著者: George A Gates, John H Mills
雑誌名: Lancet. 2005 Sep 24-30;366(9491):1111-20. doi: 10.1016/S0140-6736(05)67423-5.
Abstract/Text
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.
PMID
16182900 Lancet. 2005 Sep 24-30;366(9491):1111-20. doi: 10.1016/･･･
著者: Bevan Yueh, Nina Shapiro, Catherine H MacLean, Paul G Shekelle
雑誌名: JAMA. 2003 Apr 16;289(15):1976-85. doi: 10.1001/jama.289.15.1976.
Abstract/Text
CONTEXT: Hearing loss is the third most prevalent chronic condition in older adults and has important effects on their physical and mental health. Despite these effects, most older patients are not assessed or treated for hearing loss.
OBJECTIVE: To review the evidence on screening and management of hearing loss of older adults in the primary care setting.
DATA SOURCES AND STUDY SELECTION: We performed a search from 1985 to 2001 using MEDLINE, HealthSTAR, EMBASE, Ageline, and the National Guideline Clearinghouse for articles and practice guidelines about screening and management of hearing loss in older adults, as well as reviewed references in these articles and those suggested by experts in hearing impairment.
DATA EXTRACTION: We reviewed articles for the most clinically important information, emphasizing randomized clinical trials, where available, and identified 1595 articles.
DATA SYNTHESIS: Screening tests that reliably detect hearing loss are use of an audioscope, a hand-held combination otoscope and audiometer, and a self-administered questionnaire, the Hearing Handicap Inventory for the Elderly-Screening version. The value of routine screening for improving patient outcomes has not been evaluated in a randomized clinical trial. Screening is endorsed by most professional organizations, including the US Preventive Services Task Force. While most hearing loss in older adults is sensorineural and due to presbycusis, cerumen impaction and chronic otitis media may be present in up to 30% of elderly patients with hearing loss and can be treated by the primary care clinician. In randomized trials, hearing aids have been demonstrated to improve outcomes for patients with sensorineural hearing loss. Nonadherence to use of hearing aids is high. Prompt recognition of potentially reversible causes of hearing loss, such as sudden sensorineural hearing loss, is important to maximize the possibility of functional recovery.
CONCLUSION: While untested in a clinical trial, older adults can be screened for hearing loss using simple methods, and effective treatments exist and are available for many forms of hearing loss.
PMID
12697801 JAMA. 2003 Apr 16;289(15):1976-85. doi: 10.1001/jama.28･･･
著者: Tatsuya Yamasoba, Shinichi Someya, Chikako Yamada, Richard Weindruch, Tomas A Prolla, Masaru Tanokura
雑誌名: Hear Res. 2007 Apr;226(1-2):185-93. doi: 10.1016/j.heares.2006.06.004. Epub 2006 Jul 25.
Abstract/Text
Mitochondrial DNA (mtDNA) mutations/deletions are considered to be associated with the development of age-related hearing loss (AHL). We assessed the role of accumulation of mtDNA mutations in the development of AHL using Polg(D257A) knock-in mouse, which exhibited increased spontaneous mtDNA mutation rates during aging and showed accelerated aging primarily due to increased apoptosis. They exhibited moderate hearing loss and degeneration of the hair cells, spiral ganglion cells and stria vascularis by 9 month of age, while wild-type animals did not. We next examined if mitochondrial damage induced by systemic application of germanium dioxide caused progressive hearing loss and cochlear damage. Guinea pigs and mice given germanium dioxide exhibited degeneration of the muscles and kidney and developed hearing loss due to degeneration of cochlear tissues, including the stria vascularis. Calorie restriction, which causes a metabolic shift toward increased energy metabolism in some organs, has been shown to attenuate AHL and age-related cochlear degeneration and to lower quantity of mtDNA deletions in the cochlea of mammals. Together these findings indicate that decreased energy metabolism due to accumulation of mtDNA mutations/deletions and decline of respiratory chain function play an important role in the manifestation of AHL.
PMID
16870370 Hear Res. 2007 Apr;226(1-2):185-93. doi: 10.1016/j.hear･･･
著者: Shinichi Someya, Jinze Xu, Kenji Kondo, Dalian Ding, Richard J Salvi, Tatsuya Yamasoba, Peter S Rabinovitch, Richard Weindruch, Christiaan Leeuwenburgh, Masaru Tanokura, Tomas A Prolla
雑誌名: Proc Natl Acad Sci U S A. 2009 Nov 17;106(46):19432-7. doi: 10.1073/pnas.0908786106. Epub 2009 Nov 9.
Abstract/Text
Age-related hearing loss (AHL), known as presbycusis, is a universal feature of mammalian aging and is the most common sensory disorder in the elderly population. The molecular mechanisms underlying AHL are unknown, and currently there is no treatment for the disorder. Here we report that C57BL/6J mice with a deletion of the mitochondrial pro-apoptotic gene Bak exhibit reduced age-related apoptotic cell death of spiral ganglion neurons and hair cells in the cochlea, and prevention of AHL. Oxidative stress induces Bak expression in primary cochlear cells, and Bak deficiency prevents apoptotic cell death. Furthermore, a mitochondrially targeted catalase transgene suppresses Bak expression in the cochlea, reduces cochlear cell death, and prevents AHL. Oral supplementation with the mitochondrial antioxidants alpha-lipoic acid and coenzyme Q(10) also suppresses Bak expression in the cochlea, reduces cochlear cell death, and prevents AHL. Thus, induction of a Bak-dependent mitochondrial apoptosis program in response to oxidative stress is a key mechanism of AHL in C57BL/6J mice.
PMID
19901338 Proc Natl Acad Sci U S A. 2009 Nov 17;106(46):19432-7. ･･･
著者: Shinichi Someya, Tatsuya Yamasoba, Richard Weindruch, Tomas A Prolla, Masaru Tanokura
雑誌名: Neurobiol Aging. 2007 Oct;28(10):1613-22. doi: 10.1016/j.neurobiolaging.2006.06.024. Epub 2006 Aug 4.
Abstract/Text
Presbycusis is characterized by an age-related progressive decline of auditory function, and arises mainly from the degeneration of hair cells or spiral ganglion (SG) cells in the cochlea. Here we show that caloric restriction suppresses apoptotic cell death in the mouse cochlea and prevents late onset of presbycusis. Calorie restricted (CR) mice, which maintained body weight at the same level as that of young control (YC) mice, retained normal hearing and showed no cochlear degeneration. CR mice also showed a significant reduction in the number of TUNEL-positive cells and cleaved caspase-3-positive cells relative to middle-age control (MC) mice. Microarray analysis revealed that CR down-regulated the expression of 24 apoptotic genes, including Bak and Bim. Taken together, our findings suggest that loss of critical cells through apoptosis is an important mechanism of presbycusis in mammals, and that CR can retard this process by suppressing apoptosis in the inner ear tissue.
PMID
16890326 Neurobiol Aging. 2007 Oct;28(10):1613-22. doi: 10.1016/･･･
著者: Shinichi Someya, Wei Yu, William C Hallows, Jinze Xu, James M Vann, Christiaan Leeuwenburgh, Masaru Tanokura, John M Denu, Tomas A Prolla
雑誌名: Cell. 2010 Nov 24;143(5):802-12. doi: 10.1016/j.cell.2010.10.002.
Abstract/Text
Caloric restriction (CR) extends the life span and health span of a variety of species and slows the progression of age-related hearing loss (AHL), a common age-related disorder associated with oxidative stress. Here, we report that CR reduces oxidative DNA damage in multiple tissues and prevents AHL in wild-type mice but fails to modify these phenotypes in mice lacking the mitochondrial deacetylase Sirt3, a member of the sirtuin family. In response to CR, Sirt3 directly deacetylates and activates mitochondrial isocitrate dehydrogenase 2 (Idh2), leading to increased NADPH levels and an increased ratio of reduced-to-oxidized glutathione in mitochondria. In cultured cells, overexpression of Sirt3 and/or Idh2 increases NADPH levels and protects from oxidative stress-induced cell death. Therefore, our findings identify Sirt3 as an essential player in enhancing the mitochondrial glutathione antioxidant defense system during CR and suggest that Sirt3-dependent mitochondrial adaptations may be a central mechanism of aging retardation in mammals.
Copyright © 2010 Elsevier Inc. All rights reserved.
PMID
21094524 Cell. 2010 Nov 24;143(5):802-12. doi: 10.1016/j.cell.20･･･
