of the oval window into electrochemical signals in the cochlear hair cells, and finally, neural signals travel to the central auditory system, via the auditory division of the 8th cranial nerve. The majority of people above 60 years have some form of age-related hearing loss, also known as presbycusis. However, the biological mechanisms of presbycusis are complex and not yet fully delineated. In the present article, we highlight ion channels and transport proteins, which are integral for the proper functioning of the auditory system, facilitating the diffusion of various ions across auditory structures for signal transduction and processing. Like most other physiological systems, hearing abilities decline with age, hence, it is imperative to fully understand inner ear aging changes, so ion channel functions should be further investigated in the aging cochlea. In this review article, we discuss key various ion channels in the auditory system and how their functions change with age. Understanding the roles of ion channels in auditory processing could enhance the development of potential biotherapies for age-related hearing loss.

scholarly journals Oxidative Stresses and Mitochondrial Dysfunction in Age-Related Hearing Loss

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Chisato Fujimoto ◽  
Tatsuya Yamasoba
Keyword(s):  
Hearing Loss ◽  
Mitochondrial Dysfunction ◽  
Stria Vascularis ◽  
Spiral Ganglion ◽  
Organ Of Corti ◽  
The Elderly ◽  
Laboratory Animals ◽  
Age Related ◽  
Ganglion Neurons ◽  
Age Related Hearing Loss

Age-related hearing loss (ARHL), the progressive loss of hearing associated with aging, is the most common sensory disorder in the elderly population. The pathology of ARHL includes the hair cells of the organ of Corti, stria vascularis, and afferent spiral ganglion neurons as well as the central auditory pathways. Many studies have suggested that the accumulation of mitochondrial DNA damage, the production of reactive oxygen species, and decreased antioxidant function are associated with subsequent cochlear senescence in response to aging stress. Mitochondria play a crucial role in the induction of intrinsic apoptosis in cochlear cells. ARHL can be prevented in laboratory animals by certain interventions, such as caloric restriction and supplementation with antioxidants. In this review, we will focus on previous research concerning the role of the oxidative stress and mitochondrial dysfunction in the pathology of ARHL in both animal models and humans and introduce concepts that have recently emerged regarding the mechanisms of the development of ARHL.

scholarly journals Biased Auditory Nerve Central Synaptopathy Exacerbates Age-related Hearing Loss

2020 ◽  
Author(s):  
Meijian Wang ◽  
Chuangeng Zhang ◽  
Shengyin Lin ◽  
Yong Wang ◽  
Benjamin J. Seicol ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Auditory Processing ◽  
Auditory Nerve ◽  
Spiral Ganglion ◽  
Central Auditory Processing ◽  
Endbulb Of Held ◽  
Age Related ◽  
Central Synapses ◽  
Ganglion Neurons ◽  
Age Related Hearing Loss

SUMMARYSound information is transmitted from the cochlea to the brain by different subtypes of spiral ganglion neurons (SGN), which show varying degrees of vulnerbility under pathological conditions. It remains unclear how information from these SGNs reassemble among target neurons in the cochlear nucleus (CN) at the auditory nerve (AN) central synapses, and how different synapses change during hearing loss. Combining immunohistochemistry with electrophysiology, we investigated the giant endbulb of Held synapses and their postsynaptic bushy neurons in mice under normal hearing and age-related hearing loss (ARHL). We found that calretinin-expressing and non-calretinin-expressing endbulbs converge at continuously different ratios onto bushy neurons with varying physiological properties. Endbulbs degenerate during ARHL, and the degeneration is more severe in non-calretinin-expressing synapses, which correlates with a gradual decrease in neuronal subpopulation predominantly innervated by these inputs. Our findings suggest that biased AN central synaptopathy and shifted CN neuronal composition underlie reduced auditory input and altered central auditory processing during ARHL.

scholarly journals Age-Related Hearing Loss in Mn-SOD Heterozygous Knockout Mice

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Makoto Kinoshita ◽  
Takashi Sakamoto ◽  
Akinori Kashio ◽  
Takahiko Shimizu ◽  
Tatsuya Yamasoba
Keyword(s):  
Hearing Loss ◽  
Manganese Superoxide Dismutase ◽  
Stria Vascularis ◽  
Spiral Ganglion ◽  
Cell Loss ◽  
Auditory Brainstem ◽  
Spiral Ganglion Cell ◽  
Age Related ◽  
Brainstem Response ◽  
Age Related Hearing Loss

Age-related hearing loss (AHL) reduces the quality of life for many elderly individuals. Manganese superoxide dismutase (Mn-SOD), one of the antioxidant enzymes acting within the mitochondria, plays a crucial role in scavenging reactive oxygen species (ROS). To determine whether reduction in Mn-SOD accelerates AHL, we evaluated auditory function in Mn-SOD heterozygous knockout (HET) mice and their littermate wild-type (WT) C57BL/6 mice by means of auditory brainstem response (ABR). Mean ABR thresholds were significantly increased at 16 months when compared to those at 4 months in both WT and HET mice, but they did not significantly differ between them at either age. The extent of hair cell loss, spiral ganglion cell density, and thickness of the stria vascularis also did not differ between WT and HET mice at either age. At 16 months, immunoreactivity of 8-hydroxydeoxyguanosine was significantly greater in the SGC and SV in HET mice compared to WT mice, but that of 4-hydroxynonenal did not differ between them. These findings suggest that, although decrease of Mn-SOD by half may increase oxidative stress in the cochlea to some extent, it may not be sufficient to accelerate age-related cochlear damage under physiological aging process.

scholarly journals Auditory Processing Performance of the Middle-Aged and Elderly: Auditory or Cognitive Decline?

2018 ◽  
Vol 29 (01) ◽  
pp. 005-014 ◽  
Author(s):  
Cristina F. B. Murphy ◽  
Camila M. Rabelo ◽  
Marcela L. Silagi ◽  
Leticia L. Mansur ◽  
Doris E. Bamiou ◽  
...  
Keyword(s):  
Working Memory ◽  
Hearing Loss ◽  
Cognitive Decline ◽  
Auditory Processing ◽  
The Elderly ◽  
Regression Analyses ◽  
Frequency Pattern ◽  
Speech In Noise ◽  
Age Related ◽  
Age Related Hearing Loss

AbstractDespite the well-established relationship between aging and auditory processing decline, identifying the extent to which age effect is the main factor on auditory processing performance remains a great challenge due to the co-occurrence of age-related hearing loss and age-related cognitive decline as potential confounding factors.To investigate the effects of age-related hearing loss and working memory on the clinical evaluation of auditory processing of middle-aged and elderly.Cross-sectional study.A total of 77 adults between 50 and 70 yr of age were invited to participate in the study.The participants were recruited from a larger study that focused on the assessment and management of sensory and cognitive skills in elderly participants. Only participants with normal hearing or mild-to-moderate age-related hearing loss, with no evidence of cognitive, psychological, or neurological conditions were included. Speech-in-noise, dichotic digit, and frequency pattern tests were conducted as well as a working memory test. The hearing loss effect was investigated using an audibility index, calculated from the audiometric threshold. The performance on the digit span test was used to investigate working memory effects. Both hearing loss and working memory effects were investigated via correlation and regression analyses, partialling out age effects. The significance level was set at p < 0.05.The results demonstrated that, while hearing loss was associated to the speech-in-noise performance, working memory was associated to the frequency pattern and dichotic digit performances. Regression analyses confirmed the relative contribution of hearing loss to the variance in speech-in-noise and working memory test to the variance in frequency pattern and dichotic digit test performance.The performance decline of the elderly in auditory processing tests may be partially attributable to the working memory performance and, consequently, to the cognitive decline exhibited by this population. Mild-to-moderate hearing loss seems to affect performance on specific auditory processing tasks, such as speech in noise, reinforcing the idea that auditory processing disorder in the elderly might also be associated to auditory peripheral deficits.

scholarly journals Deafness and Cochlear Fibrocyte Alterations in Mice Deficient for the Inner Ear Protein Otospiralin

2005 ◽  
Vol 25 (2) ◽  
pp. 847-853 ◽  
Author(s):  
Benjamin Delprat ◽  
Jérôme Ruel ◽  
Matthieu J. Guitton ◽  
Ghyslaine Hamard ◽  
Marc Lenoir ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Hair Cells ◽  
Unknown Function ◽  
Stria Vascularis ◽  
Type Ii ◽  
Auditory Function ◽  
Age Related ◽  
Cochlear Physiology ◽  
Auditory Organ ◽  
Age Related Hearing Loss

ABSTRACT In the cochlea, the mammalian auditory organ, fibrocytes of the mesenchymal nonsensory regions play important roles in cochlear physiology, including the maintenance of ionic and hydric components in the endolymph. Occurrence of human deafness in fibrocyte alterations underlines their critical roles in auditory function. We recently described a novel gene, Otos, which encodes otospiralin, a small protein of unknown function that is produced by the fibrocytes of the cochlea and vestibule. We now have generated mice with deletion of Otos and found that they show moderate deafness, with no frequency predominance. Histopathology revealed a degeneration of type II and IV fibrocytes, while hair cells and stria vascularis appeared normal. Together, these findings suggest that impairment of fibrocytes caused by the loss in otospiralin leads to abnormal cochlear physiology and auditory function. This moderate dysfunction may predispose to age-related hearing loss.

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