Age-related deafness, or age-related deafness, is the most common disorder of the human auditory system. The prevalence of deafness increases significantly with age, with 25% of people in the 50-65 age group having a hearing threshold greater than 30 dB in at least one ear. more than one-third of people aged 65 and older have symptoms of hearing loss, and one-half of the population aged 75 and older have symptoms. Despite the high prevalence of deafness, the biological mechanisms of age-related deafness remain unclear. Age-related deafness is a complex disease that is influenced by environmental and genetic factors. The current view is that degenerative changes in the cochlear Corti’s apparatus, afferent neurons and vascular striae lead to different types of age-related deafness: sensorineural, neurological, and vascular. 50% of patients with age-related deafness have a single type of deafness, 25% have a mixture of two or more types, and another 25% have pathological changes that are not associated with the type of hearing loss. correlate with the type of hearing loss. The different histopathological changes indirectly suggest a genetic heterogeneity in the etiology of age-related deafness and the involvement of environmental factors in its development. The environmental aspects associated with age-related deafness have been well studied, but the genetic risk factors associated with it remain to be clarified. Although some degree of senile deafness is attributed to environmental exposures, it is estimated that 35-55% of sensorineural senile deafness is attributed to genetic alterations, an idea derived from a Swedish study that found a clear familial aggregation of senile deafness. In terms of genetic studies, experimental animal studies have found that geriatric deafness susceptibility arises as a result of a combination of germline specific genetic characteristics including Cdh23, mitochondrial DNA and Ahl2 genes. Foreign scholars have confirmed that in rodents, mitochondrial deletion: mtDNA4,834 deletion is thought to be associated with senile deafness. A similar deletion was found in the temporal bone pool of human patients with senile deafness: mtDNA4,977. Loss of antioxidant substances is also involved in the aging process, and enzymes related to glutathione metabolism are antioxidant enzymes in the cochlea. Variations in the gene expression products of the enzyme family related to glutathione metabolism can also lead to increased susceptibility to senile deafness. Research on the genetics of age-related deafness is being conducted intensively in many countries, including China, and no breakthrough findings have been made yet. It is expected that one day, the genetic mechanism of senile deafness will be elucidated and people will be able to predict whether they have genetic susceptibility to senile deafness through genetic testing, so that early prevention can be carried out.