Abstract
Hearing loss is a prevalent and growing health issue; currently, over 1.5 billion worldwide, approximately 20% of the global population, experience hearing loss, with the incidence of disabling hearing loss increasing with age. Presbycusis, also known as age-related hearing loss (ARHL), is the most prevalent type of sensory disorder among the elderly population, resulting in permanent sensorineural hearing loss. Presbycusis is characterized by bilateral hearing loss, particularly pronounced in high frequencies, resulting in psychophysical issues and a poor quality of life. It is well-defined that aging is associated with functional and morphological changes in the sensory organs, including the auditory system. Numerous studies show that epigenetic factors, in addition to genetics, are a potential risk factor for this complex disease. Here we present a study examining whether DNA methylation, an epigenetic modifier, is involved as a biomarker in Presbycusis. A Hospital-based cohort study of adults with presbycusis, comprising 55 ARHL subjects and 79 controls, was selected. Hearing measurements were used to determine the patients’ audioprofiles. A quantitative interrogation of methylation sites across the genome was achieved using the Illumina Infinium® Methylation EPIC Beadchip array. The C57BL/6J-Tnfrsf25 em1C/Cya was generated by CRISPR/Cas-mediated genome engineering to study the function of the tnfrsf25 gene and validate our preliminary findings. Our data demonstrate a strong correlation between patients’ audiometric thresholds and CpG sites methylation. Interestingly, CpG sites located in ESPN and TNFRSF25 show an increase in methylation at each hearing frequency as the patients' hearing declines.