Treatment Of Age-related Hearing Loss Research Articles

Barriers to Hearing Health Care for Aging Adults: Reframing the Conversation.

Untreated age-related hearing loss (ARHL) is associated with poor health and social outcomes. Treating hearing loss can mitigate these serious issues. Although there are documented barriers to care, we can look at these barriers and potential solutions differently if we view ARHL as a gradual onset, chronic condition. This provides a framework from which to solve problems in line with how other chronic health conditions experienced by aging adults are approached. With this lens, it becomes evident that early identification and treatment of ARHL can be supported by universal senior hearing screening, appropriate Medicare coverage for devices and services, and direct access to audiological care as well as avenues for self-care are necessary ingredients to change the hearing health care landscape.

Excessive processing and acetylation of OPA1 aggravate age-related hearing loss via the dysregulation of mitochondrial dynamics.

The pathogenesis of age-related hearing loss (ARHL) remains unclear. OPA1 is the sole fusion protein currently known to be situated in the inner mitochondrial membrane, which is pivotal for maintaining normal mitochondrial function. While it has already been demonstrated that mutations in OPA1 may lead to hereditary deafness, its involvement in the occurrence and development of ARHL has not been previously explored. In our study, we constructed D-gal-induced senescent HEI-OC1 cells and the cochlea of C57BL/6J mice with a mutated SUMOylation site of SIRT3 using CRISPR/Cas9 technology. We found enhanced L-OPA1 processing mediated by activated OMA1, and increased OPA1 acetylation resulting from reductions in SIRT3 levels in senescent HEI-OC1 cells. Consequently, the fusion function of OPA1 was inhibited, leading to mitochondrial fission and pyroptosis in hair cells, ultimately exacerbating the aging process of hair cells. Our results suggest that the dysregulation of mitochondrial dynamics in cochlear hair cells in aged mice can be ameliorated by activating the SIRT3/OPA1 signaling. This has the potential to alleviate the senescence of cochlear hair cells and reduce hearing loss in mice. Our study highlights the significant roles played by the quantities of long and short chains and the acetylation activity of OPA1 in the occurrence and development of ARHL. This finding offers new perspectives and potential targets for the prevention and treatment of ARHL.

Col1a1 mediates the focal adhesion pathway affecting hearing in miR-29a mouse model by RNA-seq analysis

Age-related hearing loss (ARHL) is a common neurodegenerative disease. Its molecular mechanisms have not been fully elucidated. In the present study, we obtained differential mRNA expression in the cochlea of 2-month-old miR-29a+/+ mice and miR-29a−/− mice by RNA-seq. Gene ontology (GO) analysis was used to identify molecular functions associated with hearing in miR-29a−/− mice, including being actin binding (GO: 0003779) and immune processes. We focused on the intersection of differential genes, miR-29a target genes and the sensory perception of sound (GO:0007605) genes, with six mRNA at this intersection, and we selected Col1a1 as our target gene. We validated Col1a1 as the direct target of miR-29a by molecular and cellular experiments. Total 6 pathways involved in Col1a1 were identified by through Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. We selected the focal adhesion pathway as our target pathway based. Their expression levels in miR-29a−/− mice were verified by qRT-PCR and Western blot. Compared with miR-29a+/+ mice, the expression levels of Col1a1, Itga4, Itga2, Itgb3, Itgb7, Pik3r3 and Ptk2 were different in miR-29a−/− mice. Immunofluorescence was used to locate genes in the cochlea. Col1a1, Itga4 and Itgb3 were differentially expressed in the basilar membranes and stria vascularis and spiral ganglion neurons compared to miR-29a+/+ mice. Pik3r3 and Ptk2 were differentially expressed in the basilar membranes and stria vascularis, but not at the s spiral ganglion neurons compared to miR-29a+/+ mice.Our results show that when miR-29a is knocked out, the Col1a1 mediates the focal adhesion pathway may affect the hearing of miR-29a−/− mice. These findings may provide a new direction for effective treatment of age-related hearing loss.

PIN1 protects auditory hair cells from senescence via autophagy.

Age-related hearing loss is an increasing sensorineural hearing loss. But the pathogenesis of ARHL has not been clarified. Herein, we studied the role and significance of PIN1 in regulating autophagy activity in senescence HEI-OC1cells and HCs. C57BL/6 mice and HEI-OC1 cells were contained in our research. Transfection of plasmids and juglone were used to upregulate or inhibit the PIN 1 expression. Immunofluorescence and Western blot were used to detect the expression of PIN1, LC3, p62, p21 and p16 protein levels in the hair cells of C57BL/6 mice cochleae and HEI-OC1 cells. Senescence-associated β-galactosidase (SA-β-gal) staining was used to investigate the senescent level.The results of this study showed that the level of autophagy increased in the senescent auditory hair cells. When inhibited the autophagy level with 3-MA, the senescent HEI-OC1 cells were alleviated. The autophagy activity in senescent HEI-OC1 cells also could be reduced by overexpressing PIN1 protein. On the contrary, inhibiting PIN1 could increase the autophagy level of senescent cells and cochlear hair cells. PIN1 might regulate autophagy activity to induce the senescent of HEI-OC1cells and HCs, which will provide a theoretical support for the prevention and treatment of age-related hearing loss.

Two Loci Contribute to Age-Related Hearing Loss Resistance in the Japanese Wild-Derived Inbred MSM/Ms Mice

An MSM/Ms strain was established using Japanese wild mice, which exhibit resistance to several phenotypes associated with aging, such as obesity, inflammation, and tumorigenesis, compared to common inbred mouse strains. MSM/Ms strain is resistant to age-related hearing loss, and their auditory abilities are sustained for long durations. The age-related hearing loss 3 (ahl3) locus contributes to age-related hearing in MSM/Ms strain. We generated ahl3 congenic strains by transferring a genomic region on chromosome 17 from MSM/Ms mice into C57BL/6J mice. Although C57BL/6J mice develop age-related hearing loss because of the ahl allele of the cadherin 23 gene, the development of middle- to high-frequency hearing loss was significantly delayed in an ahl3 congenic strain. Moreover, the novel age-related hearing loss 10 (ahl10) locus associated with age-related hearing resistance in MSM/Ms strain was mapped to chromosome 12. Although the resistance effects in ahl10 congenic strain were slightly weaker than those in ahl3 congenic strain, slow progression of age-related hearing loss was confirmed in ahl10 congenic strain despite harboring the ahl allele of cadherin 23. These results suggest that causative genes and polymorphisms of the ahl3 and ahl10 loci are important targets for the prevention and treatment of age-related hearing loss.

Network pharmacology and experimental evidence reveal the protective mechanism of Yi-Qi Cong-Ming decoction on age-related hearing loss

Context Yi-Qi Cong-Ming (YQCM) decoction has been widely used to prevent age-related hearing loss (ARHL), the most prevalent neurodegenerative disease in the elderly. Objective To explore the mechanism of YQCM decoction in the treatment of ARHL. Materials and methods The chemical constituents of YQCM were screened from the Traditional Chinese Medicine Systems Pharmacology Database. Potential targets of YQCM against ARHL were predicted by DrugBank, GeneCards, and OMIM database. Protein-protein network and enrichment analysis were used for exploring possible molecular mechanisms. Molecular docking and an in vitro model of ARHL by exposing auditory cells with 100 μM H2O2 for 3 h were applied. Cell viability and mitochondrial membrane potential (ΔΨM) were detected by CCK-8 and high-content analysis. γH2AX and cleaved caspase-3 were detected by Western blot. Results The main compounds have good affinities with hub targets, especially AKT1, PTGS2, and CASP3. GO and KEGG analysis showed that the main biological process and key targets were related to negative regulation of the apoptotic process. H2O2 treatment could reduce the cell viability by 68% and impaired ΔΨM, while 90 μg/mL YQCM pre-treatment could restore the cell viability by 97.45% and increase ΔΨM (2-fold higher). YQCM pre-treatment also reduced γH2AX and cleaved caspase-3 protein levels. Conclusions Our study suggested that YQCM prevents ARHL by modulating the apoptosis process in auditory hair cells. Moreover, this study proved that bioinformatics analysis combined with molecular docking and cell model is a promising method to explore other possible pharmacological interventions of ARHL.

Prediction of the Molecular Mechanisms Underlying Erlong Zuoci Treatment of Age-Related Hearing Loss via Network Pharmacology-Based Analyses Combined with Experimental Validation.

Background: The traditional Chinese medicine formula ErLong ZuoCi (ELZC) has been extensively used to treat age-related hearing loss (ARHL) in clinical practice in China for centuries. However, the underlying molecular mechanisms are still poorly understood. Objective: Combine network pharmacology with experimental validation to explore the potential molecular mechanisms underlying ELZC with a systematic viewpoint. Methods: The chemical components of ELZC were collected from the Traditional Chinese Medicine System Pharmacology database, and their possible target proteins were predicted using the SwissTargetPrediction database. The putative ARHL-related target proteins were identified from the database: GeneCards and OMIM. We constructed the drug-target network as well as drug-disease specific protein-protein interaction networks and performed clustering and topological property analyses. Functional annotation and signaling pathways were performed by gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis. Finally, in vitro experiments were also performed to validate ELZC’s key target proteins and treatment effects on ARHL. Results: In total, 63 chemical compounds from ELZC and 365 putative ARHL-related targets were identified, and 1860 ARHL-related targets were collected from the OMIM and GeneCards. A total of 145 shared targets of ELZC and ARHL were acquired by Venn diagram analysis. Functional enrichment analysis suggested that ELZC might exert its pharmacological effects in multiple biological processes, such as cell proliferation, apoptosis, inflammatory response, and synaptic connections, and the potential targets might be associated with AKT, ERK, and STAT3, as well as other proteins. In vitro experiments revealed that ELZC pretreatment could decrease senescence-associated β-galactosidase activity in hydrogen peroxide-induced auditory hair cells, eliminate DNA damage, and reduce cellular senescence protein p21 and p53. Finally, Western blot analysis confirmed that ELZC could upregulate the predicted target ERK phosphorylation. Conclusion: We provide an integrative network pharmacology approach, in combination with in vitro experiments to explore the underlying molecular mechanisms governing ELZC treatment of ARHL. The protective effects of ELZC against ARHL were predicted to be associated with cellular senescence, inflammatory response, and synaptic connections which might be linked to various pathways such as JNK/STAT3 and ERK cascade signaling pathways. As a prosperous possibility, our experimental data suggest phosphorylation ERK is essential for ELZC to prevent degeneration of cochlear.

Treatment of Age-Related Hearing Loss Alters Audiovisual Integration and Resting-State Functional Connectivity: A Randomized Controlled Pilot Trial.

Untreated age-related hearing loss increases audiovisual integration and impacts resting state functional brain connectivity. Further, there is a relation between crossmodal plasticity and audiovisual integration strength in cochlear implant patients. However, it is currently unclear whether amplification of the auditory input by hearing aids influences audiovisual integration and resting state functional brain connectivity. We conducted a randomized controlled pilot study to investigate how the McGurk illusion, a common measure for audiovisual integration, and resting state functional brain connectivity of the auditory cortex are altered by six-month hearing aid use. Thirty-two older participants with slight-to-moderate, symmetric, age-related hearing loss were allocated to a treatment or waiting control group and measured one week before and six months after hearing aid fitting with functional magnetic resonance imaging. Our results showed a statistical trend for an increased McGurk illusion after six months of hearing aid use. We further demonstrated that an increase in McGurk susceptibility is related to a decreased hearing aid benefit for auditory speech intelligibility in noise. No significant interaction between group and time point was obtained in the whole-brain resting state analysis. However, a region of interest (ROI)-to-ROI analysis indicated that hearing aid use of six months was associated with a decrease in resting state functional connectivity between the auditory cortex and the fusiform gyrus and that this decrease was related to an increase of perceived McGurk illusions. Our study, therefore, suggests that even short-term hearing aid use alters audiovisual integration and functional brain connectivity between auditory and visual cortices.

Characteristics of hearing loss in elderly outpatients over 60 years of age: an annual cross-sectional study

Background The prevention and treatment of presbycusis becomes a serious health challenge and socio-economic problem. Objectives We performed a cross-sectional analysis of the audiometry results of all elderly patients who visited our department throughout the year of 2018. Material and methods A total of 5520 people aged 60 and over were included and divided into three groups: young-old group (60–74 years old), old-old group (75–89 years old), and longevous group (over 90 years old). Pure-tone audiometry results of all patients were analyzed. Results Among the 5520 patients, there were 4445 cases in the young-old group, 1029 cases in the old-old group, and 46 cases in the longevous group, accounting for 80.53, 18.64, and 0.83%, respectively. In the young-old group, normal hearing and mild-moderate hearing loss were the most common, while moderate and severe hearing loss were more common among the old-old group and the longevous group. The hearing curve showed typical age-related hearing loss with a drop at high frequencies. Conclusions With an increase in age, patients tend to suffer from more serious hearing disorders. Presbycusis was associated with specific frequency and age characteristics. Understanding these characteristics is of great significance for the prevention and treatment of age-related hearing loss.

Safety and Efficacy for the Combination of Alpha Lipoic Acid, Gingko Biloba, Vitamin C, Zinc, Magnesium, Vitamin B6, Methylcobalamin, Vitamin E and Chromium Picolinate for the Medical Management of Age Related Hearing Loss: Post Marketing Surveillance Study

Introduction: Age related hearing loss is defined as a bilateral, progressive, symmetrical age-related sensorineural hearing loss, which is most pronounced at the higher frequencies. It is considered that oxidative stress has a central role in the pathology of age-related hearing loss so, this study was conducted to test the efficacy and safety for the combination of antioxidants for the treatment of age-related hearing loss. Methodology: This was a multi-centric study conducted at 11 clinical trial sites. Out of total 176 enrolled, 160 trial subjects completed the study. For efficacy assessment, 2 parameters were used including hearing related quality of life score and score obtained from hearing impairment questionnaire on day 0 (visit 1), 45 (visit 2) and 90 (visit 3). Results: At visit 1, the mean hearing related quality of life score was 4.437 increased to 5.725 at visit 2 and further increased to 6.906 at visit 3. At visit 2 and 3, the increase in hearing related quality of life score was 29.028% and 55.645% respectively as compared to baseline. The score obtained from hearing impairment questionnaire was 25.581 at visit 1 reduced to 16.200 and further reduced to 9.943 at visit 3. Conclusion: The combination of Alpha lipoic acid, Gingko biloba, Vitamin C, Zinc, Magnesium, Vitamin B6, Methyl cobalamin, Vitamin E and Chromium Picolinate can be used for the medical management of age related hearing loss.

The effect of the duration of treatment with antioxidants on age-related hearing loss

Background and aims The effect of antioxidants depends on several factors, including the type, dose, timing, and treatment duration. Several studies have demonstrated that antioxidants can prevent age-related hearing loss (ARHL), however, a few studies have focussed on the role of factors influencing the effects of antioxidant therapy. This study aimed to investigate the effect of duration of treatment on ARHL using an herbal antioxidant, silymarin, in a D-galactose-induced ageing rat model. Method 40 three-months-old Wistar rats were divided into four groups: a short-term silymarin-treated group that received 500 mg/kg/day D-galactose (8 consecutive weeks) +200 mg/kg/day silymarin (4 consecutive weeks), long-term silymarin-treated group received 500 mg/kg/day D-galactose (8 consecutive weeks)+ 200 mg/kg/day silymarin (8 consecutive weeks), placebo group received 500 mg/kg/day D-galactose + placebo (propylene glycol; 8 consecutive weeks), and control group received normal saline (8 consecutive weeks). Auditory Brainstem Response (ABR) was measured at 4, 8, 12, and 16 kHz frequencies before and after the intervention. Results No significant differences were found in ABR absolute and inter-peak latencies between groups. In contrast, there was a significant difference in ABR threshold shift between the placebo and the long-term silymarin-treated groups at 4 and 16 kHz frequencies (p ≤ .05), but without a similar difference through comparison with the short-term silymarin-treated group (p > .05). Additionally, a significant decrease in ABR amplitude of PI and PII was observed in the placebo group at 4 kHz frequency compared to the long-term silymarin-treated group (p ≤ .05), but not to the short-term silymarin-treated group (p > .05). Conclusion The present study results indicate that the duration of treatment with antioxidants influences the successful prevention and treatment of ARHL. Consequently, this factor must be considered in the antioxidant therapy of ARHL. However, further studies are required to fully evaluate the effects of optimal treatment duration with antioxidants on ARHL along with the other influencing factors.

FOXG1 promotes aging inner ear hair cell survival through activation of the autophagy pathway

ABSTRACT Presbycusis is the cumulative effect of aging on hearing. Recent studies have shown that common mitochondrial gene deletions are closely related to deafness caused by degenerative changes in the auditory system, and some of these nuclear factors are proposed to participate in the regulation of mitochondrial function. However, the detailed mechanisms involved in age-related degeneration of the auditory systems have not yet been fully elucidated. In this study, we found that FOXG1 plays an important role in the auditory degeneration process through regulation of macroautophagy/autophagy. Inhibition of FOXG1 decreased the autophagy activity and led to the accumulation of reactive oxygen species and subsequent apoptosis of cochlear hair cells. Recent clinical studies have found that aspirin plays important roles in the prevention and treatment of various diseases by regulating autophagy and mitochondria function. In this study, we found that aspirin increased the expression of FOXG1, which further activated autophagy and reduced the production of reactive oxygen species and inhibited apoptosis, and thus promoted the survival of mimetic aging HCs and HC-like OC-1 cells. This study demonstrates the regulatory function of the FOXG1 transcription factor through the autophagy pathway during hair cell degeneration in presbycusis, and it provides a new molecular approach for the treatment of age-related hearing loss. Abbreviations: AHL: age-related hearing loss; baf: bafilomycin A1; CD: common deletion; D-gal: D-galactose; GO: glucose oxidase; HC: hair cells; mtDNA: mitochondrial DNA; RAP: rapamycin; ROS: reactive oxygen species; TMRE: tetramethylrhodamine, ethyl ester

Ninjinyoeito Has a Protective Effect on the Auditory Nerve and Suppresses the Progression of Age-Related Hearing Loss in Mice.

Currently, there are limited reports available regarding the treatment and prevention of progressive age-related hearing loss. This is because age-related hearing loss is not a critical disease with direct fatalities and has several well-established countermeasures such as hearing aids and cochlear implants. This study evaluated the efficacy of Ninjinyoeito (NYT) in the treatment of age-related hearing loss. C57BL/6J mice were divided into three groups: baseline group, untreated group, and NYT-treated group, with the latter receiving NYT treatment for 2 months. The mice were fed with NYT extract mixed with 4% mouse normal chow. Hearing loss was confirmed by a reduction in intact cell density of the auditory nerve from the age of 5–7 months. The suppression of hearing loss with aging and decrease in the intact cell density of the auditory nerve were significant in mice fed with NYT for 2 months. NYT has been reported to improve blood flow and enhance mitochondrial activity and may exert its protective effects on spiral neurons through these mechanisms. There was no decrease in the size of the stria vascularis from the age of 5–7 months in C57BL/6J mice. The present model failed to reveal the effect of NYT on atrophy of the stria vascularis of the cochlear duct. In conclusion, NYT appears to have a protective effect on the auditory nerve and suppress the progression of age-related hearing loss by reducing age-related auditory nerve degeneration.

Auditory Dysfunction in Aging: Prospects for Stem Cell Therapy

Age-related hearing loss is the most common cause of adult auditory dysfunction. It is characterized by bilateral, progressive auditory deterioration associated with the aging process. There currently are limited options for the treatment as hearing aids or cochlear implants. To establish novel strategies for the treatment of this entity, it is crucial to elucidate the mechanisms of age-related hearing loss. Its etiology is believed to be multifactorial including both intrinsic and extrinsic factors. Oxidative damage, as seen in other aging organs systems, may play an essential role in the pathogenesis of the age-related hearing loss. Studies on animal models and human temporal bones have indicated a close relationship between degeneration of the cochlear lateral wall and hearing loss. Additional therapies that may prove beneficial in the treatment of age-related hearing loss include stem cell therapy, which we intend to review in this manuscript.

Age-Related Hearing Loss and Its Association with Depression in Later Life

To evaluate the association between age-related hearing loss (ARHL) and depressive symptoms in older adults over time. Data from the Health Aging and Body Composition study (N = 3075, aged 70-79 at baseline) were used previously to conduct a longitudinal latent class analysis to evaluate depression trajectories (Center for Epidemiologic Studies Depression [CES-D] Scale) over 10 years. Restricting to the subset of subjects who had hearing information available (N = 1204), self-reported hearing categories were evaluated over the same period. Association between depression classes and hearing categories were assessed via multinomial logistic regression analyses. Correlation analyses and two-sample t-tests were used to assess cross-sectional associations between depression status and audiometric hearing measures. Low-probability (N = 644), increasing-probability (N = 385), and high-probability (N = 175) trajectories of depressive symptoms were identified for the 10-year period. Impaired/Worsening (N = 182) and Healthy/Improving (N = 1,022) hearing categories were defined using self-reports. With the low-probability depression trajectory as the reference group, subjects reporting Impaired/Worsening hearing had 1.63 times increased odds of having an increasing- (p = 0.0088, 95% CI [1.13, 2.34]) and 1.85 times increased odds of having a high-probability depression trajectory (p = 0.0102, 95% CI [1.16, 2.96]). At Year 5, individuals with depressive symptoms (10CES-D ≥ 10) had impaired hearing ability measured by audiometric threshold for low-frequency (Adjusted mean difference = 2.29 dBHL, p = 0.0005) and mid-frequency sounds (Adjusted mean difference = 2.28 dBHL,p = 0.0049) compared to those with 10CES-D < 10. ARHL was associated with increased depressive symptoms in older adults. Future studies should investigate whether treatment of ARHL may be an effective prevention and/or therapeutic strategy for depressive symptoms.

MiR-29b overexpression induces cochlear hair cell apoptosis through the regulation of SIRT1/PGC-1α signaling: Implications for age-related hearing loss

It has been reported that the degeneration of cochlear hair cells is the typical cause of presbycusis (or age-related hearing loss). However, the molecular mechanisms that mediate cochlear hair cell apoptosis are not yet fully understood and there is no effective treatment for this disorder. MicroRNAs (miRNAs or miRs) have been increasingly shown to be associated with age-related diseases and are emerging as promising therapeutic targets. In this study, we investigated whether miR-29b is involved in the degeneration of cochlear hair cells. To examine our hypothesis, nuclear staining and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) were used to quantify the hair cell counts. RT-qPCR and western blot analysis were used to examine miR-29b/sirtuin 1 (SIRT1)/proliferator-activated receptor-gamma coactivator 1α (PGC-1α) signaling in cochlear hair cells. We found that there was a significant degeneration of cochlear hair cells and a higher expression of miR-29b in aged C57BL/6 mice compared with young mice. There was also an age-related decrease in the expression of SIRT1 and PGC-1α. In the inner ear cell line, HEI-OC1, miR-29b overexpression (by transfection with miR-29b mimic) inhibited SIRT1 and PGC-1α expression, leading to an increase in mitochondrial dysfunction and apoptosis. Moreover, the inhibition of miR-29b (by transfection with miR-29b inhibitor) increased SIRT1 and PGC-1α expression, while it decreased apoptosis. Taken together, our findings support a link between age-related cochlear hair cell apoptosis and miR-29b/SIRT1/PGC-1α signaling, which may present an attractive pharmacological target for the development of novel drugs for the treatment of age-related hearing loss.

NAD(+) Metabolism in Age-Related Hearing Loss.

Age-related hearing loss (ARHL), a degenerative disorder characterized by age-dependent progressive increase in the threshold of auditory sensitivity, affects 40% of people over the age of 65, and it has emerged as an important social and public health problem. Various factors, including genetic and environmental components, are known to affect both the onset and severity of ARHL. In particular, age-dependent changes in cellular oxidative stress and inflammatory responses accompanied by altered cellular signaling and gene expression progressively affect the function of the auditory system and eventually lead to hearing impairment. Recent findings suggest that a disturbance of intracellular NAD(+) levels is clinically related to the progression of age-associated disorders. Therefore, maintenance of optimal intracellular NAD(+) levels may be a critical factor for cellular senescence, and thus, understanding its molecular signaling pathways would provide critical insights into the prevention and treatment of ARHL as well as other age-related diseases. In this review, we describe the role of NAD(+) metabolism in aging and age-related diseases, including ARHL, and discuss a potential strategy for prevention or treatment of ARHL with a particular interest in NAD(+)-dependent cellular pathways.

Comprehensive management of presbycusis: central and peripheral.

The prevailing otolaryngologic approach to treatment of age-related hearing loss (ARHL), presbycusis, emphasizes compensation of peripheral functional deficits (ie, hearing aids and cochlear implants). This approach does not address adequately the needs of the geriatric population, 1 in 5 of whom is expected to consist of the "old old" in the coming decades. Aging affects both the peripheral and central auditory systems, and disorders of executive function become more prevalent with advancing age. Growing evidence supports an association between age-related hearing loss and cognitive decline. Thus, to facilitate optimal functional capacity in our geriatric patients, a more comprehensive management strategy of ARHL is needed. Diagnostic evaluation should go beyond standard audiometric testing and include measures of central auditory function, including dichotic tasks and speech-in-noise testing. Treatment should include not only appropriate means of peripheral compensation but also auditory rehabilitative training and counseling.

Treatment of Age-Related Hearing Loss in Dogs with the Vibrant Soundbridge Middle Ear Implant: Short-Term Results in 3 Dogs

Age-related hearing loss (ARHL), or presbycusis, is the most common form of acquired hearing loss in dogs. Middle ear implants have been used successfully in people with ARHL who cannot benefit from conventional hearing aids. Audibility improves in dogs with ARHL after implantation of the Vibrant Soundbridge (VSB) middle ear implant. Three Beagle dogs with ARHL, mean age 11.1 years. The dogs were assessed pre- and postoperatively by brainstem-evoked response audiometry (BERA), otoscopy, and computed tomography scans of the ears. A VSB middle ear implant was implanted unilaterally. Three months later the functionality of the implants was assessed by auditory steady-state responses (ASSRs), after which the dogs were euthanized for histopathological examination. The VSB was implanted successfully in all dogs. Recovery from surgery was uneventful, except for transient facial nerve paralysis in 2 dogs. ASSRs showed that hearing improved after activation of the implants with a mean of 20.7, 13, and 16.3 dB at 1, 2, and 4 kHz, respectively. The implantation procedure did not affect residual hearing (with inactive implants) as measured by BERA. Implantation of the VSB resulted in lower ASSR thresholds, but only at the higher gain settings of the audioprocessor. As in humans, a more powerful audioprocessor is required to treat sensorineural hearing loss exceeding 20 dB in dogs. A substantial improvement in patient-owner communication will have to be demonstrated in future studies before the procedure can be recommended in clinical practice.