Current concepts in age-related hearing loss: Epidemiology and mechanistic pathways

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Abstract

Age-related hearing loss (AHL), also known as presbycusis, is a universal feature of mammalian aging and is characterized by a decline of auditory function, such as increased hearing thresholds and poor frequency resolution. The primary pathology of AHL includes the hair cells, stria vascularis, and afferent spiral ganglion neurons as well as the central auditory pathways. A growing body of evidence in animal studies has suggested that cumulative effect of oxidative stress could induce damage to macromolecules such as mitochondrial DNA (mtDNA) and that the resulting accumulation of mtDNA mutations/deletions and decline of mitochondrial function play an important role in inducing apoptosis of the cochlear cells, thereby the development of AHL. Epidemiological studies have demonstrated four categories of risk factors of AHL in humans: cochlear aging, environment such as noise exposure, genetic predisposition, and health co-morbidities such as cigarette smoking and atherosclerosis. Genetic investigation has identified several putative associating genes, including those related to antioxidant defense and atherosclerosis. Exposure to noise is known to induce excess generation of reactive oxygen species (ROS) in the cochlea, and cumulative oxidative stress can be enhanced by relatively hypoxic situations resulting from the impaired homeostasis of cochlear blood supply due to atherosclerosis, which could be accelerated by genetic and co-morbidity factors. Antioxidant defense system may also be influenced by genetic backgrounds. These may explain the large variations of the onset and extent of AHL among elderly subjects.

This article is part of a Special Issue entitled “Annual Reviews 2013”.

Highlights

▸ We did comprehensive review of human and animal studies of age-related hearing loss. ▸ Epidemiologic studies indicated four categories of risk factors. ▸ Genetic investigation identified several associating genes. ▸ Animal studies supported the role of oxidative stress and mitochondrial dysfunction. ▸ We proposed conceptual model of the development of AHL.

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