ArticleHearing research2010
Separate and combined effects of Sod1 and Cdh23 mutations on age-related hearing loss and cochlear pathology in C57BL/6J mice.
Article in Hearing research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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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.
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Who cites it
33 citing papers in PubMed, 57 citations in OpenAlex.
- Foxg1 gene mutation impairs auditory cortex response and reduces sound tolerance.Cerebral cortex (New York, N.Y. : 1991) · 2025Article
- Protection from cisplatin-induced hearing loss with lentiviral vector-mediated ectopic expression of the anti-apoptotic protein BCL-XL.Molecular therapy. Nucleic acids · 2024Article
- Article
- Hearing impairment in murine model of Down syndrome.Frontiers in genetics · 2022Article
- The KEAP1-NRF2 System in Healthy Aging and Longevity.Antioxidants (Basel, Switzerland) · 2021Review
- Roles of Bak and Sirt3 in Paraquat-Induced Cochlear Hair Cell Damage.Neurotoxicity research · 2021Article
- Mitochondrial calcium uniporter is essential for hearing and hair cell preservation in congenic FVB/NJ mice.Scientific reports · 2021Article
- Age-Related Changes in the Cochlea and Vestibule: Shared Patterns and Processes.Frontiers in neuroscience · 2021Review
- Mechanistic Analysis of Age-Related Clinical Manifestations in Down Syndrome.Frontiers in aging neuroscience · 2021Article
- Activation of the NRF2 pathway in Keap1-knockdown mice attenuates progression of age-related hearing loss.NPJ aging and mechanisms of disease · 2020Article
- Can auditory brain stem response accurately reflect the cochlear function?Journal of neurophysiology · 2020Article
- Phenotypic characteristics of commonly used inbred mouse strains.Journal of molecular medicine (Berlin, Germany) · 2020Review
- Functional organization of mouse primary auditory cortex in adult C57BL/6 and F1 (CBAxC57) mice.Scientific reports · 2020Article
- Homeostatic maintenance and age-related functional decline in the Drosophila ear.Scientific reports · 2020Article
- Redox activation of excitatory pathways in auditory neurons as mechanism of age-related hearing loss.Redox biology · 2020Article
- Article
- N-acetylcysteine Treatment Reduces Age-related Hearing Loss and Memory Impairment in the Senescence-Accelerated Prone 8 (SAMP8) Mouse Model.Aging and disease · 2018Article
- Malformation of the Posterior Cerebellar Vermis Is a Common Neuroanatomical Phenotype of Genetically Engineered Mice on the C57BL/6 Background.Cerebellum (London, England) · 2018Article
- Hidden Age-Related Hearing Loss and Hearing Disorders: Current Knowledge and Future Directions.Hearing, balance and communication · 2018Article
- Effects of Cdh23 single nucleotide substitutions on age-related hearing loss in C57BL/6 and 129S1/Sv mice and comparisons with congenic strains.Scientific reports · 2017Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Both the ahl allele of Cdh23 and the null mutation of Sod1 have been shown to contribute to age-related hearing loss (AHL) in mice, but mixed strain backgrounds have confounded analyses of their individual and combined effects. To test for the effects of Sod1 deficiency independently from those of Cdh23(ahl), we produced mice with four digenic genotypes: Sod1(+/+)Cdh23(ahl)(/ahl), Sod1(+/+)Cdh23(+/+), Sod1(-/-)Cdh23(ahl)(/ahl), and Sod1(-/-)Cdh23(+/+), all on a uniform C57BL(/)6J strain background. We assessed hearing loss by ABR threshold measurements and evaluated cochlear pathologies in age-matched mice of each digenic combination. ABR analysis showed that Sod1(+/+)Cdh23(+/+) mice retain normal hearing up to 15 months of age and that hearing loss of Sod1(+/+)Cdh23(ahl)(/ahl) mice is more age and frequency dependent than that of Sod1(-/-)Cdh23(+/+) mice. ABR results also showed that mice with both gene mutations (Sod1(-/-)Cdh23(ahl)(/ahl)) exhibit the earliest onset and most severe hearing loss, greater than predicted for strictly additive effects. Histological analysis of cochleas showed that hair cell lesions are most severe in Sod1(-)(/-)Cdh23(ahl)(/ahl) mice followed closely by Sod1(+)(/+)Cdh23(ahl)(/ahl) mice and much smaller in Sod1(-)(/-)Cdh23(+)(/+) and Sod1(+)(/+)Cdh23(+)(/+) mice. Despite extensive damage to cochlear hair cells, vestibular hair cells appeared remarkably normal in all strains. Although both Sod1(-/-) and Cdh23(ahl)(/ahl) genotypes had strong effects on hearing loss, the Cdh23(ahl/ahl) genotype was primarily responsible for the increase in hair cell loss, suggesting that the two mutations have different underlying mechanisms of pathology.
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