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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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      Frailty in Older Adults: Evidence for a Phenotype

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        Clinical and biomarker changes in dominantly inherited Alzheimer's disease.

        The order and magnitude of pathologic processes in Alzheimer's disease are not well understood, partly because the disease develops over many years. Autosomal dominant Alzheimer's disease has a predictable age at onset and provides an opportunity to determine the sequence and magnitude of pathologic changes that culminate in symptomatic disease. In this prospective, longitudinal study, we analyzed data from 128 participants who underwent baseline clinical and cognitive assessments, brain imaging, and cerebrospinal fluid (CSF) and blood tests. We used the participant's age at baseline assessment and the parent's age at the onset of symptoms of Alzheimer's disease to calculate the estimated years from expected symptom onset (age of the participant minus parent's age at symptom onset). We conducted cross-sectional analyses of baseline data in relation to estimated years from expected symptom onset in order to determine the relative order and magnitude of pathophysiological changes. Concentrations of amyloid-beta (Aβ)(42) in the CSF appeared to decline 25 years before expected symptom onset. Aβ deposition, as measured by positron-emission tomography with the use of Pittsburgh compound B, was detected 15 years before expected symptom onset. Increased concentrations of tau protein in the CSF and an increase in brain atrophy were detected 15 years before expected symptom onset. Cerebral hypometabolism and impaired episodic memory were observed 10 years before expected symptom onset. Global cognitive impairment, as measured by the Mini-Mental State Examination and the Clinical Dementia Rating scale, was detected 5 years before expected symptom onset, and patients met diagnostic criteria for dementia at an average of 3 years after expected symptom onset. We found that autosomal dominant Alzheimer's disease was associated with a series of pathophysiological changes over decades in CSF biochemical markers of Alzheimer's disease, brain amyloid deposition, and brain metabolism as well as progressive cognitive impairment. Our results require confirmation with the use of longitudinal data and may not apply to patients with sporadic Alzheimer's disease. (Funded by the National Institute on Aging and others; DIAN ClinicalTrials.gov number, NCT00869817.).
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          What is cognitive reserve? Theory and research application of the reserve concept.

           Yaakov Stern (2002)
          The idea of reserve against brain damage stems from the repeated observation that there does not appear to be a direct relationship between the degree of brain pathology or brain damage and the clinical manifestation of that damage. This paper attempts to develop a coherent theoretical account of reserve. One convenient subdivision of reserve models revolves around whether they envision reserve as a passive process, such as in brain reserve or threshold, or see the brain as actively attempting to cope with or compensate for pathology, as in cognitive reserve. Cognitive reserve may be based on more efficient utilization of brain networks or of enhanced ability to recruit alternate brain networks as needed. A distinction is suggested between reserve, the ability to optimize or maximize normal performance, and compensation, an attempt to maximize performance in the face of brain damage by using brain structures or networks not engaged when the brain is not damaged. Epidemiologic and imaging data that help to develop and support the concept of reserve are presented.
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            Author and article information

            Affiliations
            1Clinical Research, Ear Science Institute Australia , Subiaco, WA, Australia
            2School of Surgery, University of Western Australia , Perth, WA, Australia
            3School of Medicine, University of Notre Dame Australia , Fremantle, WA, Australia
            4Biomedical Sciences, Macquarie University , Sydney, NSW, Australia
            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

            Contributors
            Journal
            Front Neurosci
            Front Neurosci
            Front. Neurosci.
            Frontiers in Neuroscience
            Frontiers Media S.A.
            1662-4548
            1662-453X
            05 March 2018
            2018
            : 12
            5844959
            10.3389/fnins.2018.00125
            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.

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            Figures: 2, Tables: 0, Equations: 0, References: 252, Pages: 16, Words: 15480
            Categories
            Neuroscience
            Review

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