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Original Contribution

February 2011

Hearing Loss and Incident Dementia

Frank R. Lin, MD, PhDE. Jeffrey Metter, MDRichard J. O’Brien, MD, PhD; et alSusan M. Resnick, PhDAlan B. Zonderman, PhDLuigi Ferrucci, MD, PhD

Author Affiliations Article Information

Arch Neurol. 2011;68(2):214-220. doi:10.1001/archneurol.2010.362


Objective  To determine whether hearing loss is associated with incident all-cause dementia and Alzheimer disease (AD).

Design  Prospective study of 639 individuals who underwent audiometric testing and were dementia free in 1990 to 1994. Hearing loss was defined by a pure-tone average of hearing thresholds at 0.5, 1, 2, and 4 kHz in the better-hearing ear (normal, <25 dB [n = 455]; mild loss, 25-40 dB [n = 125]; moderate loss, 41-70 dB [n = 53]; and severe loss, >70 dB [n = 6]). Diagnosis of incident dementia was made by consensus diagnostic conference. Cox proportional hazards models were used to model time to incident dementia according to severity of hearing loss and were adjusted for age, sex, race, education, diabetes mellitus, smoking, and hypertension.

Setting  Baltimore Longitudinal Study of Aging.

Participants  Six hundred thirty-nine individuals aged 36 to 90 years.

Main Outcome Measure  Incident caces of all-cause dementia and AD until May 31, 2008.

Results  During a median follow-up of 11.9 years, 58 cases of incident all-cause dementia were diagnosed, of which 37 cases were AD. The risk of incident all-cause dementia increased log linearly with the severity of baseline hearing loss (1.27 per 10-dB loss; 95% confidence interval, 1.06-1.50). Compared with normal hearing, the hazard ratio (95% confidence interval) for incident all-cause dementia was 1.89 (1.00-3.58) for mild hearing loss, 3.00 (1.43-6.30) for moderate hearing loss, and 4.94 (1.09-22.40) for severe hearing loss. The risk of incident AD also increased with baseline hearing loss (1.20 per 10 dB of hearing loss) but with a wider confidence interval (0.94-1.53).

Conclusions  Hearing loss is independently associated with incident all-cause dementia. Whether hearing loss is a marker for early-stage dementia or is actually a modifiable risk factor for dementia deserves further study.

The prevalence of dementia is projected to double every 20 years such that by 2050, more than 100 million people or nearly 1 in 85 persons will be affected worldwide.1,2 The devastating impact of dementia on affected individuals and the burden imposed on their families and society has made the prevention and treatment of dementia a public health priority. Interventions that could merely delay the onset of dementia by 1 year would lead to a more than 10% decrease in the global prevalence of dementia in 2050.3 Unfortunately, there are no known interventions that currently have such effectiveness.

Epidemiologic approaches have focused on the identification of putative risk factors that could be targeted for prevention based on the assumption that dementia is easier to prevent than to reverse. Candidate factors include low involvement in leisure activities and social interactions, sedentary state, diabetes mellitus, and hypertension.4 Some researchers have also suggested that hearing loss, by reducing stimulatory input and hampering social interaction, may be associated with dementia,5,6 but, to our knowledge, this hypothesis has never been prospectively studied. Given the growing number of people with hearing loss7 and the array of technological interventions currently available for aural rehabilitation, understanding whether hearing loss is a risk factor for dementia is important. We performed the present study to investigate the prospective association of hearing loss with incident dementia within the cohort of the Baltimore Longitudinal Study of Aging (BLSA).



Subjects were participants in the BLSA, an ongoing prospective study of the effects of aging that was initiated in 1958 by the National Institute on Aging.8 The BLSA cohort consists of community-dwelling volunteers who travel to the National Institute on Aging in Baltimore biennially for 2½ days of intensive testing. From 1990 through 1994, 1305 participants completed at least 1 study visit, of whom 976 underwent audiometry and 749 had both audiometry and cognitive testing. Some participants had missing audiometry or cognitive testing data because of inadequate time for testing or tester unavailability during study visits. After excluding individuals with prevalent dementia (n = 58), those with more than 3 errors on the Blessed Information Memory Concentration Test (n = 39), and those with suspected dementia (n = 13), our baseline cohort consisted of 639 participants who were followed up until May 31, 2008 (median participant follow-up of 11.9 years) (Figure 1). For participants with more than 1 visit during this period, data from the first assessment were used. All participants provided written informed consent, and the BLSA study protocol was approved by the institutional review board.

Cognitive testing and diagnosis of dementia

The protocol for adjudication of dementia in the BLSA has been used continuously since 1986 and has been described previously.9 Participants 65 years or older underwent a complete neurological and neuropsychological examination using a standard battery of tests. Participants younger than 65 years first underwent screening with the Blessed Information Memory Concentration Test and underwent further examination if they made 3 or more errors. Dementia diagnosis was established during a multidisciplinary consensus diagnostic conference using the Diagnostic and Statistical Manual of Mental Disorders (Third Edition Revised) for diagnosis of dementia10 and the National Institute of Neurological and Communicative Disorders and Stroke–Alzheimer Disease and Related Disorders Association criteria for diagnosis of Alzheimer disease (AD).11 If participants were determined to have clinically significant cognitive decline (typically memory) but did not meet criteria for dementia, they were classified as having suspected dementia, which corresponds to the current diagnosis of mild cognitive impairment.12 Participants initially underwent evaluation for dementia every 2 years during their routine BLSA follow-up visits. In 1997, follow-up was shifted to a sliding-scale schedule to reduce participant burden and improve data collection. Participants older than 80 years were examined annually; those aged 60 to 80 years, biennially; and those younger than 60 years, every 4 years.


Audiometry was performed in the BLSA from 1958 to 1994. During the entire period from 1990 through 1994, when the baseline evaluation for this analysis was performed, hearing thresholds were measured using an automated testing device (Audiometer Model 320; Virtual Equipment Co, Portland, Oregon) in a soundproof chamber under unaided conditions. A pure-tone average (PTA) of air conduction thresholds at 0.5, 1, 2, and 4 kHz was calculated for each ear, and the PTA in the better-hearing ear was used for subsequent analyses because that ear would be the principal determinant of hearing and speech perception ability on an everyday basis. We used the PTA in decibels as both a continuous variable and a categorical variable defined by the following commonly used levels of hearing loss: normal (<25 dB), mild loss (25-40 dB), moderate loss (41-70 dB), and severe loss (>70 dB). Before 1990, audiometric testing was performed using a Bekesy audiometer (GSI 1701; Grason Stadler, Littleton, Massachusetts), and these data were used in analyses of prebaseline hearing trajectories.

Other covariates

A diagnosis of diabetes mellitus was based on a fasting glucose level of more than 125 mg/dL (to convert to millimoles per liter, multiply by 0.0555), a pathologic oral glucose tolerance test result, or history of a physician diagnosis plus treatment with oral antidiabetic drugs or insulin. The diagnosis of hypertension was based on a systolic blood pressure of greater than 140 mm Hg and/or diastolic blood pressure of at least 90 mm Hg or treatment with antihypertensive medications. Race (white/black/other), education (in years), smoking status (current/former/never), and hearing aid use were based on self-report.

Statistical analyses

Baseline characteristics of cohort members were compared using 1-way analysis of variance for continuous variables and χ2 or Fisher exact test for categorical variables. Cox proportional hazards models were used to study time to incident all-cause dementia or AD. Participants not diagnosed as having dementia were censored at the time of their last negative cognitive evaluation finding. Time-on-study (ie, time of entry into the baseline study cohort) was used as the time scale with the exception of 1 model that used age as the time scale.

All Cox models included covariates of sex, age, race, education, diabetes, smoking, and hypertension. Diabetes and hypertension were included as covariates in the analysis because they have been found to be risk factors for dementia.4 Additional models included baseline Blessed scores (residual variability in cognition after definition of the baseline cohort) and hearing aid use. All covariates were treated as time-constant variables. Cox model proportionality assumptions and the linear association between hearing loss and dementia were tested using the Schoenfeld residuals method.13 To examine the graphical association between hearing threshold and dementia, we used a smoothing spline for the hearing threshold and age in the Cox proportional hazards model.14 A locally weighted scatterplot smoother (loess smoother) was then applied to the exponential of the partial residuals derived from the hazards model against the hearing threshold. A bootstrap procedure was used to generate 10 000 data sets that were then used to estimate the 95% confidence interval (CI) for the loess smoother. Analysis of hearing loss trajectories before baseline was performed using a random effects analysis and adjusted for age. Population-attributable risk (PAR) was calculated using the following equation15:

PAR = (Pexposed([R – 1])/(1 + Pexposed[RR – 1]),

where Pexposed was the prevalence of baseline hearing loss of at least 25 dB and RR was the rate ratio (hazard ratio [HR]) of dementia risk associated with hearing loss. Participants with missing data were excluded from analyses; this represented less than 0.2% of the study sample (1 participant) for all analyses except for analyses incorporating hearing aid use, in which there were more extensive missing data (typically among normal-hearing participants who did not respond). Significance testing for all analyses was 2 sided with a type I error of .05. The statistical software used was a free available software environment (R, version 2.9.1;


Baseline demographic characteristics of participants by hearing loss category are presented in Table 1. In general, participants with greater hearing loss were more likely to be older, male, and hypertensive. Blessed scores did not differ by hearing loss category (P = .08), although the range of errors was narrow (0-3) because participants with more than 3 errors were excluded from the study cohort at baseline.

Baseline covariates associated with an increased risk of incident all-cause dementia are hearing loss, age, hypertension, hearing aid use, and Blessed score (Table 2). Independent of age, in the 15 years before baseline assessment (520 participants with 2678 observations), participants who later developed incident dementia experienced an average PTA loss of 0.52 dB/y (95% CI, 0.34-0.70 dB/y) compared with 0.27 dB/y (0.21-0.33 dB/y) in those who did not develop dementia.

In Cox proportional hazards models adjusted for sex, age, race, education, diabetes, smoking, and hypertension (base model), the excess risk of incident dementia per 10 dB of hearing loss was 1.27 (95% CI, 1.06-1.50) (Table 3). The risk of incident dementia became evident for hearing loss of greater than 25 dB and thereafter increased log linearly with more severe loss (Figure 2). This association remained significant after censoring participants who developed dementia within a 2-, 4-, or 6-year washout period from baseline (P = .008, P = .003, and P = .04, respectively).

Confirmatory analyses from models including baseline Blessed error score (to account for baseline cognitive function) or models using age as the time scale rather than time-on-study (to account for residual confounding between age and hearing loss) produced virtually unchanged findings (cf Table 3). Restricting the analytical cohort to participants 65 years or older at baseline (n = 315) or excluding participants at baseline with a history of stroke or transient ischemic attack (n = 19) also did not substantially change the main findings (Table 3). There was no evidence to suggest that self-reported hearing aid use was associated with a reduction in dementia risk (HR, 0.97; P = .92).

In subsequent analyses, we categorized hearing loss according to commonly accepted levels of hearing loss severity. Compared with those with normal hearing, participants with mild hearing loss had an HR for incident dementia of 1.89 (95% CI, 1.00-3.58; P = .049), those with moderate hearing loss had an HR of 3.00 (1.43-6.30; P = .004), and those with severe hearing loss (n = 6) had an HR of 4.94 (1.09-22.40; P = .04).

When the outcome of the analysis was restricted to incident AD (37 of the 58 cases of dementia), hearing loss was associated with an excess risk of 1.20 per 10 dB of hearing loss (95% CI, 0.94-1.53). This result is comparable to the risk seen for all-cause dementia (Table 3) but with a wider CI, possibly owing to the smaller sample size.

We estimated the proportion of incident all-cause dementia risk that was attributable to hearing loss for participants older than 60 years in our cohort, assuming that hearing loss could be causally associated with dementia. Hearing loss of at least 25 dB in the better-hearing ear was present in 43% of this subcohort, and the relative risk (HR) of dementia associated with hearing loss was 2.32 (95% CI, 1.32- 4.07). Thus, the attributable risk of dementia associated with hearing loss in this subcohort was 36.4% (95% CI, 12.8%-58.6%).


In this study, hearing loss was independently associated with incident all-cause dementia after adjustment for sex, age, race, education, diabetes, smoking, and hypertension, and our findings were robust to multiple sensitivity analyses. The risk of all-cause dementia increased log linearly with hearing loss severity, and for individuals older than 60 years in our cohort, more than one-third of the risk of incident all-cause dementia was associated with hearing loss.

Our findings contribute significantly to the discussion in the literature on whether hearing loss is a risk factor for dementia. Previous studies suggested that individuals with hearing loss are more likely to have a diagnosis of dementia5,6 and poorer cognitive function.16 Supporting this hypothesis, smaller prospective studies have observed that hearing loss is associated with accelerated cognitive decline in individuals with prevalent dementia.17,18 Although a prospective study19 of cognitively normal elderly volunteers failed to find any meaningful association between hearing loss at study entry and later cognitive function, the results of that study are questionable because of the short (5-year) follow-up and a 50% dropout rate. In our study, hearing loss, a condition that is highly prevalent in older adults and that often remains untreated,20 was strongly and prospectively associated with incident dementia.

A number of mechanisms may be theoretically implicated in the observed association between hearing loss and incident dementia. There may be an overdiagnosis of dementia in individuals affected by hearing loss or, vice versa, an overdiagnosis of hearing loss in individuals with cognitive impairment at baseline. An overdiagnosis of dementia in our study is unlikely because the diagnostic protocol for incident dementia relied on a consensus conference that examined information from multiple sources. We also conducted sensitivity analyses censoring individuals diagnosed as having dementia during a 6-year washout period from baseline that did not affect our results. In such an analysis, individuals would already have had normal findings on several cognitive examinations with hearing loss before being diagnosed as having dementia, likely indicating that the dementia diagnosis was not confounded by poor communication. Hearing loss (short of profound deafness) also minimally impairs face-to-face communication in quiet environments (ie, during cognitive testing), particularly in the setting of testing by experienced examiners who are accustomed to working with older adults.21

An overdiagnosis of hearing loss is also unlikely because no evidence suggests that mild cognitive impairment would affect the reliability of audiometric testing. Pure-tone audiometry has been performed in children as young as 5 years. We also excluded any individuals with recognized cognitive impairment at baseline (mild cognitive impairment or Blessed score >3), and our results were robust to models controlling for baseline Blessed scores.

Another possibility is that hearing loss and progressive cognitive impairment are caused by a common neuropathologic process, possibly the same that leads to AD. However, pure-tone audiometry is typically considered a measure of the auditory periphery because detection of pure tones relies solely on cochlear transduction and neuronal afferents to brainstem nuclei and the primary auditory cortex. Perception of pure tones does not require higher levels of auditory cortical processing,22 and results of auditory brainstem response testing of these pathways are usually normal in patients with AD.23 In contrast, central auditory nuclei required for higher-order auditory processing can be affected by AD neuropathology,24-26 and tests of central auditory function have been found to be associated with AD.27

The likelihood of another neurobiological process such as vascular disease or factors related to family history (eg, apolipoprotein E [ApoE] status) causing hearing loss and dementia also cannot be fully excluded. However, risk factors for vascular disease such as diabetes, smoking, and hypertension were adjusted for in our models, and a preliminary study has not found a positive association between ApoE status and hearing loss.28 Other variables, such as mental and leisure activities, were not included as covariates in our models because these variables would not be expected to cause hearing loss and act as meaningful confounders in our models. Our results were also robust to excluding individuals at baseline who had a history of stroke or transient ischemic attack.

Finally, hearing loss may be causally related to dementia, possibly through exhaustion of cognitive reserve, social isolation, environmental deafferentation, or a combination of these pathways. Cognitive reserve reflects interindividual differences in neurocognitive processing that allow some individuals to cope better with neuropathology than others.29 Functional magnetic resonance imaging studies showing interindividual variation in efficiency of task-related neural processing provide some evidence of this concept.30,31 Cognitive reserve has also been used to explain discrepancies between the extent of neuropathology seen at autopsy and clinical expression of dementia.32 The potential effect of hearing loss on cognitive reserve is suggested by studies demonstrating that, under conditions in which auditory perception is difficult (ie, hearing loss), greater cognitive resources are dedicated to auditory perceptual processing to the detriment of other cognitive processes such as working memory.33,34 This reallocation of neural resources to auditory processing could deplete the cognitive reserve available to other cognitive processes and possibly lead to the earlier clinical expression of dementia.35

Communication impairments caused by hearing loss can also lead to social isolation in older adults,36,37 and epidemiologic38,39 and neuroanatomic studies40 have demonstrated associations between poor social networks and dementia. Our results also seem to support this possible pathway because the risk of dementia associated with hearing loss appeared to only increase at hearing thresholds of greater than 25 dB, which is considered the threshold at which hearing loss begins to impair verbal communication.41 Finally, a hypothetical mechanism by which hearing loss could directly affect AD neuropathology is suggested by animal studies demonstrating that environmental enrichment (possibly analogous in humans to having access to auditory and environmental stimuli) can reduce β-amyloid levels in transgenic mouse models.42 This hypothesis is also supported by studies showing that individuals who remain engaged in leisure activities have a lower risk of dementia.43

In the present study, self-reported hearing aid use was not associated with a significant reduction in dementia risk, but data on other key variables (eg, type of hearing aid used, hours worn per day, number of years used, characteristics of participants choosing to use hearing aids, use of other communicative strategies, and adequacy of rehabilitation) that would affect the success of aural rehabilitation and affect any observed association were not gathered. Consequently, whether hearing devices and aural rehabilitative strategies could affect cognitive decline and dementia remains unknown and will require further study.

Our study has limitations. First, only the severity of hearing loss at baseline was considered in the analysis, and information was not available on the trajectory of hearing loss after baseline assessment or on the possible etiology of the hearing loss. However, it is unlikely that this limitation substantially biased our findings given that reversible hearing loss is rare, and hearing loss tends to only worsen with time. Residual confounding by other environmental, genetic, or neuropathologic processes is also plausible but speculative based on our current knowledge of established risk factors for hearing loss and dementia. Given the very close association between age and both hearing loss and dementia, there is a possibility of unaccounted residual confounding. However, this is unlikely because we also confirmed our findings in a statistical model using age rather than time-on-study as the time scale to account for nonlinear effects of age on hearing and cognition.44 Our findings were also unchanged after restricting our cohort to participants 65 years or older at baseline.

Finally, caution must be applied when generalizing the results of our current study because the BLSA is a volunteer cohort of individuals of high socioceconomic status. Further confirmation of our results will need to be performed in larger studies using more representative, community-based samples. However, this potential limitation to broad generalizability could strengthen the internal validity of our findings given the relative homogeneity of the study cohort in observed and likely unobservable characteristics.

If confirmed in other independent cohorts, the findings of our study could have substantial implications for individuals and public health. Hearing loss in older adults may be preventable45 and can be practically addressed with current technology (eg, digital hearing aids and cochlear implants) and with other rehabilitative interventions focused on optimizing social and environmental conditions for hearing. With the increasing number of people with hearing loss, research into the mechanistic pathways linking hearing loss with dementia and the potential of rehabilitative strategies to moderate this association are critically needed.

Correspondence: Frank R. Lin, MD, PhD, Department of Otolaryngology–Head and Neck Surgery, The Johns Hopkins School of Medicine, JHOC 6120, 601 N Caroline St, Baltimore, MD 21287 (

Accepted for Publication: April 29, 2010.

Author Contributions: Drs Metter and Ferrucci had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design: Lin, Metter, and Ferrucci. Acquisition of data: Metter, O’Brien, Resnick, Zonderman, and Ferrucci. Analysis and interpretation of data: Lin, Metter, O’Brien, Resnick, Zonderman, and Ferrucci. Drafting of the manuscript: Lin and Metter. Critical revision of the manuscript for important intellectual content: Lin, O’Brien, Resnick, Zonderman, and Ferrucci. Statistical analysis: Lin, Metter, Zonderman, and Ferrucci. Obtained funding: O’Brien and Resnick. Administrative, technical, or material support: O’Brien and Zonderman. Study supervision: Resnick and Ferrucci.

Financial Disclosure: None reported.

Funding/Support: This work was supported by the Intramural Research Program of the National Institute on Aging and grant 1K23DC011279-01 from the National Institute on Deafness and Other Communication Disorders (Dr Lin).

Role of the Sponsor: The National Institute on Aging funded the design and conduct of the study; collection, management, analysis, and interpretation of the data; and preparation and review of the manuscript. The sponsor was not involved in manuscript approval.



Ferri  CPPrince  MBrayne  C  et al. Alzheimer's Disease International, Global prevalence of dementia: a Delphi consensus study.  Lancet 2005;366 (9503) 2112- 2117PubMedGoogle ScholarCrossref


Alzheimer's Disease International, World Alzheimer Report 2009. Prince  MJackson  J London, England Alzheimer's Disease International2009;


Brookmeyer  RJohnson  EZiegler-Graham  KArrighi  HM Forecasting the global burden of Alzheimer's disease.  Alzheimers Dement 2007;3 (3) 186- 191PubMedGoogle ScholarCrossref


Coley  NAndrieu  SGardette  V  et al.  Dementia prevention: methodological explanations for inconsistent results.  Epidemiol Rev 2008;3035- 66PubMedGoogle ScholarCrossref


Uhlmann  RFLarson  EBRees  TSKoepsell  TDDuckert  LG Relationship of hearing impairment to dementia and cognitive dysfunction in older adults.  JAMA 1989;261 (13) 1916- 1919
ArticlePubMedGoogle ScholarCrossref


Ives  DGBonino  PTraven  NDKuller  LH Characteristics and comorbidities of rural older adults with hearing impairment.  J Am Geriatr Soc 1995;43 (7) 803- 806PubMedGoogle Scholar


Agrawal  YPlatz  EANiparko  JK Prevalence of hearing loss and differences by demographic characteristics among US adults: data from the National Health and Nutrition Examination Survey, 1999-2004.  Arch Intern Med 2008;168 (14) 1522- 1530
ArticlePubMedGoogle ScholarCrossref


Shock  NGreulich  RAndres  R  et al.  Normal Human Aging: The Baltimore Longitudinal Study of Aging  Washington, DC National Institutes of Health1984;NIH publication 84-2450


Kawas  CGray  SBrookmeyer  RFozard  JZonderman  A Age-specific incidence rates of Alzheimer's disease: the Baltimore Longitudinal Study of Aging.  Neurology 2000;54 (11) 2072- 2077PubMedGoogle ScholarCrossref


American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised.  Washington, DC American Psychiatric Association1987;


McKhann  GDrachman  DFolstein  MKatzman  RPrice  DStadlan  EM Clinical diagnosis of Alzheimer's disease: report of the NINCDS-ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer's Disease.  Neurology 1984;34 (7) 939- 944PubMedGoogle ScholarCrossref


Petersen  RCSmith  GEWaring  SCIvnik  RJTangalos  EGKokmen  E Mild cognitive impairment: clinical characterization and outcome.  Arch Neurol 1999;56 (3) 303- 308
ArticlePubMedGoogle ScholarCrossref


Schoenfeld  D Partial residuals for the proportional hazards regression model.  Biometrika 1982;69 (1) 239- 241Google ScholarCrossref


Therneau  TGrambsch  P Modeling Survival Data: Extending the Cox Model.  New York, NY Springer Publishing Co Inc2000;


Northridge  ME Public health methods: attributable risk as a link between causality and public health action.  Am J Public Health 1995;85 (9) 1202- 1204PubMedGoogle ScholarCrossref


Cacciatore  FNapoli  CAbete  PMarciano  ETriassi  MRengo  F Quality of life determinants and hearing function in an elderly population: Osservatorio Geriatrico Campano Study Group.  Gerontology 1999;45 (6) 323- 328PubMedGoogle ScholarCrossref


Peters  CAPotter  JFScholer  SG Hearing impairment as a predictor of cognitive decline in dementia.  J Am Geriatr Soc 1988;36 (11) 981- 986PubMedGoogle Scholar


Uhlmann  RFLarson  EBKoepsell  TD Hearing impairment and cognitive decline in senile dementia of the Alzheimer's type.  J Am Geriatr Soc 1986;34 (3) 207- 210PubMedGoogle Scholar


Gennis  VGarry  PJHaaland  KYYeo  RAGoodwin  JS Hearing and cognition in the elderly: new findings and a review of the literature.  Arch Intern Med 1991;151 (11) 2259- 2264
ArticlePubMedGoogle ScholarCrossref


Popelka  MMCruickshanks  KJWiley  TLTweed  TSKlein  BEKlein  R Low prevalence of hearing aid use among older adults with hearing loss: the Epidemiology of Hearing Loss Study.  J Am Geriatr Soc 1998;46 (9) 1075- 1078PubMedGoogle Scholar


Gordon-Salant  S Hearing loss and aging: new research findings and clinical implications.  J Rehabil Res Dev 2005;42 (4) ((suppl 2)) 9- 24PubMedGoogle ScholarCrossref


Pickles  JO An Introduction to the Physiology of Hearing.  Bingley, England Emerald Group Publishing2008;


Grimes  AMGrady  CLPikus  A Auditory evoked potentials in patients with dementia of the Alzheimer type.  Ear Hear 1987;8 (3) 157- 161PubMedGoogle ScholarCrossref


Sinha  UKHollen  KMRodriguez  RMiller  CA Auditory system degeneration in Alzheimer's disease.  Neurology 1993;43 (4) 779- 785PubMedGoogle ScholarCrossref


Parvizi  JVan Hoesen  GWDamasio  A The selective vulnerability of brainstem nuclei to Alzheimer's disease.  Ann Neurol 2001;49 (1) 53- 66PubMedGoogle ScholarCrossref


Baloyannis  SJMauroudis  IManolides  SLManolides  LS Synaptic alterations in the medial geniculate bodies and the inferior colliculi in Alzheimer's disease: a Golgi and electron microscope study.  Acta Otolaryngol 2009;129 (4) 416- 418PubMedGoogle ScholarCrossref


Gates  GABeiser  ARees  TSD’Agostino  RBWolf  PA Central auditory dysfunction may precede the onset of clinical dementia in people with probable Alzheimer's disease.  J Am Geriatr Soc 2002;50 (3) 482- 488PubMedGoogle ScholarCrossref


O’Grady  GBoyles  ALSpeer  MDeRuyter  FStrittmatter  WWorley  G Apolipoprotein E alleles and sensorineural hearing loss.  Int J Audiol 2007;46 (4) 183- 186PubMedGoogle ScholarCrossref


Stern  Y Cognitive reserve.  Neuropsychologia 2009;47 (10) 2015- 2028PubMedGoogle ScholarCrossref


Holtzer  RRakitin  BCSteffener  JFlynn  JKumar  AStern  Y Age effects on load-dependent brain activations in working memory for novel material.  Brain Res 2009;1249148- 161PubMedGoogle ScholarCrossref


Zarahn  ERakitin  BAbela  DFlynn  JStern  Y Age-related changes in brain activation during a delayed item recognition task.  Neurobiol Aging 2007;28 (5) 784- 798PubMedGoogle ScholarCrossref


Savva  GMWharton  SBInce  PGForster  GMatthews  FEBrayne  CMedical Research Council Cognitive Function and Ageing Study, Age, neuropathology, and dementia.  N Engl J Med 2009;360 (22) 2302- 2309PubMedGoogle ScholarCrossref


Tun  PAMcCoy  SWingfield  A Aging, hearing acuity, and the attentional costs of effortful listening.  Psychol Aging 2009;24 (3) 761- 766PubMedGoogle ScholarCrossref


Pichora-Fuller  MKSchneider  BADaneman  M How young and old adults listen to and remember speech in noise.  J Acoust Soc Am 1995;97 (1) 593- 608PubMedGoogle ScholarCrossref


Boyle  PAWilson  RSSchneider  JABienias  JLBennett  DA Processing resources reduce the effect of Alzheimer pathology on other cognitive systems.  Neurology 2008;70 (17) 1534- 1542PubMedGoogle ScholarCrossref


Strawbridge  WJWallhagen  MIShema  SJKaplan  GA Negative consequences of hearing impairment in old age: a longitudinal analysis.  Gerontologist 2000;40 (3) 320- 326PubMedGoogle ScholarCrossref


Weinstein  BEVentry  IM Hearing impairment and social isolation in the elderly.  J Speech Hear Res 1982;25 (4) 593- 599PubMedGoogle Scholar


Fratiglioni  LWang  HXEricsson  KMaytan  MWinblad  B Influence of social network on occurrence of dementia: a community-based longitudinal study.  Lancet 2000;355 (9212) 1315- 1319PubMedGoogle ScholarCrossref


Barnes  LLMendes de Leon  CFWilson  RSBienias  JLEvans  DA Social resources and cognitive decline in a population of older African Americans and whites.  Neurology 2004;63 (12) 2322- 2326PubMedGoogle ScholarCrossref


Bennett  DASchneider  JATang  YArnold  SEWilson  RS The effect of social networks on the relation between Alzheimer's disease pathology and level of cognitive function in old people: a longitudinal cohort study.  Lancet Neurol 2006;5 (5) 406- 412PubMedGoogle ScholarCrossref


Dalton  DSCruickshanks  KJKlein  BEKlein  RWiley  TLNondahl  DM The impact of hearing loss on quality of life in older adults.  Gerontologist 2003;43 (5) 661- 668PubMedGoogle ScholarCrossref


Lazarov  ORobinson  JTang  YP  et al.  Environmental enrichment reduces Aβ levels and amyloid deposition in transgenic mice.  Cell 2005;120 (5) 701- 713PubMedGoogle ScholarCrossref


Verghese  JLipton  RBKatz  MJ  et al.  Leisure activities and the risk of dementia in the elderly.  N Engl J Med 2003;348 (25) 2508- 2516PubMedGoogle ScholarCrossref


Korn  ELGraubard  BIMidthune  D Time-to-event analysis of longitudinal follow-up of a survey: choice of the time-scale.  Am J Epidemiol 1997;145 (1) 72- 80PubMedGoogle ScholarCrossref


Zhan  WCruickshanks  KJKlein  BE  et al.  Generational differences in the prevalence of hearing impairment in older adults.  Am J Epidemiol 2010;171 (2) 260- 266PubMedGoogle ScholarCrossref

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