ArticleAging cell2022
Cochlear Neurotrophin-3 overexpression at mid-life prevents age-related inner hair cell synaptopathy and slows age-related hearing loss.
Article in Aging cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- A single-nucleus transcriptomic atlas of human inner ear development.Nature neuroscience · 2026Article
- Neural Hearing Loss: Mechanisms, Diagnosis and Treatment Horizons.Journal of the Association for Research in Otolaryngology : JARO · 2026Review
- Advances in pathogenesis, novel therapeutic strategies and interventions for age-related hearing loss.Frontiers in molecular neuroscience · 2026Review
- Engineering exosomes in the treatment of sensorineural hearing loss: from basic research to clinical applications.Frontiers in molecular neuroscience · 2026Review
- TNFAIP8L2 maintains hair cell function and regulates age-related hearing loss via mTORC1 signaling.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Conditional Overexpression of Neuritin in Supporting Cell Protects Cochlear Hair Cell and Delays Age-Related Hearing Loss by Enhancing Autophagy.International journal of molecular sciences · 2025Article
- The differential expression profiles of miRNA in serum-derived exosomes and its potential role in age-related hearing loss.Frontiers in aging neuroscience · 2025Article
- Population coding of auditory space in the dorsal inferior colliculus persists with altered binaural cues.bioRxiv : the preprint server for biology · 2024Article
- From hidden hearing loss to supranormal auditory processing by neurotrophin 3-mediated modulation of inner hair cell synapse density.PLoS biology · 2024Article
- Eurycomanone fromJournal of clinical biochemistry and nutrition · 2024Article
- Oxidative Stress Plays an Important Role in Glutamatergic Excitotoxicity-Induced Cochlear Synaptopathy: Implication for Therapeutic Molecules Screening.Antioxidants (Basel, Switzerland) · 2024Article
- Age-related hearing loss: An updated and comprehensive review of the interventions.Iranian journal of basic medical sciences · 2024Review
- Candidate Key Proteins in Tinnitus: A Bioinformatic Study of Synaptic Transmission in Spiral Ganglion Neurons.Cellular and molecular neurobiology · 2023Article
- Neural Degeneration in Normal-Aging Human Cochleas: Machine-Learning Counts and 3D Mapping in Archival Sections.Journal of the Association for Research in Otolaryngology : JARO · 2023Article
- Regeneration of Hair Cells from Endogenous Otic Progenitors in the Adult Mammalian Cochlea: Understanding Its Origins and Future Directions.International journal of molecular sciences · 2023Review
- Progress on mechanisms of age-related hearing loss.Frontiers in neuroscience · 2023Review
- Cochlear Neurotrophin-3 overexpression at mid-life prevents age-related inner hair cell synaptopathy and slows age-related hearing loss.Aging cell · 2022Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Age-related hearing loss (ARHL) is the most prevalent sensory deficit in the elderly. This progressive pathology often has psychological and medical comorbidities, including social isolation, depression, and cognitive decline. Despite ARHL's enormous societal and economic impact, no therapies to prevent or slow its progression exist. Loss of synapses between inner hair cells (IHCs) and spiral ganglion neurons (SGNs), a.k.a. IHC synaptopathy, is an early event in cochlear aging, preceding neuronal and hair cell loss. To determine if age-related IHC synaptopathy can be prevented, and if this impacts the time-course of ARHL, we tested the effects of cochlear overexpression of neurotrophin-3 (Ntf3) starting at middle age. We chose Ntf3 because this neurotrophin regulates the formation of IHC-SGN synapses in the neonatal period. We now show that triggering Ntf3 overexpression by IHC supporting cells starting in middle age rapidly increases the amplitude of sound-evoked neural potentials compared with age-matched controls, indicating that Ntf3 produces a positive effect on cochlear function when the pathology is minimal. Furthermore, near the end of their lifespan, Ntf3-overexpressing mice have milder ARHL, with larger sound-evoked potentials along the ascending auditory pathway and reduced IHC synaptopathy compared with age-matched controls. Our results also provide evidence that an age-related decrease in cochlear Ntf3 expression contributes to ARHL and that Ntf3 supplementation could serve as a therapeutic for this prevalent disorder. Furthermore, these findings suggest that factors that regulate synaptogenesis during development could prevent age-related synaptopathy in the brain, a process involved in several central nervous system degenerative disorders.
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