Abstract
Age-related hearing loss (ARHL) is the most common sensory disorder in the elderly population. SAMP8 mouse model presents accelerated senescence and has been identified as a model of gerontological research. SAMP8 displays a progressive age-related decline in brain function associated with a progressive hearing loss mimicking human aging memory deficits and ARHL. The molecular mechanisms associated with SAMP8 senescence process involve oxidative stress leading to chronic inflammation and apoptosis. Here, we studied the effect of N-acetylcysteine (NAC), an antioxidant, on SAMP8 hearing loss and memory to determine the potential interest of this model in the study of new antioxidant therapies. We observed a strong decrease of auditory brainstem response thresholds from 45 to 75 days of age and an increase of distortion product amplitudes from 60 to 75 days in NAC treated group compared to vehicle. Moreover, NAC treated group presented also an increase of memory performance at 60 and 105 days of age. These results confirm that NAC delays the senescence process by slowing the age-related hearing loss, protecting the cochlear hair cells and improving memory, suggesting that antioxidants could be a pharmacological target for age-related hearing and memory loss.
Highlights
Age-related hearing loss (ARHL) is the most common sensory disorder in the elderly population
We showed that NAC treatment improved memory in SAMP8 mice
We hypothesized that NAC reduced the overexpression of reactive oxygen species (ROS) produced by mitochondria leading to a reduction of cellular and mitochondrial damage and preventing cochlear hair cell and neuron apoptosis
Summary
Age-related hearing loss (ARHL) is the most common sensory disorder in the elderly population. The most common form of sensory impairment in elderly people is the age-related hearing loss (ARHL) [2]. This disorder is characterized by symmetric sensorineural hearing loss that starts at high frequencies with a prevalence of 35% of individuals over 65 years of age [3]. SAMP8 mice have been identified as suitable for use as models in gerontological research [7] This strain has been widely used in aging research to study phenotypes such as immune dysfunction, osteoporosis, and brain atrophy [6,7]. A recent study demonstrated that the molecular mechanisms associated with premature SAMP8 senescence involves oxidative stress, altered levels of anti-oxidant enzymes and decreased activity of Complexes I, II and IV which in turn lead to chronic inflammation and triggering of apoptotic cell death pathways [9]
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