ReviewJournal of neuroscience research2020
Pathology and mechanisms of cochlear aging.
Review in Journal of neuroscience research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
142 citing papers in PubMed, 243 citations in OpenAlex.
- Trial
- Workplace noise exposure and the prevalence and 10-year incidence of age-related hearing loss.PloS one · 2021Trial
- Cycloastragenol Provides Pharmacokinetic Advantages over Astragaloside IV with Enhanced Cochlear Exposure and Protection Against Age-Associated Hearing Dysfunction.Pharmaceutics · 2026Article
- The Relationships Among Tinnitus Intensity, Complexity, Sound Intolerance, and Psychiatric Symptoms.Journal of clinical medicine · 2026Article
- The Relationship Between Reduced Glomerular Filtration Rate and Hearing Impairment: A Study Based on Western and Eastern Population.Journal of clinical medicine · 2026Article
- Presbycusis Across the Lifespan: Genetic, Molecular, and Multi-Omics Contributions.Audiology research · 2026Review
- Investigation of the Effects of Cadherin 23 and Oncomodulin on Early Progressive Hearing Loss Using a New Oncomodulin Mouse Model.International journal of molecular sciences · 2026Article
- Prevalence and sex differences in moderate-to-severe hearing loss among older adults: a cross-sectional study.BMC geriatrics · 2026Article
- AAV-mediated surtuin 1 overexpression in the cochlear inner hair cells protects ribbon synapses of D-galactose-induced aging mice.Molecular biology reports · 2026Article
- Upregulation of TRPV2 exacerbates age-related hearing loss by promoting oxidative stress in spiral ganglion neurons.Molecular brain · 2026Article
- Identification of sensorineural hearing loss subtypes using unsupervised machine learning and assessment of their replicability.Scientific reports · 2026Article
- Article
- Metformin alleviates presbycusis by activating the SIRT1/PINK1/GPX4 pathway in vitro and in vivo.Inflammopharmacology · 2026Article
- Siglec-1 upregulation and macrophage activation in age-related hearing loss: insights from integrated transcriptomic studies in mice and humans.Frontiers in cellular neuroscience · 2026Article
- Precision Diagnostics in Age-Related Hearing Loss: Emerging Molecular Biomarkers for Early Detection and Targeted Prevention.International journal of general medicine · 2026Review
- Peripheral adaptive immune remodeling associated with severe hearing loss in older adults: a single-center flow-cytometry study with mouse cochlear transcriptomic context.Frontiers in aging · 2026Article
- Cochlear endoplasmic reticulum stress causes connexin 26 degradation is involved in age-related hearing loss.iScience · 2025Article
- Review
- Ferroptosis and hearing loss: from molecular mechanisms to therapeutic interventions.Journal of enzyme inhibition and medicinal chemistry · 2025Review
- Prognostic Significance of Isolated Low-Frequency Hearing Loss: A Longitudinal Audiometric Study.Journal of clinical medicine · 2025Article
82 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Presbycusis, or age-related hearing loss (ARHL), occurs in most mammals with variations in the age of onset, rate of decline, and magnitude of degeneration in the central nervous system and inner ear. The affected cochlear structures include the stria vascularis and its vasculature, spiral ligament, sensory hair cells and auditory neurons. Dysfunction of the stria vascularis results in a reduced endocochlear potential. Without this potential, the cochlear amplification provided by the electro-motility of the outer hair cells is insufficient, and a high-frequency hearing-loss results. Degeneration of the sensory cells, especially the outer hair cells also leads to hearing loss due to lack of amplification. Neuronal degeneration, another hallmark of ARHL, most likely underlies difficulties with speech discrimination, especially in noisy environments. Noise exposure is a major cause of ARHL. It is well-known to cause sensory cell degeneration, especially the outer hair cells at the high frequency end of the cochlea. Even loud, but not uncomfortable, sound levels can lead to synaptopathy and ultimately neuronal degeneration. Even in the absence of a noisy environment, aged cells degenerate. This pathology most likely results from damage to mitochondria and contributes to degenerative changes in the stria vascularis, hair cells, and neurons. The genetic underpinnings of ARHL are still unknown and most likely involve various combinations of genes. At present, the only effective strategy for reducing ARHL is prevention of noise exposure. If future strategies can improve mitochondrial activity and reduce oxidative damage in old age, these should also bring relief.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.