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      Impact of Aging on the Auditory System and Related Cognitive Functions: A Narrative Review

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          Abstract

          Age-related hearing loss (ARHL), presbycusis, is a chronic health condition that affects approximately one-third of the world's population. The peripheral and central hearing alterations associated with age-related hearing loss have a profound impact on perception of verbal and non-verbal auditory stimuli. The high prevalence of hearing loss in the older adults corresponds to the increased frequency of dementia in this population. Therefore, researchers have focused their attention on age-related central effects that occur independent of the peripheral hearing loss as well as central effects of peripheral hearing loss and its association with cognitive decline and dementia. Here we review the current evidence for the age-related changes of the peripheral and central auditory system and the relationship between hearing loss and pathological cognitive decline and dementia. Furthermore, there is a paucity of evidence on the relationship between ARHL and established biomarkers of Alzheimer's disease, as the most common cause of dementia. Such studies are critical to be able to consider any causal relationship between dementia and ARHL. While this narrative review will examine the pathophysiological alterations in both the peripheral and central auditory system and its clinical implications, the question remains unanswered whether hearing loss causes cognitive impairment or vice versa.

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          Dementia prevention, intervention, and care

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            The role of oxidative stress in noise-induced hearing loss.

            Modern research has provided new insights into the biological mechanisms of noise-induced hearing loss, and with these new insights comes hope for possible prevention or treatment. Underlying the classic set of cochlear pathologies that occur as a result of noise exposure are increased levels of reactive oxygen species (ROS) that play a significant role in noise-induced hair cell death. Both necrotic and apoptotic cell death have been identified in the cochlea. Included in the current review is a brief review of ROS, along with a description of sources of cochlear ROS generation and how ROS can damage cochlear tissue. The pathways of necrotic and apoptotic cell death are also reviewed. Interventions are discussed that target the prevention of noise-induced hair cell death: the use of antioxidants to scavenge and eliminate the damaging ROS, pharmacological interventions to limit the damage resulting from ROS, and new techniques aimed at interrupting the apoptotic biochemical cascade that results in the death of irreplaceable hair cells.
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              Noise-induced cochlear neuropathy is selective for fibers with low spontaneous rates.

              Acoustic overexposure can cause a permanent loss of auditory nerve fibers without destroying cochlear sensory cells, despite complete recovery of cochlear thresholds (Kujawa and Liberman 2009), as measured by gross neural potentials such as the auditory brainstem response (ABR). To address this nominal paradox, we recorded responses from single auditory nerve fibers in guinea pigs exposed to this type of neuropathic noise (4- to 8-kHz octave band at 106 dB SPL for 2 h). Two weeks postexposure, ABR thresholds had recovered to normal, while suprathreshold ABR amplitudes were reduced. Both thresholds and amplitudes of distortion-product otoacoustic emissions fully recovered, suggesting recovery of hair cell function. Loss of up to 30% of auditory-nerve synapses on inner hair cells was confirmed by confocal analysis of the cochlear sensory epithelium immunostained for pre- and postsynaptic markers. In single fiber recordings, at 2 wk postexposure, frequency tuning, dynamic range, postonset adaptation, first-spike latency and its variance, and other basic properties of auditory nerve response were all completely normal in the remaining fibers. The only physiological abnormality was a change in population statistics suggesting a selective loss of fibers with low- and medium-spontaneous rates. Selective loss of these high-threshold fibers would explain how ABR thresholds can recover despite such significant noise-induced neuropathy. A selective loss of high-threshold fibers may contribute to the problems of hearing in noisy environments that characterize the aging auditory system.
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                Author and article information

                Contributors
                Journal
                Front Neurosci
                Front Neurosci
                Front. Neurosci.
                Frontiers in Neuroscience
                Frontiers Media S.A.
                1662-4548
                1662-453X
                05 March 2018
                2018
                : 12
                : 125
                Affiliations
                [1] 1Clinical Research, Ear Science Institute Australia , Subiaco, WA, Australia
                [2] 2School of Surgery, University of Western Australia , Perth, WA, Australia
                [3] 3School of Medicine, University of Notre Dame Australia , Fremantle, WA, Australia
                [4] 4Biomedical Sciences, Macquarie University , Sydney, NSW, Australia
                [5] 5School of Medical and Health Sciences, Edith Cowan University , Joondalup, WA, Australia
                Author notes

                Edited by: Stefano L. Sensi, Università degli Studi G. d'Annunzio Chieti e Pescara, Italy

                Reviewed by: Aurel Popa-Wagner, University of Rostock, Germany; Cristina Sanchez-Castañeda, University of Barcelona, Spain

                *Correspondence: Hamid R. Sohrabi h.sohrabi@ 123456ecu.edu.au

                This article was submitted to Neurodegeneration, a section of the journal Frontiers in Neuroscience

                Article
                10.3389/fnins.2018.00125
                5844959
                29556173
                dfabd30c-219a-43c2-a2e2-86f1b43ccb6a
                Copyright © 2018 Jayakody, Friedland, Martins and Sohrabi.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 18 September 2017
                : 15 February 2018
                Page count
                Figures: 2, Tables: 0, Equations: 0, References: 252, Pages: 16, Words: 15480
                Categories
                Neuroscience
                Review

                Neurosciences
                age-related hearing loss,presbycusis,aging,auditory system,cognitive functions,dementia
                Neurosciences
                age-related hearing loss, presbycusis, aging, auditory system, cognitive functions, dementia

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