Abstract

Age-related hearing loss (AHL), also known as presbycusis, is one of the most prevalent chronic degenerative conditions; it progresses with age and affects tens of millions of the elderly worldwide. It is characterized by a decline in auditory function, which is reflected by higher hearing thresholds and poor frequency resolution [1], resulting in the inability to understand words and making it difficult to understand everyday language. The primary pathology of AHL includes the loss of sensory hair cells and spiral ganglion neurons, and strial atrophy [2], in addition to degeneration of the central auditory pathways. AHL is caused by the interaction of multiple factors and shows large variations in the onset and extent of hearing loss. These multiple factors complicate the interpretation of basic and clinical research in AHL [3]. Human epidemiological studies have identified four risk factor categories for AHL, including cochlear aging (individual age), environment (occupational and leisure noise exposure, ototoxic medications, socioeconomic status), genetic predisposition (sex, race, specific genetic loci/genes), and health comorbidities (hypertension, diabetes, stroke, cigarette smoking) [4-6]. Genetic investigation has identified several putative gene associations, including with genes related to antioxidant defense systems, such as glutathione S-transferase and atherosclerosis.