Submitted Successfully!
To reward your contribution, here is a gift for you: A free trial for our video production service.
Thank you for your contribution! You can also upload a video entry or images related to this topic.
Version Summary Created by Modification Content Size Created at Operation
1 Presbycusis is the most common sensory impairment seen in the elderly. As our cochlea, the peripheral organ of hearing, ages, we tend to experience a decline in hearing and are at greater risk of cochlear sensory-neural cell degeneration and exacerbated a + 2871 word(s) 2871 2020-01-19 07:54:57 |
2 format change -996 word(s) 1875 2020-10-23 06:08:17 |

Video Upload Options

Do you have a full video?

Confirm

Are you sure to Delete?
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
Wang, J.; Puel, J. Age-Related Hearing Loss. Encyclopedia. Available online: https://encyclopedia.pub/entry/269 (accessed on 28 March 2024).
Wang J, Puel J. Age-Related Hearing Loss. Encyclopedia. Available at: https://encyclopedia.pub/entry/269. Accessed March 28, 2024.
Wang, Jing, Jean-Luc Puel. "Age-Related Hearing Loss" Encyclopedia, https://encyclopedia.pub/entry/269 (accessed March 28, 2024).
Wang, J., & Puel, J. (2020, February 03). Age-Related Hearing Loss. In Encyclopedia. https://encyclopedia.pub/entry/269
Wang, Jing and Jean-Luc Puel. "Age-Related Hearing Loss." Encyclopedia. Web. 03 February, 2020.
Age-Related Hearing Loss
Edit

Age-related hearing impairment, also referred to as presbycusis, is the most common sensory impairment seen in the elderly. As our cochlea, the peripheral organ of hearing, ages, we tend to experience a decline in hearing and are at greater risk of cochlear sensory-neural cell degeneration and exacerbated age-related hearing impairments (e.g., gradual hearing loss, deterioration in speech comprehension, difficulty in the localization sound sources, and ringing sensations in the ears). Here, we outline recent research into major causal factors of age-related hearing loss including both extrinsic (e.g. noise and ototoxic medication), and intrinsic factors (e.g. genetic predisposition, epigenetic factors and aging).

Age-related hearing loss Presbycusis Causal factors

1. Introduction

The clinical presentation of presbycusis, the rate of the progression, age at onset, and ultimate severity of hearing loss varies from patient to patient. Whereas the majority of elderly patients present clear hearing losses, a significant fraction of the geriatric population has almost normal hearing. This is due to intrinsic (genetic predisposition, epigenetic factors, and aging), and extrinsic factors (e.g., noise- or ototoxic drug-exposure, head trauma, cigarette smoking) that are either the sole etiology for hearing loss, or several work in synergy with the physiopathology of presbycusis[1].

2. Biological Aging on Hearing

2.1. Aging and Hearing in Healthy People

The clinical diagnosis of presbycusis is based on bilateral progressive loss of hearing starting from a high-frequency region of the hearing spectrum. Loss of hearing can begin in young adulthood, but is initially evident at 60 years for most people. Over time, the threshold elevation progresses to lower and lower frequency areas. However, presbycusis studies in humans are limited by the genetic heterogeneity and the difficulty in controlling deleterious auditory exposures over time. Despite these limitations, it has been reported that in a cohort unscreened for noise exposure, ototoxic drug exposure, and otologic disease history, presbycusis develops earlier and to a greater extent than in a highly screened cohort (without history of significant noise exposure or diseases that affect the ear)[2]. It has been suggested that the onset of hearing loss induced by biological aging is very late. Indeed, the Mabaan tribe living in the Sudanese desert retains their hearing into old age[3]. Because the hearing of the young Mabaans was the same as those of young people from other countries, the good preservation of hearing in the tribe has been attributed to their quiet living environment and generally healthy condition[4]. However, it can be argued that this difference might be caused by genetic differences between the populations. To answer this question, Goycoolea et al.[5] compared the hearing of natives of Easter Island, people living in a pre-industrial society, with those who had emigrated to Chile and spent varying amounts of time in modern society. Results showed that hearing in males that had lived or were living in Chile was significantly worse than that of males who had lived their entire lives on Easter Island, and that the poorer hearing was related to the number of years lived in modern society. Contrary to these early investigations, more recent studies showed that hearing thresholds decline with age and the rate of decline accelerates with age in presbycusis patients without noise-exposure or diseases that may affect the ear[6]. In addition, the differences of hearing thresholds between presbycusis patients with or without noise exposure are limited[7]. These results thus supported the belief that age is one of the major causal factors of ARHL.

2.2. Aging and Hearing in Animals

To study the impact of cochlear aging on hearing, animal models are a useful tool due to their short lifespan, controlled environments and diet composition, and limited genetic heterogeneity. Gerbils that grew up in quiet environments[8] showed various degrees of threshold shifts with age. The threshold shift profile was a relatively flat loss across low and mid frequencies, with the greatest losses at the higher frequencies resembling that often seen in human presbycusis[9]. These animals also showed a decline of the endocochlear potential[10][11] and reduced amplitudes of compound action potentials of the auditory nerve[12]. Reduced amplitudes of compound action potentials in aging ears suggested asynchronous or poorly synchronized neural activity in the auditory nerve of quiet-aged gerbils[12]. Cochlear morphological examination of gerbils raised in quiet demonstrated that the most important age-related degeneration site is the stria vascularis[13]. The stria vascularis is essential for maintaining the endocochlear potential which is the main driving force for the transmission of sound signals from the ear to the brain. The degeneration of marginal and intermediate cells of the stria vascularis began in both the base and apex of the cochlea, extending to the mid-cochlear regions as age increased. In addition, there was a loss of Na-K-ATPase[14] and losses of the strial capillary area in aged animals[15]. Certainly, more work with other species aged in quiet is needed in this area. However, existing data from quiet-aged gerbils make it clear that in gerbils, cochlear aging impacts specifically the stria vascularis and probably the neural structures.

3. Genetic Predispositions

Presbycusis shows a clear familial association. Heritability studies of presbycusis in humans have estimated that 25% to 75% of the variance in this pathology has a genetic component[1][16][17]. Genetic polymorphisms in the genes coding detoxification enzymes, such as glutathion S-transferase (GSTM1 and the GSTT1 null genotypes) and N-acetyltransferase 2 (NAT2*6A)[18][19][20]  were reported to be linked to ARHL. SOD2 promoter variants (−38C > G) of the SOD2 gene encoding a ubiquitous mitochondrial superoxide dismutase enzyme (MnSOD) may link to the ARHL risk in men[21]. The main function of uncoupling protein 2 (UCP2) is the control of mitochondria-derived oxygen species (ROS)[22]. In a Japanese population, UCP2 Ala55Val polymorphisms exhibited a significant association with ARHL[23].

An increased individual susceptibility to ARHL may rely on single nucleotide polymorphisms in the grainyhead-like 2 gene (GRHL2), nonsyndromic sensorineural deafness type 5 (DFNA5) and potassium voltage-gated channel subfamily q Member 4 (KCNQ4) genes, whose mutations are responsible for DFNA28, DFNA2, and DFNA5, respectively[24][25][26], but also in the glutamate metabotrophic receptor 7 gene (GRM7, e.g., OMIM ID: 604101)[27][28]. Finally, a common mtDNA 4977-bp deletion was frequently found in presbycusic patients[24].

Some genes associated with ARHL have also been identified in mice, including age-related hearing loss gene 1 (Ahl1), localized in chromosome 10, Ahl2[29] on chromosome 5 (associated with early-onset hearing loss when combined with a homozygous disease allele at the Ahl1 locus), and Ahl3 on chromosome 17[30]. The Ahl candidate region contains several interesting candidate genes, including genes encoding gap-junction proteins and several collagens. Mouse strains exhibiting ARHL are also more sensitive to noise-induced hearing loss than are other strains. Collectively, polymorphisms in some monogenic deafness-causing genes, neurotransmitter-related genes, and genes involved in detoxification of oxidative stress and mitochondrial function are clearly associated with ARHL.

4. Epigenetic Factors

Traditionally, genetics and adult lifestyle factors are considered to be among the main determinants of aging-associated pathological conditions. Accumulating evidence, however, suggests that epigenetic factors may contribute to these conditions[31][32]. The term epigenetics is defined as a change in phenotype that is not caused by a change in DNA sequence[33]. Epigenetic regulation of gene expression may change over time due to environmental exposures in common complex traits. The two most well understood mechanisms of epigenetic alterations that lead to these phenotypic changes are DNA methylation and histone modifications.

4.1. DNA Methylation

Age-related changes in DNA methylation include global hypomethylation and region-specific hypermethylation[34]. In the cochlea, the first evidence showing that involvement of aberrant DNA methylation in presbycusis came from a study focused on the gap junction protein b-2 (GJB2), in the cochlea of mimetic aging rats. In this study, Wu et al.[35] showed that hypermethylation of the promoter region of GJB2 gene resulted in connexin 26 down-regulation and an increased risk for presbycusis. Furthermore, Xu et al. [36] reported that hypermethylation of hearing-loss genes such as solute carrier family 26 member 4 (SLC26A4, DFNB4) and purinergic receptor P2X 2 (P2RX2, DFNA41) resulted in an increased risk for presbycusis in men. In addition, reduced expression of P2RX2, KCNQ5, ERBB3, and SOCS3 genes through DNA hypermethylation in elderly women was associated with presbycusis[37]. More recently, Bouzid et al. demonstrated that hypermethylation of CpG site in the cadherin-23 (CDH23) gene is likely to be associated with presbycusis in elderly women[37]. These results implicate complex pathogenic mechanisms underlying ARHL.

4.2. Histone Modification

Histone proteins including H1/H5, H2A, H2B, H3, and H4 are the chief proteins of chromatin and play an important role in maintaining the shape and structure of a nucleosome. In the last few years, the role of histone modifications in aging and age-related diseases has emerged. Watanabe and Bloch[38] investigated the modification of histones in the aged cochlea of mice using immunohistochemistry. Acetylated histone H3 was detected in the spiral ganglion cells and the organ of Corti of young cochlea, but not in those of aged cochlea. Conversely, dimethylatedhistone H3 was detected in the aged group, but not in the young group. The degeneration was severest in the spira lganglion cells and the organ of Corti of the basal turn. These results suggested that histone modifications may be involved in cochlear aging regulation.

5. Environmental Factors

The complexity of etiological factors for presbycusis begins with the number of environmental risk factors, such as occupational or leisure noise, ototoxic medication (aminoglycoside, cisplatin, salicylate, loop diuretics…), cigarette smoking, and alcohol abuse[39]. However, to date, it is not clear whether these environmental factors produce some kind of early onset and/or accelerated progression of cochlear aging or whether they act on specific pathophysiological mechanisms. In this part of our review, we will focus on the two most-studied environmental factors: noise exposure and ototoxic medication.

5.1. Noise Exposure

A retrospective clinical study from a large cohort of men in the Framingham Heart Study observed that in ears with presumed cochlear damage from previous noise exposure, subsequent progression of ARHL was exacerbated at frequencies outside the original noise-induced hearing loss[40]. These observations suggest an age-noise interaction that exacerbates age-related hearing loss in previously noise-damaged ears.

Increasing evidence from animal aging models indicates that early noise exposure renders the inner ears significantly more vulnerable to aging and may have an impact on the onset and/or progression of ARHL[41][42][43]. Indeed, Kujawa and Liberman[41] found that noise exposure in young CBA/CaJ mice, an inbred mouse strain used as “good hearing” mouse model, could trigger progressive neuronal loss and exacerbate the ARHL. Furthermore, Fernandez et al.[43] showed that interactions between noise and aging might require an acute synaptopathy to accelerate cochlear aging. In addition, repeated exposure to a short duration sound (1 h/110 dB SPL) over a long period also led to an early onset of ARHL (at six months of age) in Wistar rats when compared to non-exposed rats in which the onset of ARHL was around 12 months of age[44][45]. Although the long-term effects of early noise exposure on the aging ear are poorly understood, these clinical and experimental results indicate that noise exposure may modify the onset and/or progression of ARHL, particularly for neural presbycusis.

5.2. Ototoxic Medications

To date, the influence of other environmental risk factors such as ototoxic medications, cigarette smoking, or alcohol abuse on ARHL is less clear and often controversial. Recently, a large longitudinal cohort study (n = 3753) aimed at elucidating the association of ototoxic medications exposure with the risk of developing hearing loss during the 10-year follow-up period demonstrated that ototoxicity-age interactions may also exacerbate age-related hearing loss in older adults[46].

References

  1. George A. Gates; Nat N. Couropmitree; Richard H. Myers; Genetic Associations in Age-Related Hearing Thresholds. Archives of Otolaryngology–Head & Neck Surgery 1999, 125, 654-659, 10.1001/archotol.125.6.654.
  2. Maya Guest; May Boggess; John Attia; Relative risk of elevated hearing threshold compared to ISO1999 normative populations for Royal Australian Air Force male personnel. Hearing Research 2012, 285, 65-76, 10.1016/j.heares.2012.01.007.
  3. Samuel Rosen; Moe Bergman; Dietrich Plester; Aly El-Mofty; Mohamed Hamad Satti; LXII Presbycusis Study of a Relatively Noise-Free Population in the Sudan. Annals of Otology, Rhinology & Laryngology 1962, 71, 727-743, 10.1177/000348946207100313.
  4. Moe Bergman; Hearing in the Mabaans: A Critical Review of Related Literature. Archives of Otolaryngology–Head & Neck Surgery 1966, 84, 411-415, 10.1001/archotol.1966.00760030413007.
  5. Marcos V. Goycoolea; Hortensia G. Goycoolea; Corina R. Farfan; Leonardo G. Rodriguez; Gumaro C. Martinez; Ricardo Vidal; EFFECT OF LIFE IN INDUSTRIALIZED SOCIETIES ON HEARING IN NATIVES OF EASTER ISLAND. The Laryngoscope 1986, 96, 1391-1396, 10.1288/00005537-198612000-00015.
  6. Eric C. Bielefeld; Chiemi Tanaka; Guang-Di Chen; Donald Henderson; Age-related hearing loss: Is it a preventable condition?. Hearing Research 2010, 264, 98-107, 10.1016/j.heares.2009.09.001.
  7. Andrea Ciorba; A Benatti; C Bianchini; C Aimoni; Stefano Volpato; Roberto Bovo; Alessandro Martini; High frequency hearing loss in the elderly: effect of age and noise exposure in an Italian group. The Journal of Laryngology & Otology 2011, 125, 776-780, 10.1017/s0022215111001101.
  8. Richard A. Schmiedt; John H. Mills; Joe C. Adams; Tuning and suppression in auditory nerve fibers of aged gerbils raised in quiet or noise. Hearing Research 1990, 45, 221-236, 10.1016/0378-5955(90)90122-6.
  9. Harold F. Schuknecht; Kozo Watanuki; Tadahiko Takahashi; A. Aziz Belal; Robert S. Kimura; Diane Deleo Jones; Carol Y. Ota; Harold F. Shuknecht; ATROPHY OF THE STRIA VASCULARIS, A COMMON CAUSE FOR HEARING LOSS. The Laryngoscope 1974, 84, 1777-1821, 10.1288/00005537-197410000-00012.
  10. M.A. Gratton; R.A. Schmiedt; B.A. Schulte; Age-related decreases in endocochlear potential are associated with vascular abnormalities in the stria vascularis.. Hearing Research 1996, 102, 181-190, 10.1016/s0378-5955(96)90017-9.
  11. M.A Gratton; B J Smyth; C F Lam; F A Boettcher; R A Schmiedt; Decline in the endocochlear potential corresponds to decreased Na,K-ATPase activity in the lateral wall of quiet-aged gerbils.. Hearing Research 1997, 108, 9-16, 10.1016/s0378-5955(97)00034-8.
  12. Lisa I. Hellstrom; Richard A. Schmiedt; Compound action potential input/output functions in young and quiet-aged gerbils. Hearing Research 1990, 50, 163-174, 10.1016/0378-5955(90)90042-n.
  13. George A Gates; John H Mills; Presbycusis. The Lancet 2005, 366, 1111-1120, 10.1016/s0140-6736(05)67423-5.
  14. Bradley A. Schulte; Richard A. Schmiedt; Lateral wall Na, K-ATPase and endocochlear potentials decline with age in quiet-reared gerbils. Hearing Research 1992, 61, 35-46, 10.1016/0378-5955(92)90034-k.
  15. M.A Gratton; B A Schulte; Alterations in microvasculature are associated with atrophy of the stria vascularis in quiet-aged gerbils.. Hearing Research 1995, 82, 44-52.
  16. Kaare Christensen; Henrik Frederiksen; Howard J. Hoffman; Genetic and Environmental Influences on Self‐Reported Reduced Hearing in the Old and Oldest Old. Journal of the American Geriatrics Society 2001, 49, 1512-1517, 10.1046/j.1532-5415.2001.4911245.x.
  17. Anne Viljanen; Pertti Era; Jaakko Kaprio; Ilmari Pyykkö; Markku Koskenvuo; Taina Rantanen; Genetic and environmental influences on hearing in older women.. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 2007, 62, 447-452, 10.1093/gerona/62.4.447.
  18. Murat Unal; Lülüfer Tamer; Zeynep Nil Doğruer; Hatice Yildirim; Yusuf Vayisoğlu; Handan Camdeviren; N-Acetyltransferase 2 Gene Polymorphism and Presbycusis. The Laryngoscope 2005, 115, 2238-2241, 10.1097/01.mlg.0000183694.10583.12.
  19. Els Van Eyken; Guy Van Camp; Erik Fransen; Vedat Topsakal; Jan-Jaap Hendrickx; Kelly Demeester; Paul Van De Heyning; Elina Mäki-Torkko; Samuli Hannula; Martti Sorri; et al.Mona JensenAgnete ParvingMichael BilleManuela BaurMarcus PfisterAmanda BonaconsaManuela MazzoliEva OrzanAngeles EspesoDafydd StephensKatia VerbruggenJoke HuygheI DhoogePatrick HuygenHannie KremerC W R J CremersSylvia KunstMinna ManninenIlmari PyykkoAmalia Díaz-LacavaMichael SteffensThomas WienkerLut Van Laer Contribution of the N-acetyltransferase 2 polymorphism NAT2*6A to age-related hearing impairment. Journal of Medical Genetics 2007, 44, 570-578, 10.1136/jmg.2007.049205.
  20. Anthony Bared; Xiaomei Ouyang; Simon Angeli; Li Lin Du; Kimberly Hoang; Denise Yan; Xue-Zhong Liu; MD Xue Zhong Liu; Antioxidant enzymes, presbycusis, and ethnic variability. Otolaryngology–Head and Neck Surgery 2010, 143, 263-268, 10.1016/j.otohns.2010.03.024.
  21. Lisa S. Nolan; Barbara A. Cadge; Miriam Gomez-Dorado; Sally J. Dawson; A functional and genetic analysis of SOD2 promoter variants and their contribution to age-related hearing loss. Mechanisms of Ageing and Development 2013, 134, 298-306, 10.1016/j.mad.2013.02.009.
  22. Denis Arsenijevic; Hiroki Onuma; Claire Pecqueur; Serge Raimbault; Brian S. Manning; Bruno Miroux; Elodie Couplan; Marie-Clotilde Alves-Guerra; Marc Goubern; Richard Surwit; et al.Frédéric BouillaudDenis RichardSheila CollinsDaniel Ricquier Disruption of the uncoupling protein-2 gene in mice reveals a role in immunity and reactive oxygen species production. Nature Genetics 2000, 26, 435-439, 10.1038/82565.
  23. Saiko Sugiura; Yasue Uchida; Tsutomu Nakashima; Fujiko Ando2); Hiroshi Shimokata; The association between gene polymorphisms in uncoupling proteins and hearing impairment in Japanese elderly. Acta Oto-Laryngologica 2009, 130, 487-492, 10.3109/00016480903283758.
  24. Yasue Uchida; Saiko Sugiura; Michihiko Sone; Hiromi Ueda; Tsutomu Nakashima; Progress and Prospects in Human Genetic Research into Age-Related Hearing Impairment. BioMed Research International 2014, 2014, 1-10, 10.1155/2014/390601.
  25. Lut Van Laer; Els Van Eyken; Erik Fransen; Jeroen R. Huyghe; Vedat Topsakal; Jan-Jaap Hendrickx; Samuli Hannula; Elina Mäki-Torkko; Mona Jensen; Kelly Demeester; et al.Manuela BaurAmanda BonaconsaManuela MazzoliAngeles EspesoKatia VerbruggenJoke HuyghePatrick HuygenSylvia KunstMinna ManninenAnnelies KoningsAmalia N. Diaz-LacavaMichael SteffensThomas F. WienkerIlmari PyykköCor W.R.J. CremersHannie KremerIngeborg J. DhoogeDafydd StephensEva OrzanMarkus PfisterMichael BilleAgnete ParvingMartti SorriPaul Van De HeyningGuy Van Camp The grainyhead like 2 gene (GRHL2), alias TFCP2L3, is associated with age-related hearing impairment. Human Molecular Genetics 2007, 17, 159-169, 10.1093/hmg/ddm292.
  26. E. Van Eyken; L. Van Laer; E Fransen; V. Topsakal; N. Lemkens; W. Laureys; N. Nelissen; A. Vandevelde; T. Wienker; Paul Van De Heyning; et al.Guy Van Camp KCNQ4: a gene for age-related hearing impairment?. Human Mutation 2006, 27, 1007-1016, 10.1002/humu.20375.
  27. Rick A. Friedman; Lut Van Laer; Matthew J. Huentelman; Sonal S. Sheth; Els Van Eyken; Jason J. Corneveaux; Waibhav D. Tembe; Rebecca F. Halperin; Ashley Q. Thorburn; Sofie Thys; et al.Sarah BonneuxErik FransenJeroen HuygheIlmari PyykköC. W. R. J. CremersHannie KremerIngeborg DhoogeDafydd StephensEva OrzanMarkus PfisterMichael BilleAgnete ParvingMartti SorriPaul H. Van De HeyningLinna MakmuraJeffrey D. OhmenFrederick H. LinthicumJose N. FayadJohn V. PearsonDavid W. CraigDietrich A. StephanGuy Van Camp GRM7 variants confer susceptibility to age-related hearing impairment. Human Molecular Genetics 2008, 18, 785-796, 10.1093/hmg/ddn402.
  28. Dina L. Newman; Laurel M. Fisher; Jeffrey Douglass Ohmen; Robert Parody; Chin-To Fong; Susan T. Frisina; Frances Mapes; David A. Eddins; D. Robert Frisina; Robert D. Frisina; et al.Rick A. Friedman GRM7 variants associated with age-related hearing loss based on auditory perception. Hearing Research 2012, 294, 125-132, 10.1016/j.heares.2012.08.016.
  29. Kenneth R. Johnson; Qing Yin Zheng; Ahl2, a Second Locus Affecting Age-Related Hearing Loss in Mice. Genomics 2002, 80, 461-464, 10.1006/geno.2002.6858.
  30. Yuka Morita; Sachiko Hirokawa; Yoshiaki Kikkawa; Tomoyuki Nomura; Hiromichi Yonekawa; Toshihiko Shiroishi; Sugata Takahashi; Ryo Kominami; Fine mapping of Ahl3 affecting both age-related and noise-induced hearing loss. Biochemical and Biophysical Research Communications 2007, 355, 117-121, 10.1016/j.bbrc.2007.01.115.
  31. Alexander Vaiserman; Oleh Lushchak; Developmental origins of type 2 diabetes: Focus on epigenetics. Ageing Research Reviews 2019, 55, 100957, 10.1016/j.arr.2019.100957.
  32. Sangita Pal; Jessica K. Tyler; Epigenetics and aging. Science Advances 2016, 2, e1600584, 10.1126/sciadv.1600584.
  33. Matthew J. Provenzano; Frederick E. Domann; A role for epigenetics in hearing: Establishment and maintenance of auditory specific gene expression patterns. Hearing Research 2007, 233, 1-13, 10.1016/j.heares.2007.07.002.
  34. Fu-Hui Xiao; Qing-Peng Kong; Benjamin Perry; Yong-Han He; Progress on the role of DNA methylation in aging and longevity. Briefings in Functional Genomics 2016, 15, elw009-459, 10.1093/bfgp/elw009.
  35. Xia Wu; Yanjun Wang; Yu Sun; Sen Chen; Shuai Zhang; Ling Shen; Xiang Huang; Xi Lin; Wei-Jia Kong; Reduced expression of Connexin26 and its DNA promoter hypermethylation in the inner ear of mimetic aging rats induced by d-galactose. Biochemical and Biophysical Research Communications 2014, 452, 340-346, 10.1016/j.bbrc.2014.08.063.
  36. Jin Xu; Jiachen Zheng; Wanjing Shen; Lili Ma; Ming Zhao; Xubo Wang; Jiyuan Tang; Jihong Yan; Zhenhua Wu; Zuquan Zou; et al.Shizhong BuYang Xi Elevated SLC26A4 gene promoter methylation is associated with the risk of presbycusis in men. Molecular Medicine Reports 2017, 16, 347-352, 10.3892/mmr.2017.6565.
  37. Amal Bouzid; Ibtihel Smeti; Leila Dhouib; Magali Roche; Imen Achour; Aida Khalfallah; Abdullah Ahmed Gibriel; Ilhem Charfeddine; Hammadi Ayadi; Joel Lachuer; et al.Abdelmonem GhorbelChristine PetitSaber Masmoudi Down-expression of P2RX2, KCNQ5, ERBB3 and SOCS3 through DNA hypermethylation in elderly women with presbycusis. Biomarkers 2018, 23, 347-356, 10.1080/1354750x.2018.1427795.
  38. Ken-Ichi Watanabe; Wilhelm Bloch; Histone methylation and acetylation indicates epigenetic change in the aged cochlea of mice. European Archives of Oto-Rhino-Laryngology 2012, 270, 1823-1830, 10.1007/s00405-012-2222-1.
  39. Erik Fransen; Nele Lemkens; Lut Van Laer; Guy Van Camp; Age-related hearing impairment (ARHI): environmental risk factors and genetic prospects.. Experimental Gerontology 2003, 38, 353-359, 10.1016/s0531-5565(03)00032-9.
  40. George A. Gates; Peter Schmid; Sharon G. Kujawa; Byung-Ho Nam; Ralph D’Agostino; Longitudinal threshold changes in older men with audiometric notches. Hearing Research 2000, 141, 220-228, 10.1016/s0378-5955(99)00223-3.
  41. Sharon G. Kujawa; Acceleration of Age-Related Hearing Loss by Early Noise Exposure: Evidence of a Misspent Youth. Journal of Neuroscience 2006, 26, 2115-2123, 10.1523/jneurosci.4985-05.2006.
  42. Anna Rita Fetoni; Pasqualina M. Picciotti; Gaetano Paludetti; Diana Etroiani; Pathogenesis of presbycusis in animal models: A review. Experimental Gerontology 2011, 46, 413-425, 10.1016/j.exger.2010.12.003.
  43. Katharine A. Fernandez; Penelope W.C. Jeffers; Kumud Lall; M. Charles Liberman; Sharon G. Kujawa; Aging after Noise Exposure: Acceleration of Cochlear Synaptopathy in "Recovered" Ears. Journal of Neuroscience 2015, 35, 7509-7520, 10.1523/jneurosci.5138-14.2015.
  44. Juan Carlos Ealvarado; Verónica Fuentes-Santamaría; María Cruz Gabaldón-Ull; José M. Juiz; Age-Related Hearing Loss Is Accelerated by Repeated Short-Duration Loud Sound Stimulation. Frontiers in Neuroscience 2019, 13, 77, 10.3389/fnins.2019.00077.
  45. Juan Carlos Ealvarado; Verã³Nica Fuentes-Santamarã­a; Marã­a C. Gabaldã³N-Ull; José Luis Eblanco; Josã© M. Juiz; Wistar rats: a forgotten model of age-related hearing loss. Frontiers in Aging Neuroscience 2014, 6, 29, 10.3389/fnagi.2014.00029.
  46. YoonMee Joo; Karen J Cruickshanks; Barbara E K Klein; Ronald Klein; Oisaeng Hong; Margaret I Wallhagen; The Contribution of Ototoxic Medications to Hearing Loss Among Older Adults. The Journals of Gerontology: Series A 2019, 75, 561-566, 10.1093/gerona/glz166.
More
Information
Subjects: Pathology
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register : ,
View Times: 823
Revisions: 2 times (View History)
Update Date: 23 Oct 2020
1000/1000