Hearing Loss and Cognitive Decline in Older Adults

Previous longitudinal studies indicate that hearing loss and cognitive impairment are associated in non-tonal language-speaking older adults. This study aimed to investigate whether there is a longitudinal association between hearing loss and cognitive decline in older adults who speak a tonal language. Chinese-speaking older adults aged 60 years and above were recruited for baseline and 12 month follow-up measurements. All participants completed a pure tone audiometric hearing test, Hearing Impaired-Montreal Cognitive Assessment Test (HI-MoCA), and a Computerized Neuropsychological Test Battery (CANTAB). The De Jong Gierveld Loneliness Scale was used to measure loneliness, and the 21-item Depression Anxiety Stress Scale (DASS-21) was used to measure aspects of mental health. Associations between baseline hearing loss and various cognitive, mental and psychosocial measures were evaluated using logistic regression. A total of 71 (29.6%) of the participants had normal hearing, 70 (29.2%) had mild hearing loss, and 99 (41.2%) had moderate or severe hearing loss at baseline, based on mean hearing thresholds in the better ear. After adjusting for demographic and other factors, baseline moderate/severe audiometric hearing loss was associated with an increased risk of cognitive impairment at follow-up (OR: 2.20, 95% CI: 1.06, 4.50). When pure-tone average (PTA) was modeled continuously, an average difference of 0.24 in HI-MoCA scores for every 10 dB increase in BE4FA existed, and an average difference of 0.07 in the change of HI-MoCA scores in a 12 month period. The results revealed a significant longitudinal relationship between age-related hearing loss and cognitive decline in this cohort of tonal language-speaking older adults. Steps should also be taken to incorporate hearing assessment and cognitive screening in clinical protocols for older adults 60 years and above in both hearing and memory clinics.

Aim: To examine the association between a healthy diet, assessed by the Healthy Diet Indicator (HDI), and cognitive decline in older adults. Methods: Data from 21,837 participants aged ≥55 years from 3 cohorts (Survey in Europe on Nutrition and the Elderly, a Concerted Action [SENECA], Rotterdam Study [RS], Nurses' Health Study [NHS]) were analyzed. HDI scores were based on intakes of saturated fatty acids, polyunsaturated fatty acids, mono- and disaccharides, protein, cholesterol, fruits and vegetables, and fiber. The Telephone Interview for Cognitive Status in NHS and Mini-Mental State Examination in RS and SENECA were used to assess cognitive function from multiple repeated measures. Using multivariable-adjusted, mixed linear regression, mean differences in annual rates of cognitive decline by HDI quintiles were estimated. Results: Multivariable-adjusted differences in rates in the highest versus the lowest HDI quintile were 0.01 (95% CI -0.01, 0.02) in NHS, 0.00 (95% CI -0.02, 0.01) in RS, and 0.00 (95% CI -0.05, 0.05) in SENECA with a pooled estimate of 0.00 (95% CI -0.01, 0.01), I² = 0%. Conclusions: A higher HDI score was not related to reduced rates of cognitive decline in European and American older adults.

I read with great interest Kawakami et al.'s paper, “Examining the combined effects of social isolation and oral dysfunction on cognitive decline in community-dwelling older Japanese adults”.1 The research highlights a significant association between social isolation (SI) and oral dysfunction (OD), individually and in combination, with cognitive decline in older adults. Although the paper effectively presents these relationships, I propose an additional layer of understanding: that SI and OD are deeply intertwined, forming a self-perpetuating vicious cycle that accelerates cognitive decline. The study's conclusion regarding the combined factors of SI and OD, and their association with cognitive decline is particularly insightful.1 My opinion is that this association is strengthened by a bidirectional relationship between SI and OD, creating a feedback loop that intensifies their negative impact on cognitive function. This vicious cycle unfolds as follows: oral dysfunction often leads to social isolation. Challenges with eating, chewing and speaking, common manifestations of OD, can cause embarrassment and discomfort, leading to a reluctance to participate in social activities, especially those involving food or conversation. Consequently, individuals might withdraw, increasing SI and loneliness. This withdrawal reduces vital cognitive stimulation, directly contributing to cognitive decline. Specific issues in geriatric dentistry, such as significant tooth loss, complexities with dentures and dry mouth (xerostomia) often induced by polypharmacy, severely impact an older adults' confidence and ability to engage socially, further driving isolation.2 Conversely, SI can profoundly worsen oral dysfunction. A lack of social engagement can diminish an individual's motivation or access to maintain diligent oral hygiene, seek regular dental checkups or address emerging oral health issues.3 Without social support, self-care, including oral health, might be neglected. The psychological stress and potential depression associated with prolonged SI can also indirectly impact oral health by altering immune responses or reducing health-seeking behaviors.4 This deterioration in oral health then perpetuates the isolation, making social interaction even more challenging. Existing barriers to dental care in older adults, such as financial constraints, transportation difficulties, and limited access to geriatric dental specialists, are exacerbated by SI, as isolated individuals might lack the support networks necessary to overcome these hurdles.5 Negative attitudes and misconceptions regarding oral health in older adults, even among some healthcare professionals, further hinder access and motivation for care for those who are socially isolated. This interplay between SI and OD creates a powerful negative synergy, amplifying cognitive decline (Figure 1). Social isolation deprives the brain of crucial cognitive stimulation and increases psychosocial stress, both well-established contributors to cognitive impairment. Simultaneously, oral dysfunction can lead to malnutrition and chronic oral inflammation, which negatively impacts brain health.6 When these factors reinforce each other, cognitive reserve erodes faster, making individuals significantly more vulnerable to cognitive decline and dementia. The combined burden of increased oral disease risk (e.g. gum disease, tooth decay) and challenges in maintaining oral hygiene due to physical or cognitive impairments creates a cascade of health issues that collectively undermine cognitive resilience.6 Understanding this vicious cycle is critical for developing more effective and holistic interventions. Beyond promoting general social engagement and improving overall oral health, a comprehensive approach must consider several intervening factors. Integrated care models are essential, where dental professionals screen for SI and cognitive decline, and social workers understand oral health's impact on social participation. Psychological support is crucial to address distress and embarrassment. Nutritional counseling can mitigate cognitive risks from malnutrition. Community-based programs combining social activities with oral health education and accessible dental screenings offer dual benefits.7 Technology-assisted interventions, such as virtual platforms for social connection or digital reminders for oral hygiene, can support homebound older adults.8 Caregiver education on the interconnectedness of these factors is also vital. Crucially, targeted geriatric oral health initiatives are needed to directly confront specific challenges: effective xerostomia management, robust support for managing tooth loss and dentures, adaptive tools for oral hygiene despite limitations, and dismantling financial/transportation barriers to specialized dental care.9 Efforts must also shift negative attitudes and misconceptions about older adults' oral health. In conclusion, Kawakami et al.'s paper provides a vital foundation for understanding the combined impact of social isolation and oral dysfunction on cognitive decline. By recognizing the potential for a vicious cycle between these two factors, and by proactively addressing the specific challenges inherent in geriatric dentistry, we can move toward more comprehensive and impactful interventions. These integrated strategies will be instrumental in promoting healthier aging, and significantly mitigating the risk of cognitive impairment and dementia. No funding was received. The author declares no conflict of interest. All aspects of this work were carried out by the sole author. Data sharing is not applicable to this article, as no new data were created or analyzed in this study.

Scarce population-based data exist on whether APOE4 modifies associations of blood-based neurodegenerative biomarkers with cognitive decline, particularly in a diverse, biracial population of community-dwelling older adults without dementia. To assess whether APOE4 carrier status is associated with an accelerated rate of cognitive decline in older adults without dementia and with elevated neurodegenerative burden. This 20-year prospective cohort study started in 1993 and was conducted through 2012 on the South Side of Chicago among community-dwelling older adults without dementia from the longitudinal biracial Chicago Health and Aging Project. The interaction of APOE4 carrier status with prospective associations of serum neurodegenerative biomarkers with global cognitive decline was examined using a mixed-effects regression model, adjusting for demographics and chronic health conditions. Statistical analyses were conducted from June 2024 to January 2025. APOE4 carrier status and serum biomarker levels for total tau (t-tau), neurofilament light (NfL) chain, and glial fibrillary acidic protein (GFAP) measured with a Quanterix Neuroplex kit at baseline. Cognitive decline calculated from composite global cognition scores across study waves. Among 1038 community-dwelling older adults (mean [SD] age, 77.1 [5.9] years; 615 Black [59.2%] and 423 White [40.8%]; 651 female [62.7%]), there was a mean (SD) of 12.8 (3.4) years of education and 343 individuals (33.0%) were APOE4 carriers. Higher levels of blood-based neurodegenerative biomarkers (ie, t-tau, NfL, and GFAP) were associated with a faster rate of cognitive decline among APOE4 carriers than noncarriers. Specifically, compared with noncarriers, APOE4 carriers had annual rates of cognitive decline per 1-log10 unit higher levels in t-tau and GFAP that were accelerated by a β (SD) of -0.03 (0.02) (P = .046) and -0.07 (0.03) (P = .02), respectively. Similarly, compared with noncarriers and participants in the lower NfL tertile, APOE4 carriers with middle and upper tertiles of NfL levels experienced accelerated cognitive decline, with a β (SD) of -0.04 (0.02) (P = .006) and -0.03 (0.02) (P = .07), respectively, although the difference was not significant for upper tertiles. This study found that higher levels of neurodegeneration (t-tau), axonal injury (NfL), and reactive astrocytes and neuroinflammation (GFAP) biomarkers were associated with accelerated cognitive decline in genetically susceptible APOE4 carriers. These findings highlight the association of APOE4 with exacerbation of neurodegenerative processes, with not only significant implications for understanding and tracking the progression of neurodegenerative diseases, but also a call for inclusivity of APOE4 status in scientific investigations and clinical trials.

Midlife obesity is a known risk factor for cognitive impairment, whereas its association in late life is complex, giving rise to the concept of the 'obesity paradox.' The weight-adjusted waist index (WWI), an indicator reflecting central obesity, has recently emerged. However, evidence regarding the association between WWI and cognitive impairment in Chinese older adults remains scarce. This study explores WWI's association with cognitive decline in older adults, addressing gaps in central obesity's role in neurocognitive health. A total of 5001 older adults aged ≥65 years with normal cognition from the Chinese Longitudinal Healthy Longevity Survey were included in this longitudinal analysis, with a median follow-up duration of 4 years. A time-varying Cox proportional hazards regression model was used to evaluate the association between WWI, waist circumference (WC), body mass index (BMI) and incident cognitive impairment. Nonlinear correlations were investigated using restricted-cubic-spline curves. Subgroup analyses and sensitivity analyses were conducted to enhance the robustness of findings. The incidence of cognitive impairment across the four WWI quartile groups (Q1-Q4) was 6.7%, 7.8%, 9.3% and 13.4%, respectively. WWI was positively associated with incident cognitive impairment, whether treated as a continuous variable (hazard ratio [HR] = 1.14, 95% confidence interval [95% CI] = 1.06-1.23) or a categorised variable (Q4 vs. Q1: HR = 1.70, 95% CI = 1.29-2.24; Q3 vs. Q1: HR = 1.43, 95% CI = 1.08-1.90) in models adjusted for multiple covariates. WC showed a similar trend, while BMI demonstrated no significant association. Associations persisted across subgroups and sensitivity analyses. Elevated WWI and WC, but not BMI, were significantly associated with an increased risk of incident cognitive impairment. The findings suggested that WWI may be a more precise indicator of the association between obesity and cognitive impairment.

BackgroundAnemia and cardiovascular disease (CVD) are two prevalent chronic conditions causing cerebral hypoxia in older adults. Although anemia and CVD often coexist in older people and potentially share underlying mechanisms, the independent effects of these two diseases with cognitive decline are largely unknown. The objective of this cohort study is to investigate the independent associations of anemia and CVD with cognitive decline in older adults, and further explore their associations with changes in MRI markers of brain aging using longitudinal MRI data.MethodThis cohort study used data from 2244 dementia‐ and stroke‐free participants in the population‐based Swedish National study on Aging and Care in Kungsholmen (age ≥60 years, female 62%). Participants were regularly followed from 2001‐2004 (baseline) through 2013‐2016. Anemia (WHO criteria) and CVD were determined at baseline. Cognitive function was assessed using a neuropsychological test battery across 12 years. A subset of participants (N = 503) underwent brain MRI examinations at baseline, and 327undertook follow‐up MRI scans after 3 and/or 6 years. Brain volumetric measures and markers of cerebral small vessel disease (cSVD) were assessed following standard methods. The associations of anemia or/and CVD with cognitive decline and changes in brain volume and cSVD markers were investigated using linear mixed‐effects models, while controlling for age, sex, lifestyle, vascular risk factors, chronic kidney disease, cancer, serum c‐reactive protein, and APOE genotype.ResultOf the 2244 participants, 5% had only anemia and 17% had only CVD. Both anemia and CVD were independently associated with a steeper decline in global cognitive composite score (anemia ‐0.01/year; 95%CI ‐0.03 to ‐0.00, CVD ‐0.02/year; 95%CI ‐0.03 to ‐0.02). Anemia was associated with faster decline in category fluency and perceptual speed, while CVD was significantly associated with an accelerated decline in all examined cognitive domains. Both anemia and CVD at baseline were associated with a steeper decline in total brain tissue volume, while CVD was additionally associated with steeper decline in volumes of hippocampus (P<0.05). Neither was significantly associated with changes in cSVD markers (i.e., white‐matter hyperintensities, lacunes).ConclusionBoth anemia and CVD are risk factors for accelerated cognitive decline and brain atrophy in older adults.

To determine the extent to which the regional brain volumes associated with slow gait speed can inform subsequent cognitive decline in older adults from the Rush Memory and Aging Project. We utilized deformation-based morphometry (DBM) in a whole-brain exploratory approach to identify the regional brain volumes associated with gait speed assessed over a short distance during an in-home assessment. We created deformation scores to summarize the gait-associated regions and entered the scores into a series of longitudinal mixed effects models to determine the extent to which deformation predicted change in cognition over time, controlling for associations between gait and cognition. In 438 older adults (81 ± 7; 76% female), DBM revealed that slower gait speed was associated with smaller volumes across frontal white matter, temporal grey matter, and subcortical areas and larger volumes in the ventricles during the same testing cycle. When a subset was followed over multiple (5 ± 2) years, slower gait speed was also associated with annual declines in global cognition, executive functioning, and memory abilities. Several of the gait-related brain structures were associated with these declines in cognition; however, larger ventricles and smaller medial temporal lobe volumes proved most robust and attenuated the association between slow gait and cognitive decline. Regional brain volumes in the ventricles and temporal lobe associated with both slow gait speed and faster cognitive decline have potential to improve risk stratification for cognitive decline in older adults.

Neurofilament light chain (NfL) has been associated with cognitive status in multiple neurodegenerative conditions. Studies about plasma NfL and cognitive decline in older adults are still limited. 504 older adults (median age 75 years) who expressed memory complaints were selected from the Multidomain Alzheimer’s Preventive Trial (MAPT) and were classified as normal cognition (NC) or mild cognitive impairment (MCI). Cognitive functions were measured as mini mental state examination (MMSE) and composite cognitive score (CCS) over a 4-year period. Plasma NfL was measured at the first or the second year of the MAPT. Mixed-effects linear models were performed to evaluate cross-sectional and longitudinal associations. In the whole population, higher plasma NfL was cross-sectionally associated with lower cognitive functions (MMSE: β = − 0.007, 95% CI [− 0.013, − 0.001]; CCS: β = − 0.003, 95% CI [− 0.006, − 0.001]). In adults with MCI, but not NC, higher plasma NfL was associated with lower CCS at the cross-sectional level (β = − 0.003, 95% CI [− 0.005, − 0.0002]). The upper quartile NfL group further demonstrated more over time decline in CCS (β = − 0.07, 95% CI [− 0.12, − 0.01]) under the MCI status. Plasma NfL can be a promising biomarker of progressive cognition decline in older adults with MCI.

Cognitive decline is a major concern for older adults with epilepsy. Whether and how much faster older adults with epilepsy experience cognitive decline beyond expected age-related cognitive change remain unclear. We sought to estimate and compare rates of cognitive decline in older adults with and without epilepsy. The Cardiovascular Health Study is a population-based longitudinal cohort study of 5888 US adults aged 65+. Cognitive function was assessed annually with Modified Mini-Mental State Exam (3MS) and Digit Symbol Substitution Test (DSST). We used linear mixed models to estimate average rates of decline in 3MS and DSST scores by epilepsy status (prevalent, incident, or no epilepsy), adjusted for risk factors associated with cognitive decline. The rate of decline in 3MS was significantly faster in prevalent epilepsy (P<.001) and after incident epilepsy (P=.002) compared with no epilepsy. Prevalent epilepsy and apolipoprotein E gene (APOE) ε4 (ApoE4) had a synergistic interaction, whereby prevalent epilepsy and ApoE4 together were associated with 1.51 points faster annual decline in 3MS than would be expected if prevalent epilepsy and ApoE4 did not interact (P<.001). Older adults with prevalent epilepsy had a significantly lower initial DSST score and faster rate of decline compared to those with no epilepsy (P<.001). Faster decline in global cognitive ability seen in this study validates concerns of patients. ApoE4 allele status was an effect modifier of the relationship between cognitive decline and prevalent epilepsy. Further research is warranted to explore biological mechanisms and possible interventions to mitigate cognitive decline.

Neurodegenerative diseases pose increasing challenges to global aging populations. Cognitive decline in older adults is an initial indicator of neurodegenerative diseases, yet comprehensive research on environmental chemical exposures related to cognitive decline is limited. This study uses Exposome-Wide Association Study (ExWAS) framework to investigate associations of environmental chemicals with cognitive function in individuals aged ≥60 years. We used the Digit Symbol Substitution Test (DSST) scores and chemical biomarker data of the US National Health and Nutrition Examination Survey (NHANES) spanning four cycles (1999-2000, 2001-2002, 2011-2012, 2013-2014). We conducted multiple survey-weighted regression to identify biomarkers associated with DSST scores, Bayesian weighted quantile sum regression to estimate odds ratio (OR) of cognitive decline from multiple exposures to the identified biomarkers, and correlation network analyses to examine relationships among possible important biomarkers and cognitive decline. After correction for multiple comparisons, among 229 biomarkers having a ≥10% detection rate, 40 were associated with DSST scores (q-value &amp;lt;0.05). When assessing the effects of chemical mixtures on cognitive decline, no association between mixtures of chemicals and DSST scores was observed. Correlation network showed that cognitive decline is directly related with age and education level and identified that thiocyanate, m-/p-xylene, triclosan, benzophenone-3 and diphenyl phosphate were weakly related to cognitive function. In conclusion, leveraging the ExWAS framework enables us to identify chemical biomarkers that were not previously discovered from traditional approaches of examining a small number of chemicals at a time. While our findings provide foundation for further research, longitudinal studies are warranted to elucidate causal relationships.

BackgroundThe COVID‐19 pandemic led to widespread social isolation and loneliness, especially among older adults aged 60 years and above. Loneliness is increasingly recognized as a significant public health concern given its association with adverse physical and mental health outcomes. However, less is known about the potential impact of loneliness on cognitive health and decline in older adults during the COVID‐19 pandemic specifically.MethodsA systematic review was conducted to examine the evidence on the relationship between loneliness and cognitive decline in older adults during the COVID‐19 pandemic. A comprehensive search was performed in MEDLINE (PubMed), CINAHL (EBSCO), PsycINFO (EBSCO), EMBASE, Scopus, AgeLine, and ProQuest for relevant studies published after January 2020 using PRISMA guidelines. Additional manual searches supplemented the database search. Inclusion criteria were studies with validated measurements of both cognitive function and COVID‐19 pandemic exposure in adults aged 60 years and older. Four paired reviewers independently assessed the identified studies for eligibility based on the predetermined criteria.ResultsThe search identified 9 eligible longitudinal studies with a total combined sample of 4,810 older adults. Three studies specifically measured loneliness using validated scales such as the UCLA Loneliness Scale. The most common assessment of cognition was the Mini‐Mental State Examination (MMSE), which was used in 8 of the 9 studies. Of the 4 studies examining the association between loneliness and cognitive decline, 3 reported a significant relationship even after adjusting for potential confounding factors including age, sex, and education level. However, the specific cognitive domains affected and magnitude of the association varied across studies.ConclusionThe available evidence from this systematic review suggests higher loneliness is significantly associated with cognitive decline in older adults during the COVID‐19 pandemic. This relationship remained even after accounting for demographic and socioeconomic characteristics. These findings highlight the need for post‐pandemic public health strategies that foster social engagement and interaction while maintaining appropriate physical distancing measures. Such approaches may help mitigate the secondary effects of the pandemic on mental and cognitive health among older adults. Further research is warranted to elucidate the complex interrelationships between social isolation, loneliness, and cognitive decline.

The association between depressive symptoms with fear of falling and cognitive decline in older adults in the Korean community: An analysis of the Korean Longitudinal Study of Aging (KLoSA), 2006–2020

Diet quality plays an important role in dementia prevention. It remains unclear how the joint effect of vegetable variety and diet quality affects cognition. This study aimed to explore the association of diet quality and vegetable variety with cognitive decline in older adults. This prospective cohort study (2011–2015) included 436 community-dwelling elders in Taipei. Diet quality, assessed by the modified Alternative Healthy Eating Index (mAHEI), was computed from a food frequency questionnaire at baseline (2011–2013). Vegetable variety indicated the number of different vegetable groups, adjusted for vegetable quantity. Multivariable linear and logistic regression models were used to explore the association of diet quality and vegetable variety with the decline of global and domain-specific cognition over two years. Our findings suggest that high diet quality (the highest tertile of mAHEI) was associated with a lower risk of both global cognitive decline (adjusted odds ratio (AOR) = 0.54, confidence interval (CI) = 0.31–0.95) and decline of attention domain (AOR = 0.56, CI = 0.32–0.99) compared with low diet quality. In elders with high vegetable variety, high diet quality was associated with a lower risk of global cognitive decline (AOR = 0.49, CI = 0.26–0.95). We therefore concluded that high diet quality along with diverse vegetable intake was associated with a lower risk of cognitive decline in older adults.

Hearing intervention versus health education control to reduce cognitive decline in older adults with hearing loss in the USA (ACHIEVE): a multicentre, randomised controlled trial

Backgroundthe prevalence of individuals with cognitive decline is increasing since the number of elderly adults is growing considerably. The literature provides promising results on the beneficial effect of exercise and vitamin supplementation on cognitive function both in cognitively healthy as well as in the demented elderly.Methods/Designthe design is a two-by-two factorial randomised controlled trial. The study population consists of independently living elderly, between 70 and 80 years old, with mild cognitive impairment (MCI). In the RCT the effect of two interventions, a walking program and vitamin supplementation, is examined. The walking program (WP) is a group-based program aimed at improving cardiovascular endurance; frequency two lessons a week; lesson duration one hour; program duration one year. Non-walking groups receive a placebo activity program (PAP) (i.e. low intensive non-aerobic group exercises, like stretching) with the same frequency, lesson and program duration. Vitamin supplementation consists of a single daily vitamin supplement containing 50 mg B6, 5 mg folic acid and 0,4 mg B12 for one year. Subjects not receiving vitamin supplements are daily taking an identically looking placebo pill, also for a year. Participants are randomised to four groups 1) WP and vitamin supplements; 2) WP and placebo supplements; 3) PAP and vitamin supplements; 4) PAP and placebo supplements. Primary outcome measures are measures of cognitive function. Secondary outcomes include psychosocial wellbeing, physical activity, cardiovascular endurance and blood vitamin levels.Discussionno large intervention study has been conducted yet on the effect of physical activity and vitamin supplementation in a population-based sample of adults with MCI. The objective of the present article is to describe the design of a randomised controlled trial examining the effect of a walking program and vitamin B supplementation on the rate of cognitive decline in older adults with MCI.