The Experts below are selected from a list of 1233 Experts worldwide ranked by ideXlab platform
John H. Mills - One of the best experts on this subject based on the ideXlab platform.
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Presbycusis.
The Lancet, 2005Co-Authors: George A. Gates, John H. MillsAbstract:The inevitable deterioration in hearing ability that occurs with age--presbycusis--is a multifactorial process that can vary in severity from mild to substantial. Left untreated, presbycusis of a moderate or greater degree affects communication and can contribute to isolation, depression, and, possibly, dementia. These psychological effects are largely reversible with rehabilitative treatment. Comprehensive rehabilitation is widely available but underused because, in part, of social attitudes that undervalue hearing, in addition to the cost and stigma of hearing aids. Remediation of presbycusis is an important contributor to quality of life in geriatric medicine and can include education about communication effectiveness, hearing aids, assistive listening devices, and cochlear implants for severe hearing loss. Primary care physicians should screen and refer their elderly patients for assessment and remediation. Where hearing aids no longer provide benefit, cochlear implantation is the treatment of choice with excellent results even in octogenarians.
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Analysis of Blood Chemistry and Hearing Levels in a Sample of Older Persons
Ear and Hearing, 1998Co-Authors: Fu-shing Lee, Lois J. Matthews, John H. Mills, Judy R. Dubno, Warren Y. AdkinsAbstract:Objective:As part of an ongoing study of Presbyacusis, the relationship between blood chemistry levels and hearing levels was investigated. Previous reports often used small sets of blood chemistry measures, and results were inconclusive. This experiment examined hearing levels and 27 measures of bl
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Presbyacusis: An overview
The Journal of the Acoustical Society of America, 1993Co-Authors: John H. MillsAbstract:Presbyacusis is defined operationally as age‐related hearing loss. It is a common problem and will become even more prevalent in the future. Age‐related histopathological changes have been discovered at nearly every location in the aging auditory system from the external ear to the cochlea to the auditory brainstem and temporal lobe. Even for a given person, histopathology can be observed at multiple sites. Moreover, for individual human subjects it remains difficult, if not impossible, to separate age‐related hearing loss from hearing loss caused by exposure to noise and other ototoxic agents (sociocusis), or from hearing loss caused by other disease processes (nosoacusis). Most of the research on Presbyacusis can be placed into three categories: cross‐sectional epidemiologic (audiometric surveys) studies; clinical studies with the emphasis on histopathology of the cochlea, psychophysics, and speech perception; and most recently, there have been a number of efforts to develop an animal model (mouse, rat,...
Judy R. Dubno - One of the best experts on this subject based on the ideXlab platform.
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Translational and interdisciplinary insights into Presbyacusis: A multidimensional disease.
Hearing research, 2020Co-Authors: Mark A. Eckert, Kelly C. Harris, Hainan Lang, Morag A. Lewis, Richard A. Schmiedt, Bradley A. Schulte, Karen P. Steel, Kenneth I. Vaden, Judy R. DubnoAbstract:Abstract There are multiple etiologies and phenotypes of age-related hearing loss or Presbyacusis. In this review we summarize findings from animal and human studies of Presbyacusis, including those that provide the theoretical framework for distinct metabolic, sensory, and neural Presbyacusis phenotypes. A key finding in quiet-aged animals is a decline in the endocochlear potential (EP) that results in elevated pure-tone thresholds across frequencies with greater losses at higher frequencies. In contrast, sensory Presbyacusis appears to derive, in part, from acute and cumulative effects on hair cells of a lifetime of environmental exposures (e.g., noise), which often result in pronounced high frequency hearing loss. These patterns of hearing loss in animals are recognizable in the human audiogram and can be classified into metabolic and sensory Presbyacusis phenotypes, as well as a mixed metabolic+sensory phenotype. However, the audiogram does not fully characterize age-related changes in auditory function. Along with the effects of peripheral auditory system declines on the auditory nerve, primary degeneration in the spiral ganglion also appears to contribute to central auditory system aging. These inner ear alterations often correlate with structural and functional changes throughout the central nervous system and may explain suprathreshold speech communication difficulties in older adults with hearing loss. Throughout this review we highlight potential methods and research directions, with the goal of advancing our understanding, prevention, diagnosis, and treatment of Presbyacusis.
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Oxford Medicine Online - Histopathological aspects of Presbyacusis
Oxford Medicine Online, 2018Co-Authors: Paul R. Lambert, Judy R. DubnoAbstract:This chapter discusses Schuknecht and Gacek’s 1993 paper on histopathological aspects of Presbyacusis including the design of the study (outcome measures, results, conclusions, and a critique).
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Characterizing individual differences: Audiometric phenotypes of age-related hearing loss
2015Co-Authors: Judy R. DubnoAbstract:Metabolic Presbyacusis, or the degeneration of the cochlear lateral wall and decline of the endocochlear potential, largely accounts for age-related threshold elevations observed in laboratory animals raised in quiet and may underlie the characteristic audiogram of older humans. The “audiometric phenotype” associated with metabolic Presbyacusis differs from audiograms associated with sensory losses resulting from ototoxic drug and noise exposures. Evidence supporting metabolic and sensory phenotypes in audiograms from older adults can be derived from demographic information (age, gender), environmental exposures (noise and ototoxic drug histories), and stability or changes in audiometric phenotypes as individuals age. When confirmed with biological markers and longitudinal analyses, well-defined audiometric phenotypes of human age-related hearing loss can contribute to explanations of individual differences in auditory function for older adults.
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Age-related changes of myelin basic protein in mouse and human auditory nerve.
PloS one, 2012Co-Authors: Yazhi Xing, Judy R. Dubno, Bradley A. Schulte, Devadoss J. Samuvel, Shawn M. Stevens, Hainan LangAbstract:Age-related hearing loss (Presbyacusis) is the most common type of hearing impairment. One of the most consistent pathological changes seen in Presbyacusis is the loss of spiral ganglion neurons (SGNs). Defining the cellular and molecular basis of SGN degeneration in the human inner ear is critical to gaining a better understanding of the pathophysiology of Presbyacusis. However, information on age-related cellular and molecular alterations in the human spiral ganglion remains scant, owing to the very limited availably of human specimens suitable for high resolution morphological and molecular analysis. This study aimed at defining age-related alterations in the auditory nerve in human temporal bones and determining if immunostaining for myelin basic protein (MBP) can be used as an alternative approach to electron microscopy for evaluating myelin degeneration. For comparative purposes, we evaluated ultrastructural alternations and changes in MBP immunostaining in aging CBA/CaJ mice. We then examined 13 temporal bones from 10 human donors, including 4 adults aged 38–46 years (middle-aged group) and 6 adults aged 63–91 years (older group). Similar to the mouse, intense immunostaining of MBP was present throughout the auditory nerve of the middle-aged human donors. Significant declines in MBP immunoreactivity and losses of MBP+ auditory nerve fibers were observed in the spiral ganglia of both the older human and aged mouse ears. This study demonstrates that immunostaining for MBP in combination with confocal microscopy provides a sensitive, reliable, and efficient method for assessing alterations of myelin sheaths in the auditory nerve. The results also suggest that myelin degeneration may play a critical role in the SGN loss and the subsequent decline of the auditory nerve function in Presbyacusis.
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Analysis of Blood Chemistry and Hearing Levels in a Sample of Older Persons
Ear and Hearing, 1998Co-Authors: Fu-shing Lee, Lois J. Matthews, John H. Mills, Judy R. Dubno, Warren Y. AdkinsAbstract:Objective:As part of an ongoing study of Presbyacusis, the relationship between blood chemistry levels and hearing levels was investigated. Previous reports often used small sets of blood chemistry measures, and results were inconclusive. This experiment examined hearing levels and 27 measures of bl
Hainan Lang - One of the best experts on this subject based on the ideXlab platform.
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Translational and interdisciplinary insights into Presbyacusis: A multidimensional disease.
Hearing research, 2020Co-Authors: Mark A. Eckert, Kelly C. Harris, Hainan Lang, Morag A. Lewis, Richard A. Schmiedt, Bradley A. Schulte, Karen P. Steel, Kenneth I. Vaden, Judy R. DubnoAbstract:Abstract There are multiple etiologies and phenotypes of age-related hearing loss or Presbyacusis. In this review we summarize findings from animal and human studies of Presbyacusis, including those that provide the theoretical framework for distinct metabolic, sensory, and neural Presbyacusis phenotypes. A key finding in quiet-aged animals is a decline in the endocochlear potential (EP) that results in elevated pure-tone thresholds across frequencies with greater losses at higher frequencies. In contrast, sensory Presbyacusis appears to derive, in part, from acute and cumulative effects on hair cells of a lifetime of environmental exposures (e.g., noise), which often result in pronounced high frequency hearing loss. These patterns of hearing loss in animals are recognizable in the human audiogram and can be classified into metabolic and sensory Presbyacusis phenotypes, as well as a mixed metabolic+sensory phenotype. However, the audiogram does not fully characterize age-related changes in auditory function. Along with the effects of peripheral auditory system declines on the auditory nerve, primary degeneration in the spiral ganglion also appears to contribute to central auditory system aging. These inner ear alterations often correlate with structural and functional changes throughout the central nervous system and may explain suprathreshold speech communication difficulties in older adults with hearing loss. Throughout this review we highlight potential methods and research directions, with the goal of advancing our understanding, prevention, diagnosis, and treatment of Presbyacusis.
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Age-dependent alterations of Kir4.1 expression in neural crest-derived cells of the mouse and human cochlea.
Neurobiology of aging, 2019Co-Authors: Ting Liu, Bradley A. Schulte, Kenyaria V. Noble, Jeremy L. Barth, Hainan LangAbstract:Abstract Age-related hearing loss (or Presbyacusis) is a progressive pathophysiological process. This study addressed the hypothesis that degeneration/dysfunction of multiple nonsensory cell types contributes to Presbyacusis by evaluating tissues obtained from young and aged CBA/CaJ mouse ears and human temporal bones. Ultrastructural examination and transcriptomic analysis of mouse cochleas revealed age-dependent pathophysiological alterations in 3 types of neural crest–derived cells, namely intermediate cells in the stria vascularis, outer sulcus cells in the cochlear lateral wall, and satellite cells in the spiral ganglion. A significant decline in immunoreactivity for Kir4.1, an inwardly rectifying potassium channel, was seen in strial intermediate cells and outer sulcus cells in the ears of older mice. Age-dependent alterations in Kir4.1 immunostaining also were observed in satellite cells ensheathing spiral ganglion neurons. Expression alterations of Kir4.1 were observed in these same cell populations in the aged human cochlea. These results suggest that degeneration/dysfunction of neural crest–derived cells maybe an important contributing factor to both metabolic and neural forms of Presbyacusis.
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Age-related changes of myelin basic protein in mouse and human auditory nerve.
PloS one, 2012Co-Authors: Yazhi Xing, Judy R. Dubno, Bradley A. Schulte, Devadoss J. Samuvel, Shawn M. Stevens, Hainan LangAbstract:Age-related hearing loss (Presbyacusis) is the most common type of hearing impairment. One of the most consistent pathological changes seen in Presbyacusis is the loss of spiral ganglion neurons (SGNs). Defining the cellular and molecular basis of SGN degeneration in the human inner ear is critical to gaining a better understanding of the pathophysiology of Presbyacusis. However, information on age-related cellular and molecular alterations in the human spiral ganglion remains scant, owing to the very limited availably of human specimens suitable for high resolution morphological and molecular analysis. This study aimed at defining age-related alterations in the auditory nerve in human temporal bones and determining if immunostaining for myelin basic protein (MBP) can be used as an alternative approach to electron microscopy for evaluating myelin degeneration. For comparative purposes, we evaluated ultrastructural alternations and changes in MBP immunostaining in aging CBA/CaJ mice. We then examined 13 temporal bones from 10 human donors, including 4 adults aged 38–46 years (middle-aged group) and 6 adults aged 63–91 years (older group). Similar to the mouse, intense immunostaining of MBP was present throughout the auditory nerve of the middle-aged human donors. Significant declines in MBP immunoreactivity and losses of MBP+ auditory nerve fibers were observed in the spiral ganglia of both the older human and aged mouse ears. This study demonstrates that immunostaining for MBP in combination with confocal microscopy provides a sensitive, reliable, and efficient method for assessing alterations of myelin sheaths in the auditory nerve. The results also suggest that myelin degeneration may play a critical role in the SGN loss and the subsequent decline of the auditory nerve function in Presbyacusis.
Stefan Stenfelt - One of the best experts on this subject based on the ideXlab platform.
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Effect of metabolic Presbyacusis on cochlear responses: a simulation approach using a physiologically-based model.
The Journal of the Acoustical Society of America, 2013Co-Authors: Amin Saremi, Stefan StenfeltAbstract:In the presented model, electrical, acoustical, and mechanical elements of the cochlea are explicitly integrated into a signal transmission line where these elements convey physiological interpretations of the human cochlear structures. As a result, this physiologically-motivated model enables simulation of specific cochlear lesions such as Presbyacusis. The hypothesis is that high-frequency hearing loss in older adults may be due to metabolic Presbyacusis whereby age-related cellular/chemical degenerations in the lateral wall of the cochlea cause a reduction in the endocochlear potential. The simulations quantitatively confirm this hypothesis and emphasize that even if the outer and inner hair cells are totally active and intact, metabolic Presbyacusis alone can significantly deteriorate the cochlear functionality. Specifically, in the model, as the endocochlear potential decreases, the transduction mechanism produces less receptor current such that there is a reduction in the battery of the somatic motor. This leads to a drastic decrease in cochlear amplification and frequency sensitivity, as well as changes in position-frequency map (tuning pattern) of the cochlea. In addition, the simulations show that the age-related reduction of the endocochlear potential significantly inhibits the firing rate of the auditory nerve which might contribute to the decline of temporal resolution in the aging auditory system.
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How differently noise exposure and metabolic Presbyacusis affect the cochlear response. A simulation approach using a physiologically-based model of the human cochlea
2013Co-Authors: Amin Saremi, Stefan StenfeltAbstract:How differently noise exposure and metabolic Presbyacusis affect the cochlear response. A simulation approach using a physiologically-based model of the human cochlea
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Simulation of Presbyacusis by a physiological signal transmission model of the human cochlea
2012Co-Authors: Amin Saremi, Stefan StenfeltAbstract:Simulation of Presbyacusis by a physiological signal transmission model of the human cochlea
Jing Wang - One of the best experts on this subject based on the ideXlab platform.
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Oxidative stress, inflammation, and autophagic stress as the key mechanisms of premature age-related hearing loss in SAMP8 mouse cochlea
Antioxidants and Redox Signaling, 2012Co-Authors: Julien Menardo, Yong Tang, Sabine Ladrech, Francois Casas, Christophe Michel, Jérôme Bourien, Jérôme Ruel, Guy Rebillard, Tangui Maurice, Jing WangAbstract:AIMS: In our aging society, age-related hearing loss (ARHL) or presbycusis is increasingly important. Here, we study the mechanism of ARHL using the senescence-accelerated mouse prone 8 (SAMP8) which is a useful model to probe the effects of aging on biological processes. RESULTS: We found that the SAMP8 strain displays premature hearing loss and cochlear degeneration recapitulating the processes observed in human presbycusis (i.e., strial, sensory, and neural degeneration). The molecular mechanisms associated with premature ARHL in SAMP8 mice involve oxidative stress, altered levels of antioxidant enzymes, and decreased activity of Complexes I, II, and IV, which in turn lead to chronic inflammation and triggering of apoptotic cell death pathways. In addition, spiral ganglion neurons (SGNs) also undergo autophagic stress and accumulated lipofuscin. INNOVATION and CONCLUSION: Our results provide evidence that targeting oxidative stress, chronic inflammation, or apoptotic pathways may have therapeutic potential. Modulation of autophagy may be another strategy. The fact that autophagic stress and protein aggregation occurred specifically in SGNs also offers promising perspectives for the prevention of neural presbycusis.