Редактирование: ABR

Active breakpoint cluster region-related protein

==Publications==

{{medline-entry
|title=[Hidden hearing loss and early identification].
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32791650
|abstract=b  The symptoms of hidden hearing loss（HHL） are concealed, mainly manifested as defects in the threshold upper auditory function, which are related to noise exposure, aging and drug damage. There is no definite evidence to prove that whether the three factors participate in mechanism of synaptic damage in the cochlea. The clinical audiological characteristics of HHL are mostly as follows: the normal threshold of PTA and the wave response of [[ABR]]; the amplitude of the CAP of [[ABR]] wave Ⅰ or ECochG is lower at medium and high stimulation intensity; the lower speech recognition rate under noise, etc. Ultra-high frequency pure tone audiometry, a series of objective audiological examinations, such as [[ABR]], ECochG and frequency-following response, speech audiometry under noise, noise exposure questionnaire evaluation were applied to detect HHL at early stage.
|mesh-terms=* Acoustic Stimulation
* Audiometry, Pure-Tone
* Auditory Threshold
* Evoked Potentials, Auditory, Brain Stem
* Hearing Loss, Noise-Induced
* Humans
* Noise
|keywords=* aging
* drug damage
* hidden hearing loss
* noise exposure
|full-text-url=https://sci-hub.do/10.13201/j.issn.2096-7993.2020.07.023
}}
{{medline-entry
|title=The effect and mechanism of 19S proteasome [[PSMD11]]/Rpn6 subunit in D-Galactose induced mimetic aging models.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32450067
|abstract=Regulating proteasome activity is a potent therapeutic aspect of age-related hearing loss, which has been proven to protect neurons from age-related damaging. [[PSMD11]], subunit of the 19S proteasome regulatory particle, is known to mainly up-regulate proteasome activity and prolong aging. However, the mechanism of [[PSMD11]] in age-related hearing loss has not been deeply explored. In the present study, we explore the function and mechanism of [[PSMD11]] protecting neurons in d-Galactose (D-Gal) mimetic aging models. Age-related pathologies were detected by Taq-PCR, [[ABR]], Transmission electron microscopy, toluidine blue and β-galactosidase staining. The relative expressions of the proteins were explored by Western blotting, oxyblot, immunoprecipitation and immunofluorescence. Flow cytometry was used to manifest the oxidative state. We discovered that proteasome activity was impaired with aging, and that ROS and toxic protein accumulated in D-Gal induced aging models. [[PSMD11]] changed with aging, and was associated with the metabolism of proteasome activity in the D-Gal treated models. Moreover, the knockdown or overexpression of [[PSMD11]] was sufficient to change the oxidative state caused by D-Gal. Our results also demonstrated that [[PSMD11]] could bond to AMPKα1/2 in the auditory cortex and PC12 cells, and AMPKα2 but not AMPKα1 was efficient to regulate the function of [[PSMD11]]. Deeper insights into the mechanisms of regulating [[PSMD11]] for the anti-aging process are needed, and may offer novel therapeutic methods for central presbycusis.

|keywords=* Age-related hearing loss
* Aging
* D-galactose
* PSMD11
* Proteasome
|full-text-url=https://sci-hub.do/10.1016/j.yexcr.2020.112093
}}
{{medline-entry
|title=Aging But Not Age-Related Hearing Loss Dominates the Decrease of Parvalbumin Immunoreactivity in the Primary Auditory Cortex of Mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32327469
|abstract=Alterations in inhibitory circuits of the primary auditory cortex (pAC) have been shown to be an aspect of aging and age-related hearing loss (AHL). Several studies reported a decline in parvalbumin (PV) immunoreactivity in aged rodent pAC of animals displaying AHL and conclude a relationship between reduced sensitivity and declined PV immunoreactivity. However, it remains elusive whether AHL or a general molecular aging is causative for decreased PV immunoreactivity. In this study, we aimed to disentangle the effects of AHL and general aging on PV immunoreactivity patterns in inhibitory interneurons of mouse pAC. We compared young and old animals of a mouse line with AHL (C57BL/6) and a mutant (C57B6.CAST-[i]Cdh23 [/i] ) that is not vulnerable to AHL according to their hearing status by measuring auditory brainstem responses ([[ABR]]s) and by an immunohistochemical evaluation of the PV immunoreactivity patterns in two dimensions (rostro-caudal and layer) in the pAC. Although AHL could be confirmed by [[ABR]] measurements for the C57BL/6 mice, both aged strains showed a similar reduction of PV  positive interneurons in both, number and density. The pattern of reduction across the rostro-caudal axis and across cortical layers was similar for both aged lines. Our results demonstrate that a reduced PV immunoreactivity is a sign of general, molecular aging and not related to AHL.

|keywords=* age-related hearing loss
* aging
* mouse primary auditoy cortex
* parvalbumin
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7210488
}}
{{medline-entry
|title=Hearing loss through apoptosis of the spiral ganglion neurons in apolipoprotein E knockout mice fed with a western diet.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31948760
|abstract=Age-related hearing loss (ARHL) is a neurodegenerative disease associated with an aged population. ARHL is influenced by biological factors such as aging, sex difference, and atherosclerosis. The mechanisms of ARHL caused by atherosclerosis have not been previously determined in apolipoprotein E knockout (ApoE KO) male mice. To investigate the onset and cause of the hearing loss, ApoE KO male mice were treated with a western diet (ApoE KO-WD) for 16 weeks. The lipid profile, atherosclerotic plaques throughout the aorta, and auditory brainstem response ([[ABR]]) thresholds were measured in the ApoE KO-WD male mice. The expression of S100 calcium-binding protein B ([[S100B]]), a neuronal damage biomarker, was also observed. Reactive oxygen species (ROS) and apoptosis rates were detected in the cochlea of the ApoE KO male mice. Atherosclerotic plaques on the aorta and [[ABR]] thresholds were significantly increased in the ApoE KO-WD male mice at 24 weeks of age. [[ABR]] thresholds had a statistically significant positive correlation with the area of atherosclerotic plaques (r = 0.783, p = 0.013) in male mice at 24 weeks of age. [[S100B]] protein expression and the dihydroethidium (DHE) reaction to ROS in the cochlear spiral ganglion neurons (SGNs) were significantly increased in the ApoE KO and ApoE KO-WD male mice. Cells positive for active caspase-3 and terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) in the SGNs were significantly increased in ApoE KO-WD male mice indicating an increased rate of cellular apoptosis. In conclusion, ROS in the SGNs were activated by increased [[S100B]] expression in ApoE KO-WD male mice, and this resulted in an increased apoptosis rate. Thus, hearing loss began at 16 weeks in ApoE KO-WD male mice. Our results suggest that the ApoE KO-WD male mice are a suitable animal model for studying ARHL associated with exacerbated atherosclerosis.
|mesh-terms=* Aging
* Animals
* Apolipoproteins E
* Apoptosis
* Diet, Western
* Disease Models, Animal
* Hearing Loss
* Male
* Mice
* Mice, Inbred C57BL
* Mice, Knockout
* Neurons
* Spiral Ganglion
|keywords=* Apoptosis
* Atherosclerosis
* Hearing loss
* Reactive oxygen specie
* Spiral ganglion neurons
|full-text-url=https://sci-hub.do/10.1016/j.bbrc.2019.12.100
}}
{{medline-entry
|title=Effects of enriched endogenous omega-3 fatty acids on age-related hearing loss in mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31771637
|abstract=Dietary intervention is a practical prevention strategy for age-related hearing loss (AHL). Omega-3 (n-3) polyunsaturated fatty acids (PUFAs) may be effective in prevention of AHL due to their anti-inflammatory and tissue-protective functions. Age-related changes in the hearing function of wild-type and Fat-1 transgenic mice derived from the C57BL/6N strain, which can convert omega-6 PUFAs to n-3 PUFAs and consequently produce enriched endogenous n-3 PUFAs, were investigated to test the efficacy of n-3 PUFAs for AHL prevention. At 2 months, the baseline auditory brainstem response ([[ABR]]) thresholds were the same in Fat-1 and wild-type mice at 8-16 kHz but were significantly higher in Fat-1 mice at 4 and 32 kHz. In contrast, the [[ABR]] thresholds of Fat-1 mice were significantly lower at 10 months. Moreover, the [[ABR]] thresholds of Fat-1 mice at low-middle frequencies were significantly lower at 13 months (12 kHz). Body weights were significantly reduced in Fat-1 mice at 13 months, but not at 2, 10, and 16-17 months. In conclusion, enriched endogenous n-3 PUFAs produced due to the expression of the Fat-1 transgene partially alleviated AHL in male C57BL/6N mice.
|mesh-terms=* Aging
* Animals
* Body Weight
* Caenorhabditis elegans Proteins
* Cochlea
* Evoked Potentials, Auditory, Brain Stem
* Fatty Acid Desaturases
* Fatty Acids, Omega-3
* Male
* Mice
* Mice, Inbred C57BL
* Mice, Transgenic
* Neurons
* Presbycusis
* Spiral Ganglion
|keywords=* Age-related hearing loss
* C57BL/6 mouse
* Cochlea
* Omega-3 (n-3) fatty acids
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6878677
}}
{{medline-entry
|title=Hearing impairment and associated morphological changes in pituitary adenylate cyclase activating polypeptide (PACAP)-deficient mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31601840
|abstract=Pituitary adenylate cyclase activating polypeptide (PACAP) is a regulatory and cytoprotective neuropeptide, its deficiency implies accelerated aging in mice. It is present in the auditory system having antiapoptotic effects. Expression of Ca -binding proteins and its PAC1 receptor differs in the inner ear of PACAP-deficient (KO) and wild-type (WT) mice. Our aim was to elucidate the functional role of PACAP in the auditory system. Auditory brainstem response ([[ABR]]) tests found higher hearing thresholds in KO mice at click and low frequency burst stimuli. Hearing impairment at higher frequencies showed as reduced [[ABR]] wave amplitudes and latencies in KO animals. Increase in neuronal activity, demonstrated by c-Fos immunolabeling, was lower in KO mice after noise exposure in the ventral and dorsal cochlear nuclei. Noise induced neuronal activation was similar in further relay nuclei of the auditory pathway of WT and KO mice. Based on the similar inflammatory and angiogenic protein profile data from cochlear duct lysates, neither inflammation nor disturbed angiogenesis, as potential pathological components in sensorineural hearing losses, seem to be involved in the pathomechanism of the presented functional and morphological changes in PACAP KO mice. The hearing impairment is probably concomitant with the markedly accelerated aging processes in these animals.
|mesh-terms=* Aging
* Animals
* Cochlea
* Evoked Potentials, Auditory, Brain Stem
* Genotype
* Hearing
* Hearing Loss
* Inflammation
* Male
* Mice
* Mice, Knockout
* Models, Animal
* Neovascularization, Pathologic
* Neurons
* Pituitary Adenylate Cyclase-Activating Polypeptide
* Proteome
* Proto-Oncogene Proteins c-fos

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6787024
}}
{{medline-entry
|title=Global nurse/midwife workforce and reproductive health through social ecology lens.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31402489
|abstract=To explore how community social ecology factors may be associated with country registered nurse/registered midwife (RN/RM) workforce supply and reproductive health globally. A cross-sectional design using a social ecology framework was employed. Data were retrieved from publicly available websites for 107 countries. Dependent variables included RN/RM density, maternal mortality ratios (MMR), and adolescent birth rates ([[ABR]]). Independent variables included gender inequality, region, country income classification, education, gross domestic product per capita, government expenditure of spending on education and health, life expectancy, percent of female seats in legislature, and labor force participation factors. The best fit multivariable model of RN/RM density showed that after adjustment for region, country income and the GII, the percent of females with some secondary education explained most of variation in RN/RM density. The best fit models of MMR and [[ABR]] showed that gender inequality explained most of the variation. Other factors in the models were the percent of female seats in legislatures, region, country income class, and mean years of schooling. Employing a social ecology model can useful in RN/RM workforce planning and development as countries seek multisectoral strategies for increasing the RN/RM supply and improving reproductive health outcomes.
|mesh-terms=* Adolescent
* Cross-Sectional Studies
* Employment
* Female
* Global Health
* Health Education
* Humans
* Income
* Life Expectancy
* Male
* Midwifery
* Pregnancy
* Reproductive Health
* Social Environment
* Socioeconomic Factors
* Workforce
|keywords=* global health
* nurse/midwife workforce
* reproductive health
* social ecology
|full-text-url=https://sci-hub.do/10.1111/phn.12648
}}
{{medline-entry
|title=Urocortin 3 signalling in the auditory brainstem aids recovery of hearing after reversible noise-induced threshold shift.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31270820
|abstract=Ongoing, moderate noise exposure does not instantly damage the auditory system but may cause lasting deficits, such as elevated thresholds and accelerated ageing of the auditory system. The neuromodulatory peptide urocortin-3 ([[UCN3]]) is involved in the body's recovery from a stress response, and is also expressed in the cochlea and the auditory brainstem. Lack of [[UCN3]] facilitates age-induced hearing loss and causes permanently elevated auditory thresholds following a single 2 h noise exposure at moderate intensities. Outer hair cell function in mice lacking [[UCN3]] is unaffected, so that the observed auditory deficits are most likely due to inner hair cell function or central mechanisms. Highly specific, rather than ubiquitous, expression of [[UCN3]] in the brain renders it a promising candidate for designing drugs to ameliorate stress-related auditory deficits, including recovery from acoustic trauma. Environmental acoustic noise is omnipresent in our modern society, with sound levels that are considered non-damaging still causing long-lasting or permanent changes in the auditory system. The small neuromodulatory peptide urocortin-3 ([[UCN3]]) is the endogenous ligand for corticotropin-releasing factor receptor type 2 and together they are known to play an important role in stress recovery. [[UCN3]] expression has been observed in the auditory brainstem, but its role remains unclear. Here we describe the detailed distribution of [[UCN3]] expression in the murine auditory brainstem and provide evidence that [[UCN3]] is expressed in the synaptic region of inner hair cells in the cochlea. We also show that mice with deficient [[UCN3]] signalling experience premature ageing of the auditory system starting at an age of 4.7 months with significantly elevated thresholds of auditory brainstem responses ([[ABR]]s) compared to age-matched wild-type mice. Following a single, 2 h exposure to moderate (84 or 94 dB SPL) noise, [[UCN3]]-deficient mice exhibited significantly larger shifts in [[ABR]] thresholds combined with maladaptive recovery. In wild-type mice, the same noise exposure did not cause lasting changes to auditory thresholds. The presence of [[UCN3]]-expressing neurons throughout the auditory brainstem and the predisposition to hearing loss caused by preventing its normal expression suggests [[UCN3]] as an important neuromodulatory peptide in the auditory system's response to loud sounds.
|mesh-terms=* Aging
* Animals
* Auditory Threshold
* Evoked Potentials, Auditory, Brain Stem
* Female
* Hair Cells, Auditory, Outer
* Hearing Loss, Noise-Induced
* Male
* Mice
* Mice, Inbred C57BL
* Mice, Knockout
* Mice, Transgenic
* Noise
* Signal Transduction
* Urocortins
|keywords=* Corticotropin-releasing hormone receptor
* DPOAEs
* acoustic trauma
* ageing
* auditory brainstem responses
* neuropeptide
* stress recovery
* urocortin
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6852351
}}
{{medline-entry
|title=Age‑associated variation in the expression and function of TMEM16A calcium‑activated chloride channels in the cochlear stria vascularis of guinea pigs.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31257512
|abstract=The present study was designed to investigate the expression and function of transmembrane protein 16 (TMEM16A), a calcium‑activated chloride channel (CaCC), in the stria vascularis (SV) of the cochlea of guinea pigs at different ages, and to understand the role of CaCCs in the pathogenesis of presbycusis (age‑related hearing loss), the most common type of sensorineural hearing loss that occurs with natural aging. Guinea pigs were divided into the following groups: 2 weeks (young group), 3 months (youth group), 1 year (adult group), D‑galactose intervention (D‑gal group; aging model induced by subcutaneous injection of D‑galactose) and T16Ainh‑A01 (intraperitoneal injection of 50 µg/kg/day TMEM16A inhibitor T16Ainh‑A01 for 2 weeks). Differences in the hearing of guinea pigs between the various age groups were analyzed using auditory brainstem response ([[ABR]]), and immunofluorescence staining was performed to detect TMEM16A expression in the SV and determine the distribution. Reverse transcription‑quantitative PCR and western blot analyses were conducted to detect the mRNA and protein levels of TMEM16A in SV in the different age groups. Morris water maze behavior analysis demonstrated that spatial learning ability and memory were damaged in the D‑gal group. Superoxide dismutase activity and malondialdehyde content assays indicated that there was oxidative stress damage in the D‑gal group. The [[ABR]] thresholds gradually increased with age, and the increase in the T16Ainh‑A01 group was pronounced. Immunofluorescence analysis in the cochlear SV of guinea pigs in different groups revealed that expression of TMEM16A increased with increasing age (2 weeks to 1 year); fluorescence intensity was reduced in the D‑gal model of aging. As the guinea pigs continued to mature, the protein and mRNA contents of TMEM16A in the cochlea SV increased gradually, but were decreased in the D‑gal group. The findings indicated that CaCCs in the cochlear SV of guinea pigs were associated with the development of hearing in guinea pigs, and that downregulation of TMEM16A may be associated with age‑associated hearing loss.
|mesh-terms=* Aging
* Animals
* Anoctamin-1
* Disease Models, Animal
* Female
* Galactose
* Gene Expression Regulation
* Guinea Pigs
* Hearing
* Injections, Intraperitoneal
* Injections, Subcutaneous
* Male
* Presbycusis
* Pyrimidines
* Stria Vascularis
* Thiazoles

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6625423
}}
{{medline-entry
|title=Hormone replacement therapy attenuates hearing loss: Mechanisms involving estrogen and the IGF-1 pathway.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30845368
|abstract=Estradiol (E) is a multitasking hormone that plays a prominent role in the reproductive system, and also contributes to physiological and growth mechanisms throughout the body. Frisina and colleagues have previously demonstrated the beneficial effects of this hormone, with E-treated subjects maintaining low auditory brainstem response ([[ABR]]) thresholds relative to control subjects (Proceedings of the National Academy of Sciences of the United States of America, 2006;103:14246; Hearing Research, 2009;252:29). In the present study, we evaluated the functionality of the peripheral and central auditory systems in female CBA/CaJ middle-aged mice during and after long-term hormone replacement therapy (HRT) via electrophysiological and molecular techniques. Surprisingly, there are very few investigations about the side effects of HRT in the auditory system after it has been discontinued. Our results show that the long-term effects of HRT are permanent on [[ABR]] thresholds and [[ABR]] gap-in-noise (GIN) amplitude levels. E-treated animals had lower thresholds and higher amplitude values compared to other hormone treatment subject groups. Interestingly, progesterone (P)-treated animals had [[ABR]] thresholds that increased but amplitude levels that remained relatively the same throughout treatment. These results were consistent with qPCR experiments that displayed high levels of IGF-1R in the stria vascularis (SV) of both E and P animal groups compared to combination treatment (E   P) animals. IGF-1R plays a vital role in mediating anti-apoptotic responses via the PI3K/AKT pathway. Overall, our findings gain insights into the neuro-protective properties of E hormone treatments as well as expand the scientific knowledge base to help women decide whether HRT is the right choice for them.
|mesh-terms=* Animals
* Cells, Cultured
* Estradiol
* Estrogens
* Female
* Hearing Loss
* Hormone Replacement Therapy
* Insulin-Like Growth Factor I
* Male
* Mice
* Mice, Inbred CBA
|keywords=* HRT
* age-related hearing loss
* aging
* auditory system
* hormone replacement therapy
* neurodegeneration
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6516159
}}
{{medline-entry
|title=Evidence for age-related cochlear synaptopathy in humans unconnected to speech-in-noise intelligibility deficits.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30710791
|abstract=Cochlear synaptopathy (or the loss of primary auditory synapses) remains a subclinical condition of uncertain prevalence. Here, we investigate whether it affects humans and whether it contributes to suprathreshold speech-in-noise intelligibility deficits. For 94 human listeners with normal audiometry (aged 12-68 years; 64 women), we measured click-evoked auditory brainstem responses ([[ABR]]s), self-reported lifetime noise exposure, and speech reception thresholds for sentences (at 65 dB SPL) and words (at 50, 65 and 80 dB SPL) in steady-state and fluctuating maskers. Based on animal research, we assumed that the shallower the rate of growth of [[ABR]] wave-I amplitude versus level function, the higher the risk of suffering from synaptopathy. We found that wave-I growth rates decreased with increasing age but not with increasing noise exposure. Speech reception thresholds in noise were not correlated with wave-I growth rates and mean speech reception thresholds were not statistically different for two subgroups of participants (N = 14) with matched audiograms (up to 12 kHz) but different wave-I growth rates. Altogether, the data are consistent with the existence of age-related but not noise-related synaptopathy. In addition, the data dispute the notion that synaptopathy contributes to suprathreshold speech-in-noise intelligibility deficits.
|mesh-terms=* Acoustic Stimulation
* Adolescent
* Adult
* Aged
* Aging
* Animals
* Auditory Perception
* Auditory Threshold
* Child
* Cochlea
* Evoked Potentials, Auditory, Brain Stem
* Female
* Hair Cells, Auditory
* Hearing Loss, High-Frequency
* Hearing Loss, Noise-Induced
* Humans
* Male
* Middle Aged
* Noise
* Otoacoustic Emissions, Spontaneous
* Speech Intelligibility
* Speech Perception
* Synapses
* Young Adult
|keywords=* Auditory brainstem response
* Auditory deafferentation
* Noise exposure
* Speech-in-noise
* Synaptopathy
|full-text-url=https://sci-hub.do/10.1016/j.heares.2019.01.017
}}
{{medline-entry
|title=Masking Differentially Affects Envelope-following Responses in Young and Aged Animals.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29953908
|abstract=Age-related hearing decline typically includes threshold shifts as well as reduced wave I auditory brainstem response ([[ABR]]) amplitudes due to cochlear synaptopathy/neuropathy, which may compromise precise coding of suprathreshold speech envelopes. This is supported by findings with older listeners, who have difficulties in envelope and speech processing, especially in noise. However, separating the effects of threshold elevation, synaptopathy, and degradation by noise on physiological representations may be difficult. In the present study, the effects of notched, low- and high-pass noise on envelope-following responses (EFRs) in aging were compared when sound levels (aged: 85-dB SPL; young: 60- to 80-dB SPL) were matched between groups peripherally, by matching wave I [[ABR]] amplitudes, or centrally by matching EFR amplitudes. Low-level notched noise reduced EFRs to sinusoidally amplitude-modulated (SAM) tones in young animals for notch widths up to 2 octaves. High-pass noise above the carrier frequency reduced EFRs. Young animals showed EFR reductions at lower noise levels. Low-pass noise did not reduce EFRs in either young or aged animals. High-pass noise may affect EFR amplitudes in young animals more than aged by reducing the contributions of high-frequency-sensitive inputs. EFRs to SAM tones in modulated noise (NAM) suggest that neurons of young animals can synchronize to NAM at lower sound levels and maintain dual AM representations better than older animals. The overall results show that EFR amplitudes are strongly influenced by aging and the presence of a competing sound that likely reduces or shifts the pool of responsive neurons.
|mesh-terms=* Acoustic Stimulation
* Age Factors
* Aging
* Animals
* Brain Stem
* Evoked Potentials, Auditory, Brain Stem
* Female
* Male
* Rats
* Rats, Inbred F344
* Reaction Time
|keywords=* age-related hearing loss
* amplitude modulation
* envelope-following responses
* masking
* neuropathy
* synaptopathy
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6076866
}}
{{medline-entry
|title=Effects of Age on Speech-in-Noise Identification: Subjective Ratings of Hearing Difficulties and Encoding of Fundamental Frequency in Older Adults.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29719950
|abstract=Numerous studies have indicated deterioration of speech perception in noisy conditions among the elderly even those with normal hearing capabilities. The aim of this study was to investigate the effects of age on the speech-in-noise identification by speech-in-noise (SIN) test, subjective ratings of hearing difficulties by speech, spatial, and qualities of hearing scale (SSQ) questionnaire and encoding of fundamental frequency (F0) by Speech auditory brainstem response ([[ABR]]) in the elderly and comparing the results with young people. The present study was conducted on 32 elderly people aged over 60 years old (17 male and 15 female) with the mean age of 68.9 (standard deviation=6.33) possessing normal peripheral hearing and 32 young subjects (16 male and 16 female) aged 18-25 years old. Findings showed that the score of SIN test is lower among the elderly people as compared with young people in signal-to-noise ratios of 0 and -10 based on Iranian version of SSQ questionnaire (p