Abstract
BackgroundSensorineural hearing loss is one of the most common sensory deficiencies. However, the molecular contribution to age-related hearing loss is not fully elucidated.MethodsWe performed genome-wide association studies (GWAS) for hearing loss-related traits in the UK Biobank (N = 362,396) and selected a high confidence set of ten hearing-associated gene products for staining in human cochlear samples: EYA4, LMX1A, PTK2/FAK, UBE3B, MMP2, SYNJ2, GRM5, TRIOBP, LMO-7, and NOX4.ResultsAll proteins were found to be expressed in human cochlear structures. Our findings illustrate cochlear structures that mediate mechano-electric transduction of auditory stimuli, neuronal conductance, and neuronal plasticity to be involved in age-related hearing loss.ConclusionsOur results suggest common genetic variation to influence structural resilience to damage as well as cochlear recovery after trauma, which protect against accumulated damage to cochlear structures and the development of hearing loss over time.
Highlights
Sensorineural hearing loss is one of the most common sensory deficiencies
Genome-wide association analyses Cohort characteristics and summaries of the phenotypic data are presented in Additional file 1: Table 1 [10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41,42,43,44,45,46,47,48,49,50,51,52,53,54,55,56,57,58,59,60,61,62,63,64,65,66,67,68,69,70,71,72,73,74,75,76,77,78,79,80,81,82,83,84,85,86,87,88,89,90,91,92,93,94,95,96,97,98,99,100,101,102,103,104,105,106,107,108,109,110,111,112,113,114,115]
There were no indications of genomic inflation for all genome-wide association studies (GWAS) except for tinnitus, which indicates that genomic inflation due to stratification may be present in this dataset (Additional file 1: Table 2)
Summary
Sensorineural hearing loss is one of the most common sensory deficiencies. the molecular contribution to age-related hearing loss is not fully elucidated. The most common form of hearing loss, which represents 90% of all cases, is related to the degenerative effects of aging on hearing, i.e., age-related hearing loss or presbycusis. This is followed by inflammatory disease of the middle ear (otitis media) and congenital anomalies such as non-syndromic deafness due to genetic factors [1] as the most common causes. The molecular mechanisms that underlie the development of hearing loss and individual variation in risk are poorly elucidated. The genetic factors that influence variation in risk, emergence, and progression of age-related hearing loss in the general population are poorly characterized
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