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Gerontology ; 58(6): 490-6, 2012.
Article in English | MEDLINE | ID: mdl-22710288

ABSTRACT

Hearing loss is a common age-associated affliction that can result from the loss of hair cells and spiral ganglion neurons (SGNs) in the cochlea. Although hair cells and SGNs are typically lost in the same cochlea, recent analysis suggests that they can occur independently, via unique mechanisms. Research has identified both environmental and genetic factors that contribute to degeneration of cochlear cells. Additionally, molecular analysis has identified multiple cell-signaling mechanisms that likely contribute to pathological changes that result in hearing deficiencies. These analyses should serve as useful primers for future work, including genomic and proteomic analysis, to elucidate the mechanisms driving cell loss in the aging cochlea. Significant progress in this field has occurred in the past decade. As our understanding of aging-induced cochlear changes continues to improve, our ability to offer medical intervention will surely benefit the growing elderly population.


Subject(s)
Presbycusis , Aged , Animals , Calcium Signaling , Cell Death , Disease Models, Animal , Female , Glucocorticoids/metabolism , Glutamic Acid/metabolism , Gonadal Steroid Hormones/metabolism , Hair Cells, Auditory/pathology , Hair Cells, Auditory/physiology , Hearing Loss, Noise-Induced/etiology , Humans , Male , Middle Aged , Noise/adverse effects , Oxidative Stress , Presbycusis/etiology , Presbycusis/pathology , Presbycusis/physiopathology , Signal Transduction , Spiral Ganglion/pathology , Spiral Ganglion/physiopathology , Stress, Physiological
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