Pub Date : 2025-01-16DOI: 10.1016/j.heares.2025.109183
Douglas S. Brungart , Gregory M. Ellis , Alyssa Davidson , Hector Galloza , Benjamin Sheffield , Jaclyn Schurman
Hearing loss has historically been mainly associated with elevated pure-tone thresholds. However, in recent years, there has been increased interest in addressing the hearing difficulties reported by individuals with normal hearing thresholds. In this study, we measured hearing thresholds, noise history, temporary threshold shift history, and hearing difficulty for a sample of 10,492 Service Members. Our data reveal that overall hearing difficulties increase systematically as a function of hearing threshold within the range that is conventionally considered to be ”normal” hearing. Noise exposure history is associated with increasing hearing difficulty at all thresholds, particularly individuals with a history of noticeable changes in their hearing after noise exposure. These results challenge some fundamental assumptions of current hearing conservation programs and suggest that variations in post-noise hearing symptoms may reflect differences in individual susceptibility to permanent damage from noise exposure.
{"title":"Not-so-normal hearing: Temporary hearing changes lead to chronic difficulties for listeners with ”normal” audiometric thresholds","authors":"Douglas S. Brungart , Gregory M. Ellis , Alyssa Davidson , Hector Galloza , Benjamin Sheffield , Jaclyn Schurman","doi":"10.1016/j.heares.2025.109183","DOIUrl":"10.1016/j.heares.2025.109183","url":null,"abstract":"<div><div>Hearing loss has historically been mainly associated with elevated pure-tone thresholds. However, in recent years, there has been increased interest in addressing the hearing difficulties reported by individuals with normal hearing thresholds. In this study, we measured hearing thresholds, noise history, temporary threshold shift history, and hearing difficulty for a sample of 10,492 Service Members. Our data reveal that overall hearing difficulties increase systematically as a function of hearing threshold within the range that is conventionally considered to be ”normal” hearing. Noise exposure history is associated with increasing hearing difficulty at all thresholds, particularly individuals with a history of noticeable changes in their hearing after noise exposure. These results challenge some fundamental assumptions of current hearing conservation programs and suggest that variations in post-noise hearing symptoms may reflect differences in individual susceptibility to permanent damage from noise exposure.</div></div>","PeriodicalId":12881,"journal":{"name":"Hearing Research","volume":"458 ","pages":"Article 109183"},"PeriodicalIF":2.5,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143046441","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-15DOI: 10.1016/j.heares.2025.109197
Suwijak Deoisres, Ghadah S. Aljarboa, Steven L. Bell, David M. Simpson
The cortical tracking of the acoustic envelope is a phenomenon where the brain's electrical activity, as recorded by electroencephalography (EEG) signals, fluctuates in accordance with changes in stimulus intensity (the acoustic envelope of the stimulus). Understanding speech in a noisy background is a key challenge for people with hearing impairments. Speech stimuli are therefore more ecologically valid than clicks, tone pips, or speech tokens (e.g., syllables) for assessing hearing. However, it remains unclear whether EEG responses to speech provide an advantage in predicting speech intelligibility. This study aimed to assess the ability of cortical responses to speech and speech-related sounds to predict behavioural speech-in-noise performance in listeners with normal hearing when they are not attending to the stimuli.
Twenty native English-speaking adults with normal hearing (aged 18 to 40 years) participated in a speech reception task, listening to English Matrix sentences presented at signal-to-noise ratios (SNRs) of -15, -10, -5, 0, and ∞ (no background noise) dB, and then identifying the words they heard in the sentences. In the EEG experiment, the participants then listened to continuous speech, broadband noise modulated by the envelope of speech, and repeating short /da/ stimuli presented at the same SNR levels as in the Matrix test. For the latter, Auditory Late Response (ALR) was estimated from the EEG, and for the former, the strength of the envelope-tracking responses was calculated.
Cortical responses to all stimuli showed monotonic relationships with the signal-to-noise ratio at the group level and in most individuals, although there was considerable variability. EEG analysis in the delta band showed no significant difference in the number of participants with predicted speech reception thresholds (SRTs) within an error margin of 7 dB—the level at which SRT prediction is considered applicable—regardless of the type of cortical response used. In the theta band, however, SRT predictions based on cortical responses to continuous speech performed worse, showing a significantly lower number of predictions within an error margin of 7 dB compared to those based on cortical responses to modulated noise and the repeating /da/ sound. The proportion of individual SRT predictions with an error margin within 7 dB was, at best, 30 %.
For people with normal hearing, cortical responses to continuous speech and modulated noise predicted speech-in-noise performance at the group level but not at the individual level, due to variability in cortical tracking of the acoustic envelope. Predicting the SRT on an individual level remains a major and clinically important challenge.
{"title":"Comparing approaches for predicting behavioural speech-in-noise performance using cortical responses to unattended stimuli","authors":"Suwijak Deoisres, Ghadah S. Aljarboa, Steven L. Bell, David M. Simpson","doi":"10.1016/j.heares.2025.109197","DOIUrl":"10.1016/j.heares.2025.109197","url":null,"abstract":"<div><div>The cortical tracking of the acoustic envelope is a phenomenon where the brain's electrical activity, as recorded by electroencephalography (EEG) signals, fluctuates in accordance with changes in stimulus intensity (the acoustic envelope of the stimulus). Understanding speech in a noisy background is a key challenge for people with hearing impairments. Speech stimuli are therefore more ecologically valid than clicks, tone pips, or speech tokens (e.g., syllables) for assessing hearing. However, it remains unclear whether EEG responses to speech provide an advantage in predicting speech intelligibility. This study aimed to assess the ability of cortical responses to speech and speech-related sounds to predict behavioural speech-in-noise performance in listeners with normal hearing when they are not attending to the stimuli.</div><div>Twenty native English-speaking adults with normal hearing (aged 18 to 40 years) participated in a speech reception task, listening to English Matrix sentences presented at signal-to-noise ratios (SNRs) of -15, -10, -5, 0, and ∞ (no background noise) dB, and then identifying the words they heard in the sentences. In the EEG experiment, the participants then listened to continuous speech, broadband noise modulated by the envelope of speech, and repeating short /da/ stimuli presented at the same SNR levels as in the Matrix test. For the latter, Auditory Late Response (ALR) was estimated from the EEG, and for the former, the strength of the envelope-tracking responses was calculated.</div><div>Cortical responses to all stimuli showed monotonic relationships with the signal-to-noise ratio at the group level and in most individuals, although there was considerable variability. EEG analysis in the delta band showed no significant difference in the number of participants with predicted speech reception thresholds (SRTs) within an error margin of 7 dB—the level at which SRT prediction is considered applicable—regardless of the type of cortical response used. In the theta band, however, SRT predictions based on cortical responses to continuous speech performed worse, showing a significantly lower number of predictions within an error margin of 7 dB compared to those based on cortical responses to modulated noise and the repeating /da/ sound. The proportion of individual SRT predictions with an error margin within 7 dB was, at best, 30 %.</div><div>For people with normal hearing, cortical responses to continuous speech and modulated noise predicted speech-in-noise performance at the group level but not at the individual level, due to variability in cortical tracking of the acoustic envelope. Predicting the SRT on an individual level remains a major and clinically important challenge.</div></div>","PeriodicalId":12881,"journal":{"name":"Hearing Research","volume":"457 ","pages":"Article 109197"},"PeriodicalIF":2.5,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143004357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-11DOI: 10.1016/j.heares.2025.109184
Marie-Anick Savard, Emily B.J. Coffey
Misophonia is a disorder in which specific common sounds such as another person breathing or chewing, or the ticking of a clock, cause an atypical negative emotional response. Affected individuals may experience anger, irritability, annoyance, disgust, and anxiety, as well as physiological autonomic responses, and may find everyday environments and contexts to be unbearable in which their ‘misophonic stimuli’ (often called ‘trigger sounds’) are present. Misophonia is gradually being recognized as a genuine problem that causes significant distress and has negative consequences for individuals and their families. It has only recently come under scientific scrutiny, as researchers and clinicians are establishing its prevalence, distinguishing it from other disorders of sensory sensitivity such as hyperacusis, establishing its neurobiological bases, and evaluating the effectiveness of potential treatments. While ideas abound as to the mechanisms involved in misophonia, few have coalesced into models. The aim of the present work is to summarize and extend recent thinking on the mechanistic basis of misophonia, with a focus on moving towards neurologically-informed cognitive models that can (a) account for extant findings, and (b) generate testable predictions. We hope this work will facilitate future refinements in our understanding of misophonia, and ultimately inform treatments.
{"title":"Toward cognitive models of misophonia","authors":"Marie-Anick Savard, Emily B.J. Coffey","doi":"10.1016/j.heares.2025.109184","DOIUrl":"10.1016/j.heares.2025.109184","url":null,"abstract":"<div><div>Misophonia is a disorder in which specific common sounds such as another person breathing or chewing, or the ticking of a clock, cause an atypical negative emotional response. Affected individuals may experience anger, irritability, annoyance, disgust, and anxiety, as well as physiological autonomic responses, and may find everyday environments and contexts to be unbearable in which their ‘misophonic stimuli’ (often called ‘trigger sounds’) are present. Misophonia is gradually being recognized as a genuine problem that causes significant distress and has negative consequences for individuals and their families. It has only recently come under scientific scrutiny, as researchers and clinicians are establishing its prevalence, distinguishing it from other disorders of sensory sensitivity such as hyperacusis, establishing its neurobiological bases, and evaluating the effectiveness of potential treatments. While ideas abound as to the mechanisms involved in misophonia, few have coalesced into models. The aim of the present work is to summarize and extend recent thinking on the mechanistic basis of misophonia, with a focus on moving towards neurologically-informed cognitive models that can (a) account for extant findings, and (b) generate testable predictions. We hope this work will facilitate future refinements in our understanding of misophonia, and ultimately inform treatments.</div></div>","PeriodicalId":12881,"journal":{"name":"Hearing Research","volume":"458 ","pages":"Article 109184"},"PeriodicalIF":2.5,"publicationDate":"2025-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058874","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-11DOI: 10.1016/j.heares.2025.109186
Robert Fettiplace, Maryline Beurg
We developed an isolated auditory papilla of the crested gecko to record from the hair cells and explore the origins of frequency tuning. Low-frequency cells displayed electrical tuning, dependent on Ca2+-activated K+ channels; high-frequency cells, overlain with sallets, showed a variation in hair bundle stiffness which when combined with sallet mass could provide a mechanical resonance of 1 to 6 kHz. Sinusoidal electrical currents injected extracellularly evoked hair bundle oscillations at twice the stimulation frequency, consistent with fast electromechanical responses from hair bundles of two opposing orientations, as occur in the sallets. Current evoked oscillations were reduced by lowering Ca2+, but not by block of the mechanotransduction channels by dihydrostreptomycin or salicylate block of prestin. We suggest the phenomenon may augment passive mechanical tuning of the sallets over the high-frequency region.
{"title":"The mechanisms of frequency tuning in gecko auditory hair cells","authors":"Robert Fettiplace, Maryline Beurg","doi":"10.1016/j.heares.2025.109186","DOIUrl":"10.1016/j.heares.2025.109186","url":null,"abstract":"<div><div>We developed an isolated auditory papilla of the crested gecko to record from the hair cells and explore the origins of frequency tuning. Low-frequency cells displayed electrical tuning, dependent on Ca<sup>2+</sup>-activated K<sup>+</sup> channels; high-frequency cells, overlain with sallets, showed a variation in hair bundle stiffness which when combined with sallet mass could provide a mechanical resonance of 1 to 6 kHz. Sinusoidal electrical currents injected extracellularly evoked hair bundle oscillations at twice the stimulation frequency, consistent with fast electromechanical responses from hair bundles of two opposing orientations, as occur in the sallets. Current evoked oscillations were reduced by lowering Ca<sup>2+</sup>, but not by block of the mechanotransduction channels by dihydrostreptomycin or salicylate block of prestin. We suggest the phenomenon may augment passive mechanical tuning of the sallets over the high-frequency region.</div></div>","PeriodicalId":12881,"journal":{"name":"Hearing Research","volume":"457 ","pages":"Article 109186"},"PeriodicalIF":2.5,"publicationDate":"2025-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143004407","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-10DOI: 10.1016/j.heares.2025.109187
Nicholas R. Lozier , Max A. Aizenstein , Essence D. Williams , Marίa E. Rubio
Sexually mature females of multiple mammalian species were previously reported to have increased peripheral auditory sensitivity, often measured as higher auditory brainstem response (ABR) wave I amplitude compared to males. Here, we determined potential hormonal and genetic (i.e., XX- vs. XY-linked genes) contributions to this sex difference by recording ABRs in gonadally intact and gonadectomized female and male wildtype (WT) and four core genotypes (FCG) C57BL/6J mice. WT females at postnatal day 38 (P38) and P65, and FCG mice with ovaries at P65 had higher wave I amplitude than males, and the difference was absent in gonadectomized mice. Furthermore, in WT mice, we addressed the initiation and duration of the sex difference in wave amplitude from pre-pubescence (P25) through maturation from post-pubescent late adolescence to early adulthood (P38, P65, and P95) in both the cochlea and cochlear nucleus. In both female and male mice, wave I amplitude decreased by 50 % from P25 to P95. However, the amplitude in females was 22 % and 11 % higher than males at P38 and P65, respectively. In gonadectomized mice, there was no sex difference in wave I amplitude at any age tested, due to a decrease in gonadectomized females. In contrast, we found that wave II amplitude remains relatively constant over these ages in both sham and gonadectomized WT female and male mice. Together, the data suggest that gonad-derived hormones differentially refine the maturation of wave I, but not wave II, amplitude between late adolescence and early adulthood.
{"title":"Gonad-derived steroid hormones mediate a sex difference in the maturation of auditory encoding in the cochlea from adolescence to early adulthood in C57BL/6J mice","authors":"Nicholas R. Lozier , Max A. Aizenstein , Essence D. Williams , Marίa E. Rubio","doi":"10.1016/j.heares.2025.109187","DOIUrl":"10.1016/j.heares.2025.109187","url":null,"abstract":"<div><div>Sexually mature females of multiple mammalian species were previously reported to have increased peripheral auditory sensitivity, often measured as higher auditory brainstem response (ABR) wave I amplitude compared to males. Here, we determined potential hormonal and genetic (i.e., XX- vs. XY-linked genes) contributions to this sex difference by recording ABRs in gonadally intact and gonadectomized female and male wildtype (WT) and four core genotypes (FCG) C57BL/6J mice. WT females at postnatal day 38 (P38) and P65, and FCG mice with ovaries at P65 had higher wave I amplitude than males, and the difference was absent in gonadectomized mice. Furthermore, in WT mice, we addressed the initiation and duration of the sex difference in wave amplitude from pre-pubescence (P25) through maturation from post-pubescent late adolescence to early adulthood (P38, P65, and P95) in both the cochlea and cochlear nucleus. In both female and male mice, wave I amplitude decreased by 50 % from P25 to P95. However, the amplitude in females was 22 % and 11 % higher than males at P38 and P65, respectively. In gonadectomized mice, there was no sex difference in wave I amplitude at any age tested, due to a decrease in gonadectomized females. In contrast, we found that wave II amplitude remains relatively constant over these ages in both sham and gonadectomized WT female and male mice. Together, the data suggest that gonad-derived hormones differentially refine the maturation of wave I, but not wave II, amplitude between late adolescence and early adulthood.</div></div>","PeriodicalId":12881,"journal":{"name":"Hearing Research","volume":"457 ","pages":"Article 109187"},"PeriodicalIF":2.5,"publicationDate":"2025-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143004405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-08DOI: 10.1016/j.heares.2025.109185
Kenneth Morse, Leah Morse
Tinnitus is the perception of a ringing, buzzing, or other sound without the presence of an external stimulus. Reduced central auditory nervous system inhibition is a commonly reported mechanism contributing to a person's tinnitus perception. Different cortical auditory evoked potential (CAEP) studies have supported the presence of reduced inhibition in people with tinnitus. Although previous CAEPs used to study tinnitus do broadly represent inhibitory function, it is not entirely clear if the different CAEPs present similarly within an individual. To address this gap in knowledge, the current study evaluated the convergent validity between different CAEPs that broadly reflect inhibitory function, called sensory gating and onset-offset CAEPs. Convergent validity between sensory gating and onset-offset CAEPs was evaluated as a function of participant tinnitus status, stimulus frequency, and CAEP quantification approach. The results indicated that sensory gating and onset-offset CAEP responses indicative of inhibitory function did not demonstrate strong convergent validity. Further, the strength of convergent validity did not differ between people with and without tinnitus. However, experimental factors that yielded more robust CAEPs, such as broadband stimuli, and more comprehensive measures of amplitude, such as total response area, resulted in better convergent validity compared to higher frequency stimuli and more isolated measures of amplitude like peak amplitude. Overall, these findings suggest that the specific inhibitory mechanisms represented by sensory gating and onset-offset CAEPs differ. Therefore, each CAEP may be better suited to study distinct populations and/or inhibitory functions.
{"title":"Convergent validity of cortical auditory evoked potential indices of central auditory nervous system inhibition in people with and without tinnitus","authors":"Kenneth Morse, Leah Morse","doi":"10.1016/j.heares.2025.109185","DOIUrl":"10.1016/j.heares.2025.109185","url":null,"abstract":"<div><div>Tinnitus is the perception of a ringing, buzzing, or other sound without the presence of an external stimulus. Reduced central auditory nervous system inhibition is a commonly reported mechanism contributing to a person's tinnitus perception. Different cortical auditory evoked potential (CAEP) studies have supported the presence of reduced inhibition in people with tinnitus. Although previous CAEPs used to study tinnitus do broadly represent inhibitory function, it is not entirely clear if the different CAEPs present similarly within an individual. To address this gap in knowledge, the current study evaluated the convergent validity between different CAEPs that broadly reflect inhibitory function, called sensory gating and onset-offset CAEPs. Convergent validity between sensory gating and onset-offset CAEPs was evaluated as a function of participant tinnitus status, stimulus frequency, and CAEP quantification approach. The results indicated that sensory gating and onset-offset CAEP responses indicative of inhibitory function did not demonstrate strong convergent validity. Further, the strength of convergent validity did not differ between people with and without tinnitus. However, experimental factors that yielded more robust CAEPs, such as broadband stimuli, and more comprehensive measures of amplitude, such as total response area, resulted in better convergent validity compared to higher frequency stimuli and more isolated measures of amplitude like peak amplitude. Overall, these findings suggest that the specific inhibitory mechanisms represented by sensory gating and onset-offset CAEPs differ. Therefore, each CAEP may be better suited to study distinct populations and/or inhibitory functions.</div></div>","PeriodicalId":12881,"journal":{"name":"Hearing Research","volume":"458 ","pages":"Article 109185"},"PeriodicalIF":2.5,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143079458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Age-related hearing loss (ARHL) is a widespread problem in the elderly, significantly impairing their quality of life. Despite its high prevalence, no fundamental treatment for ARHL has been established. Nicotinamide adenine dinucleotide (NAD+) is required for various biological processes and tissue levels of the coenzyme NAD+ are known to decrease with age. A previous report suggested that declining NAD+ levels induce age-related diseases and NAD+ supplementation might be effective for treating or preventing age-related diseases. To clarify the effect of NAD+ supplementation on ARHL, C57BL/6J mice used as an animal model of ARHL were treated with nicotinamide mononucleotide (NMN), a precursor of NAD+. Oral administration of NMN at 500 mg/kg/day effectively suppressed the development of ARHL in C57BL/6J mice. To elucidate the mechanism by which NMN administration suppressed the development of ARHL, NAD+-related metabolites were assessed, and a comprehensive transcriptomic analysis of the inner ear tissue was performed. NMN administration resulted in increased NAD+ levels in inner ear tissues and induced changes in the transcriptome, specifically in genes related to metal ion metabolism. These findings suggest that NMN administration enhanced NAD+ levels in inner ear tissues, modulating metal ion metabolism to potentially protect against oxidative stress. This study provides a novel therapeutic approach to mitigating ARHL through NAD+ supplementation.
{"title":"Administration of nicotinamide mononucleotide suppresses the progression of age-related hearing loss in mice","authors":"Kouya Hattori , Takashige Hamaguchi , Rika Azuma-Suzuki , Seiichiro Higashi , Aiko Manji , Masashi Morifuji","doi":"10.1016/j.heares.2025.109182","DOIUrl":"10.1016/j.heares.2025.109182","url":null,"abstract":"<div><div>Age-related hearing loss (ARHL) is a widespread problem in the elderly, significantly impairing their quality of life. Despite its high prevalence, no fundamental treatment for ARHL has been established. Nicotinamide adenine dinucleotide (NAD<sup>+</sup>) is required for various biological processes and tissue levels of the coenzyme NAD<sup>+</sup> are known to decrease with age. A previous report suggested that declining NAD<sup>+</sup> levels induce age-related diseases and NAD<sup>+</sup> supplementation might be effective for treating or preventing age-related diseases. To clarify the effect of NAD<sup>+</sup> supplementation on ARHL, C57BL/6J mice used as an animal model of ARHL were treated with nicotinamide mononucleotide (NMN), a precursor of NAD<sup>+</sup>. Oral administration of NMN at 500 mg/kg/day effectively suppressed the development of ARHL in C57BL/6J mice. To elucidate the mechanism by which NMN administration suppressed the development of ARHL, NAD<sup>+</sup>-related metabolites were assessed, and a comprehensive transcriptomic analysis of the inner ear tissue was performed. NMN administration resulted in increased NAD<sup>+</sup> levels in inner ear tissues and induced changes in the transcriptome, specifically in genes related to metal ion metabolism. These findings suggest that NMN administration enhanced NAD<sup>+</sup> levels in inner ear tissues, modulating metal ion metabolism to potentially protect against oxidative stress. This study provides a novel therapeutic approach to mitigating ARHL through NAD<sup>+</sup> supplementation.</div></div>","PeriodicalId":12881,"journal":{"name":"Hearing Research","volume":"457 ","pages":"Article 109182"},"PeriodicalIF":2.5,"publicationDate":"2025-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142947666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01DOI: 10.1016/j.heares.2024.109155
András Bálint , Wilhelm Wimmer , Marco Caversaccio , Christian Rummel , Stefan Weder
Objectives
Understanding brain processing of auditory and visual speech is essential for advancing speech perception research and improving clinical interventions for individuals with hearing impairment. Functional near-infrared spectroscopy (fNIRS) is deemed to be highly suitable for measuring brain activity during language tasks. However, accurate data interpretation also requires validated stimuli and behavioral measures.
Design
Twenty-six adults with normal hearing listened to sentences from the Oldenburg Sentence Test (OLSA), and brain activation in the temporal, occipital, and prefrontal areas was measured by fNIRS. The sentences were presented in one of the four different modalities: speech-in-quiet, speech-in-noise, audiovisual speech or visual speech (i.e., lipreading). To support the interpretation of our fNIRS data, and to obtain a more comprehensive understanding of the study population, we performed hearing tests (pure tone and speech audiometry) and collected behavioral data using validated questionnaires, in-task comprehension questions, and listening effort ratings.
Results
In the auditory conditions (i.e., speech-in-quiet and speech-in-noise), we observed cortical activity in the temporal regions bilaterally. During the visual speech condition, we measured significant activation in the occipital area. Following the audiovisual condition, cortical activation was observed in both regions. Furthermore, we established a baseline for how individuals with normal hearing process visual cues during lipreading, and we found higher activity in the prefrontal cortex in noise conditions compared to quiet conditions, linked to higher listening effort.
Conclusions
We demonstrated the applicability of a clinically inspired audiovisual speech-comprehension task in participants with normal hearing. The measured brain activation patterns were supported and complemented by objective and behavioral parameters.
{"title":"Brain activation patterns in normal hearing adults: An fNIRS Study using an adapted clinical speech comprehension task","authors":"András Bálint , Wilhelm Wimmer , Marco Caversaccio , Christian Rummel , Stefan Weder","doi":"10.1016/j.heares.2024.109155","DOIUrl":"10.1016/j.heares.2024.109155","url":null,"abstract":"<div><h3>Objectives</h3><div>Understanding brain processing of auditory and visual speech is essential for advancing speech perception research and improving clinical interventions for individuals with hearing impairment. Functional near-infrared spectroscopy (fNIRS) is deemed to be highly suitable for measuring brain activity during language tasks. However, accurate data interpretation also requires validated stimuli and behavioral measures.</div></div><div><h3>Design</h3><div>Twenty-six adults with normal hearing listened to sentences from the Oldenburg Sentence Test (OLSA), and brain activation in the temporal, occipital, and prefrontal areas was measured by fNIRS. The sentences were presented in one of the four different modalities: speech-in-quiet, speech-in-noise, audiovisual speech or visual speech (i.e., lipreading). To support the interpretation of our fNIRS data, and to obtain a more comprehensive understanding of the study population, we performed hearing tests (pure tone and speech audiometry) and collected behavioral data using validated questionnaires, in-task comprehension questions, and listening effort ratings.</div></div><div><h3>Results</h3><div>In the auditory conditions (i.e., speech-in-quiet and speech-in-noise), we observed cortical activity in the temporal regions bilaterally. During the visual speech condition, we measured significant activation in the occipital area. Following the audiovisual condition, cortical activation was observed in both regions. Furthermore, we established a baseline for how individuals with normal hearing process visual cues during lipreading, and we found higher activity in the prefrontal cortex in noise conditions compared to quiet conditions, linked to higher listening effort.</div></div><div><h3>Conclusions</h3><div>We demonstrated the applicability of a clinically inspired audiovisual speech-comprehension task in participants with normal hearing. The measured brain activation patterns were supported and complemented by objective and behavioral parameters.</div></div>","PeriodicalId":12881,"journal":{"name":"Hearing Research","volume":"455 ","pages":"Article 109155"},"PeriodicalIF":2.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142784967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01DOI: 10.1016/j.heares.2024.109165
Sandra Franco-Caspueñas , Carmen García-Montoya , Julio Contreras , Luis Lassaletta , Isabel Varela-Nieto , Ana M. Jiménez-Lara
Background
Vestibular schwannomas (VS) are complex and heterogeneous human tumors arising from the Schwann cell compartment of the vestibulocochlear nerve. VS cause significant neurological deficit such as hearing loss and vestibular impairment, and in some cases death due to brainstem compression. There is an urgent need to find pharmacotherapies for VS since surgical removal and stereotactic radiosurgery are the only effective treatments. Cancer therapy based in the combination of drug-induced senescence and senolytics may provide an innovative pharmacological alternative for VS management.
Methods
Senescence-associated β-galactosidase (SA-β-GAL) activity detection assay, real-time polymerase chain reaction (RT-PCR), western blotting and immunofluorescence, together with viability assays were used to analyze the response to different chemotherapy drugs of the human VS HEI-193 cell line. Human VS tumor paraffin sections were also studied for SA-β-GAL-stained cells.
Results
We found that chemotherapy compounds induced genotoxic stress and cellular senescence in HEI-193 VS cells, as characterized by increased SA-β-GAL activity, growth arrest, increased levels of the cyclin-dependent kinase inhibitor p21 and the accumulation of DNA damage. These cellular senescence markers were also accompanied by an increase of senescence-associated secretory phenotype (SASP): IL6, IL8, IL1B and MMP1. Induction of senescence by chemotherapy rendered HEI-193 VS cells as druggable targets for senolytic compounds, as navitoclax. Thus, treatment with navitoclax selectively eliminated bleomycin-induced senescent HEI-193 VS cells by activating the extrinsic and intrinsic apoptosis pathways. Our data also show the presence of senescent cells, SA-β-GAL-positive stain, in human VS tumors, which are not present in healthy great auricular nerve sections.
Conclusions
These findings suggest that a one-two punch strategy of pro-senescence therapy induced by chemotherapy treatment followed by senolytic therapy represents a new paradigm for the pharmacological treatment of VS.
背景：前庭裂神经瘤（Vestibular schwannomas，VS）是一种复杂的异质性人类肿瘤，产生于前庭裂神经的许旺细胞区。前庭裂神经瘤会导致严重的神经功能缺损，如听力损失和前庭功能障碍，在某些情况下还会因压迫脑干而导致死亡。由于手术切除和立体定向放射外科手术是唯一有效的治疗方法，因此迫切需要找到治疗 VS 的药物疗法。基于药物诱导衰老和衰老剂相结合的癌症疗法可能会为 VS 的治疗提供一种创新的药物疗法：方法：采用衰老相关β-半乳糖苷酶（SA-β-GAL）活性检测法、实时聚合酶链反应（RT-PCR）、免疫印迹法和免疫荧光法以及活力检测法来分析人VS HEI-193细胞系对不同化疗药物的反应。此外，还对人VS肿瘤石蜡切片进行了SA-β-GAL染色细胞的研究：结果：我们发现化疗药物诱导了 HEI-193 VS 细胞的基因毒性应激和细胞衰老，表现为 SA-β-GAL 活性升高、生长停滞、细胞周期蛋白依赖性激酶抑制剂 p21 水平升高和 DNA 损伤积累。这些细胞衰老标志物还伴随着衰老相关分泌表型（SASP）的增加：IL6、IL8、IL1B 和 MMP1。化疗诱导衰老使 HEI-193 VS 细胞成为纳维络克（navitoclax）等衰老溶解化合物的药物靶标。因此，用navitoclax治疗可选择性地消除博莱霉素诱导的衰老HEI-193 VS细胞，激活细胞凋亡的外在和内在途径。我们的数据还显示，人VS肿瘤中存在衰老细胞，即SA-β-GAL阳性染色，而健康的大耳廓神经切片中不存在这种细胞：这些研究结果表明，化疗诱导的促衰老疗法和衰老溶解疗法双管齐下的策略代表了VS药物治疗的新模式。
{"title":"Uncovering cellular senescence as a therapeutic target in NF2-related vestibular schwannoma","authors":"Sandra Franco-Caspueñas , Carmen García-Montoya , Julio Contreras , Luis Lassaletta , Isabel Varela-Nieto , Ana M. Jiménez-Lara","doi":"10.1016/j.heares.2024.109165","DOIUrl":"10.1016/j.heares.2024.109165","url":null,"abstract":"<div><h3>Background</h3><div>Vestibular schwannomas (VS) are complex and heterogeneous human tumors arising from the Schwann cell compartment of the vestibulocochlear nerve. VS cause significant neurological deficit such as hearing loss and vestibular impairment, and in some cases death due to brainstem compression. There is an urgent need to find pharmacotherapies for VS since surgical removal and stereotactic radiosurgery are the only effective treatments. Cancer therapy based in the combination of drug-induced senescence and senolytics may provide an innovative pharmacological alternative for VS management.</div></div><div><h3>Methods</h3><div>Senescence-associated β-galactosidase (SA-β-GAL) activity detection assay, real-time polymerase chain reaction (RT-PCR), western blotting and immunofluorescence, together with viability assays were used to analyze the response to different chemotherapy drugs of the human VS HEI-193 cell line. Human VS tumor paraffin sections were also studied for SA-β-GAL-stained cells.</div></div><div><h3>Results</h3><div>We found that chemotherapy compounds induced genotoxic stress and cellular senescence in HEI-193 VS cells, as characterized by increased SA-β-GAL activity, growth arrest, increased levels of the cyclin-dependent kinase inhibitor p21 and the accumulation of DNA damage. These cellular senescence markers were also accompanied by an increase of senescence-associated secretory phenotype (SASP): <em>IL6, IL8, IL1B</em> and <em>MMP1</em>. Induction of senescence by chemotherapy rendered HEI-193 VS cells as druggable targets for senolytic compounds, as navitoclax. Thus, treatment with navitoclax selectively eliminated bleomycin-induced senescent HEI-193 VS cells by activating the extrinsic and intrinsic apoptosis pathways. Our data also show the presence of senescent cells, SA-β-GAL-positive stain, in human VS tumors, which are not present in healthy great auricular nerve sections.</div></div><div><h3>Conclusions</h3><div>These findings suggest that a one-two punch strategy of pro-senescence therapy induced by chemotherapy treatment followed by senolytic therapy represents a new paradigm for the pharmacological treatment of VS.</div></div>","PeriodicalId":12881,"journal":{"name":"Hearing Research","volume":"455 ","pages":"Article 109165"},"PeriodicalIF":2.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794648","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01DOI: 10.1016/j.heares.2024.109168
Barbara Canlon
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