presbycusis/necrosis

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Pathologic changes of presbycusis begin in secondary processes and spread to primary processes of strial marginal cells.

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Strial atrophy underlying age-related hearing loss was investigated by ultrastructural comparisons in young and senescent gerbils. In young animals strial marginal cells (MCs) projected primary processes which gave rise to and were connected by numerous ultrathin secondary processes. In

Apoptosis-related genes change their expression with age and hearing loss in the mouse cochlea.

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To understand possible causative roles of apoptosis gene regulation in age-related hearing loss (presbycusis), apoptotic gene expression patterns in the CBA mouse cochlea of four different age and hearing loss groups were compared, using GeneChip and real-time (qPCR) microarrays. GeneChip

NADPH oxidase inhibitor apocynin decreases mitochondrial dysfunction and apoptosis in the ventral cochlear nucleus of D-galactose-induced aging model in rats.

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Presbycusis has become a common sensory deficit in humans. Oxidative damage to mitochondrial DNA and mitochondrial dysfunction is strongly associated with the aging of the auditory system. A previous study established a mimetic rat model of aging using D-galactose (D-gal) and first reported that

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