title: Molecular mechanisms of age-related hearing loss.
abstract: Age-related hearing loss, known as presbyacusis, is characterized by the progressive deterioration of auditory sensitivity associated with aging and is the most common cause of adult auditory deficiency in the United States. Presbyacusis is defined as a progressive, bilateral, high-frequency hearing loss that is manifested on audiometric assessment by a moderately sloping pure tone audiogram. This condition affects approximately 23% of the population between 65 and 75 years of age and 40% of the population older than 75 years of age. In 1980, it was estimated that 11% of the population was 76 years or older and this number is expected to nearly double by the year 2030 [, Otolaryngol. Head Neck Surg. 100, 262]. When coupled with the fact that the population over 65 years of age is experiencing the most rapid progression of hearing loss, the potential socioeconomic ramifications are staggering. Interestingly, presbyacusis varies in its frequency across differing societies. This discrepancy has been attributed to many factors such as genetics, diet, socioeconomic factors, and environmental variables [, Otolaryngol. Head Neck Surg. 100, 266;. Scand. Audiol. 26 (1997) 133]. The purpose of this discussion is to illuminate the various molecular mechanisms underlying this age-related hearing loss and to offer insights into potential ways to mitigate the effects of aging on hearing impairment.
authors.affiliation: Department of Otolaryngology, Head & Neck Surgery, Department of Otolaryngology, Division Otologic/Neurotologic Surgery, Henry Ford Hospital System, Complementary/Integrative Medicine, 6777 W. Maple Rd, W. Bloomfield, MI 48323, USA. mseidma1@hfhs.org
authors.forename: Michael D
authors.initials: MD
authors.lastname: Seidman
authors.forename: Nadir
authors.initials: N
authors.lastname: Ahmad
authors.forename: Uma
authors.initials: U
authors.lastname: Bai
mesh_terms: D000375:Aging / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D000818:Animals; D016922:Cellular Senescence; D006801:Humans; D008928:Mitochondria / Q000235:genetics / Q000502:physiology*; D009154:Mutation / Q000502:physiology; D011304:Presbycusis / Q000178:diet therapy / Q000209:etiology* / Q000235:genetics / Q000473:pathology