Description and Primary Results from an Audiometric Study of Male Twins

Karlsson, K.; Harris, Jennifer R.; Svartengren, Magnus

doi:10.1097/00003446-199704000-00003

Cited by 114 publications

(78 citation statements)

References 3 publications

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“…Presbycusis does cluster in families [35] and heritability estimates indicate that 35-55% of the variance of ARHL is attributable to the effects of genes: A Swedish study consisting of 250 monozygotic and 307 dizygotic male twins (aged 36-80) showed a heritability of 47% for the population above 65, using both questionnaire and audiometric data [36]. Using the same analytical method, the National Academy of Science-National Research Council (NAS-NRC) ageing twin panel study in the USA has estimated the heritability at 61% [37].…”

Section: Heritability Allelism and Genetic Modifiers Of Presbycusismentioning

confidence: 99%

“…Heritability index was high in pairings of women (sister-sister, 0.53; mother-daughter, 0.36). Because of the difficulty of studying an outbred and older human population that includes intrinsic and environmental variables accumulated over the course of a lifetime [36,38], most studies have identified ARHL genes in a laboratory setting using mouse models, in which rigorous genetic and experimental control can be achieved, such that age is the most significant factor in an animal model of ARHL.…”

Section: Heritability Allelism and Genetic Modifiers Of Presbycusismentioning

confidence: 99%

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Ageing and hearing loss

Yan

2007

The Journal of Pathology

278

178

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Although many adults retain good hearing as they age, hearing loss associated with ageing is common among elderly persons. There are a number of pathophysiolological processes underlying age-related changes to functional components in the inner ear. Genetic factors determine the ageing process but are under the influence of intrinsic and environmental factors. It is difficult to distinguish changes of normal ageing from those of other contributing factors. The effects of age-related deafness can have significant physical, functional and mental health consequences. Although a deficit in hearing can be corrected to some degree by a hearing aid or other appropriate amplification devices, hearing-related rehabilitative needs are much more than simply amplifying external sound. Only by better understanding the process of ageing and its effect on the auditory function can we better accommodate elderly people in our day-to-day interactions. We review here the structure and function of the inner ear, pathophysiology associated with age-related hearing loss (ARHL), heritability, allelism and modifier genes of ARHL, and evaluate the genetic analyses for identification of genetic factors that are involved.

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Section: Heritability Allelism and Genetic Modifiers Of Presbycusismentioning

confidence: 99%

Section: Heritability Allelism and Genetic Modifiers Of Presbycusismentioning

confidence: 99%

Ageing and hearing loss

Yan

2007

The Journal of Pathology

278

178

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“…Such variables do not lend themselves easily to retrospective quantification. Similarly, variability in age of onset, progression, and severity of AHL may be influenced by genetic factors (Gates et al, 1999;DeStefano et al, 2003) and heterogeneity in underlying pathology (Schuknecht and Gacek, 1993), as well as the variable contribution of other insults accumulated over the course of a lifetime (Lutman and Spencer, 1990;Karlsson et al, 1997). This variability has complicated our conduct and interpretation of investigations of NIHL and AHL in humans.…”

Section: Introductionmentioning

confidence: 99%

Acceleration of Age-Related Hearing Loss by Early Noise Exposure: Evidence of a Misspent Youth

Kujawa¹,

Liberman²

2006

J. Neurosci.

594

411

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Age-related and noise-induced hearing losses in humans are multifactorial, with contributions from, and potential interactions among, numerous variables that can shape final outcome. A recent retrospective clinical study suggests an age-noise interaction that exacerbates age-related hearing loss in previously noise-damaged ears (Gates et al., 2000). Here, we address the issue in an animal model by comparing noise-induced and age-related hearing loss (NIHL; AHL) in groups of CBA/CaJ mice exposed identically (8 -16 kHz noise band at 100 dB sound pressure level for 2 h) but at different ages (4 -124 weeks) and held with unexposed cohorts for different postexposure times (2-96 weeks). When evaluated 2 weeks after exposure, maximum threshold shifts in young-exposed animals (4 -8 weeks) were 40 -50 dB; older-exposed animals (Ն16 weeks) showed essentially no shift at the same postexposure time. However, when held for long postexposure times, animals with previous exposure demonstrated AHL and histopathology fundamentally unlike unexposed, aging animals or old-exposed animals held for 2 weeks only. Specifically, they showed substantial, ongoing deterioration of cochlear neural responses, without additional change in preneural responses, and corresponding histologic evidence of primary neural degeneration throughout the cochlea. This was true particularly for young-exposed animals; however, delayed neuropathy was observed in all noise-exposed animals held 96 weeks after exposure, even those that showed no NIHL 2 weeks after exposure. Data suggest that pathologic but sublethal changes initiated by early noise exposure render the inner ears significantly more vulnerable to aging.

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“…1,2 The involvement of genetic factors in the development of this multifactorial disorder was demonstrated by several heritability studies. [3][4][5] Only recently have the first studies aiming at the identification of these genetic factors been conducted. Hitherto, three linkage studies have been performed, [6][7][8] but only one region on chromosome 8q24.13-q24.22 reached genomewide significance.…”

Section: Introductionmentioning

confidence: 99%

A genome-wide association study for age-related hearing impairment in the Saami

et al. 2010

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This study aimed at contributing to the elucidation of the genetic basis of age-related hearing impairment (ARHI), a common multifactorial disease with an important genetic contribution as demonstrated by heritability studies. We conducted a genomewide association study (GWAS) in the Finnish Saami, a small, ancient, genetically isolated population without evidence of demographic expansion. The choice of this study population was motivated by its anticipated higher extent of LD, potentially offering a substantial power advantage for association mapping. DNA samples and audiometric measurements were collected from 352 Finnish Saami individuals, aged between 50 and 75 years. To reduce the burden of multiple testing, we applied principal component (PC) analysis to the multivariate audiometric phenotype. The first three PCs captured 80% of the variation in hearing thresholds, while maintaining biologically important audiometric features. All subjects were genotyped with the Affymetrix 100 K chip. To account for multiple levels of relatedness among subjects, as well as for population stratification, association testing was performed using a mixed model. We summarised the top-ranking association signals for the three traits under study. The top-ranked SNP, rs457717 (P-value 3.55Â10 À7 ), was associated with PC3 and was localised in an intron of the IQ motif-containing GTPase-activating-like protein (IQGAP2). Intriguingly, the SNP rs161927 (P-value 0.000149), seventhranked for PC1, was positioned immediately downstream from the metabotropic glutamate receptor-7 gene (GRM7). As a previous GWAS of a European and Finnish sample set already suggested a role for GRM7 in ARHI, this study provides further evidence for the involvement of this gene.

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Description and Primary Results from an Audiometric Study of Male Twins

Cited by 114 publications

References 3 publications

Ageing and hearing loss

Ageing and hearing loss

Acceleration of Age-Related Hearing Loss by Early Noise Exposure: Evidence of a Misspent Youth

A genome-wide association study for age-related hearing impairment in the Saami

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