The impact of education on dementia: Evidence from compulsory schooling reforms in England.

BackgroundCardiovascular risk factors are associated with a higher risk of dementia. However, whether physical activity could revert this increased risk remains uncertain. We analyzed the effect of physical activity on the risk of dementia stratified by cardiovascular risk factors.MethodsData from baseline (2002‐2003) to wave 9 (2018‐2019) of the English Longitudinal Study of Ageing (ELSA) were analyzed (n = 6,021). The wave that dementia was first detected after baseline was defined as the event time. Self‐reported physical activity (inactive, low, moderate, high) at baseline was measured using a validated questionnaire. Smoking, excessive alcohol consumption, hypertension, diabetes, and obesity were analyzed as cardiovascular risk factors. Participants with simultaneous presence of 2+ risk factors were classified with a high cardiovascular risk for dementia. Socioeconomic, behavioral, and health variables were added in the Cox proportional hazard regression model as possible confounders. The incidence and the risk of dementia for physical activity, cardiovascular risk factors, and their interaction were calculated.ResultBetween baseline and wave 9, 6.21% (95% confidence interval [CI]: 5.63 to 6.85) of the participants were diagnosed with dementia. Participants with 2+ cardiovascular risk factors had a higher risk of dementia (hazard ratio [HR]: 1.31; 95%CI: 1.04, 1.63) than low‐risk adults. Physical activity level was inversely associated with the risk of incident dementia in participants who were smokers (p for linear trend = 0.027), had hypertension (p for linear trend = 0.015), and obesity (p for linear trend = 0.014). Low physical activity level (e.g., engaging in moderate‐intensity physical activity once per week) reduced the risk of dementia in participants with hypertension (HR: 0.41; 95%CI: 0.24, 0.70), and obesity (HR: 0.37; 95%CI: 0.21, 0.67). Physical activity attenuated the increased risk of incident dementia provoked by accumulated cardiovascular risk factors. High risk participants with low (HR: 0.51; 95%CI: 0.29, 0.88), moderate (HR: 0.38; 95%CI: 0.21, 0.67) and high (HR: 0.46; 95%CI: 0.22, 0.98) physical activity level had lower risk of dementia than the high risk, inactive group. Sensitivity analyses confirmed the above‐mentioned findings.ConclusionPhysical activity starting at moderate‐intensity activities once per week attenuated the increased risk of dementia associated with cardiovascular risk factors in older adults.

Although social position plays a pivotal role in cognitive aging, most dementia prevention strategies and risk prediction models continue to emphasize biomedical and genetic factors (particularly APOE status). This disconnect raises critical questions about how social environments may shape the effect of genetic risk on dementia. We examined how APOE alleles interact with social adversity to determine dementia risk. We conducted an observational analysis using two large cohort studies-the Health and Retirement Study (HRS) and the English Longitudinal Study of Ageing (ELSA)-including individuals aged 55 years or older without dementia at baseline. A social adversity index was constructed based on the five domains of social determinants of health outlined in the Healthy People 2030 framework: education access, economic stability, healthcare quality, neighborhood environment, and social context. Participants were classified as having low (APOE-ε2), intermediate (APOE-ε3/ε3), or high (APOE-ε4) genetic risk of dementia. Dementia was ascertained via clinical diagnosis, cognitive testing, or validated caregiver report. Cox proportional hazards models were used in each cohort, and estimates were pooled using random-effects adjusting for covariates. A total of 9,849 participants (HRS = 5,797; ELSA = 4,052) were followed for up to 12 years. Genetic effects were most pronounced among individuals with social advantage (reference: APOE-ε3/ε3 with social advantage; APOE-ε2 HR = 0.67, 95%CI = 0.48-0.93; APOE-ε4 HR = 1.68, 95%CI = 1.37-2.06). In contrast, those experiencing high social adversity had elevated dementia risk regardless of genotype (reference: APOE-ε3/ε3 with social advantage; APOE-ε2 HR = 3.26, 95%CI = 2.06-5.16; APOE-ε3/ε3 HR = 3.12, 95%CI = 2.47-3.95; APOE-ε4 HR = 3.21, 95%CI = 2.34-4.41). Notably, individuals with high genetic risk but social advantage had a lower dementia risk than those with low genetic risk but high social adversity. The influence of genetic risk on dementia appears shaped by social position. Addressing social adversity may reduce dementia risk across genotypes and enhance equity in dementia prevention strategies.

This study aims to assess the relationship between modifiable dementia risk factors and both dementia and cognitive decline. Data were obtained from the Health and Retirement Study (HRS) [2008-2020], the China Health and Retirement Longitudinal Study (CHARLS) [2011-2020], and the English Longitudinal Study of Ageing (ELSA) [2010-2020]. After adjusting for confounding factors, multivariable logistic regression was utilized to analyze the relationship between modifiable dementia risk factors and dementia, while multivariable linear regression was employed to examine the relationship between these risk factors and cognitive decline. Additionally, the Cox proportional hazards model was used to assess the relationship between the number of risk factor events, clusters, and dementia risk. A total of 30,113 participants from HRS, CHARLS, and ELSA were included (44.6% male, mean age 66.04 years), with an average follow-up period of 7.29 years. A low education level was significantly associated with an increased risk of dementia and accelerated cognitive decline (Overall, OR = 2.93, 95% CI: 2.70-3.18; Overall, β = -0.25, 95% CI: -0.60 to-0.55). The presence of multiple dementia risk factors correlated with a higher dementia risk; Specifically, compared with more than 5 risk factor events, both having no dementia risk factors and having only one dementia risk factor were associated with a significantly lower risk of dementia (Overall, HR = 0.15, 95% CI: 0.11-0.22, HR = 0.22, 95% CI: 0.18-0.25). Compared to the group with no coexistence of risk factors, the clusters of excessive alcohol, diabetes, vision loss, and hearing loss (HR = 4.11; 95% CI = 3.42-4.95; p < 0.001); excessive alcohol, vision loss, smoking, and hearing loss (HR = 5.18; 95% CI = 4.30-6.23; p < 0.001); and excessive alcohol, obesity, diabetes, and smoking (HR = 5.96; 95% CI = 5.11-6.95; p < 0.001) were most strongly associated with dementia risk. Among the 11 risk factors, educational attainment has the greatest impact on dementia risk and cognitive decline. A dose-response relationship exists between the number of modifiable risk factor events and dementia risk. The coexistence of multiple risk factors is associated with dementia risk, and these associations vary by risk factor cluster.

BackgroundAlthough social position plays a pivotal role in cognitive aging, most dementia prevention strategies and risk prediction models continue to emphasize biomedical and genetic factors (particularly APOE status). This disconnect raises critical questions about how social environments may shape the effect of genetic risk on dementia. We examined how APOE alleles interact with social adversity to determine dementia risk.MethodsWe conducted an observational analysis using two large cohort studies—the Health and Retirement Study (HRS) and the English Longitudinal Study of Ageing (ELSA)—including individuals aged 55 years or older without dementia at baseline. A social adversity index was constructed based on the five domains of social determinants of health outlined in the Healthy People 2030 framework: education access, economic stability, healthcare quality, neighborhood environment, and social context. Participants were classified as having low (APOE-ε2), intermediate (APOE-ε3/ε3), or high (APOE-ε4) genetic risk of dementia. Dementia was ascertained via clinical diagnosis, cognitive testing, or validated caregiver report. Cox proportional hazards models were used in each cohort, and estimates were pooled using random-effects adjusting for covariates.ResultsA total of 9,849 participants (HRS = 5,797; ELSA = 4,052) were followed for up to 12 years. Genetic effects were most pronounced among individuals with social advantage (reference: APOE-ε3/ε3 with social advantage; APOE-ε2 HR = 0.67, 95%CI = 0.48–0.93; APOE-ε4 HR = 1.68, 95%CI = 1.37–2.06). In contrast, those experiencing high social adversity had elevated dementia risk regardless of genotype (reference: APOE-ε3/ε3 with social advantage; APOE-ε2 HR = 3.26, 95%CI = 2.06–5.16; APOE-ε3/ε3 HR = 3.12, 95%CI = 2.47–3.95; APOE-ε4 HR = 3.21, 95%CI = 2.34–4.41). Notably, individuals with high genetic risk but social advantage had a lower dementia risk than those with low genetic risk but high social adversity.ConclusionsThe influence of genetic risk on dementia appears shaped by social position. Addressing social adversity may reduce dementia risk across genotypes and enhance equity in dementia prevention strategies.

This study examined the relationship between sleep disorders and the risk of dementia in patients with newly diagnosed type 2 diabetes. This study used the Korean Health Screening Cohort data and included 39 135 subjects aged ≥40 years with new-onset type 2 diabetes between 2004 and 2007, with follow-up throughout 2013. Sleep disorders were measured by F51(sleep disorders not due to a substance or known physiological condition) or G47(sleep disorders) under International Classification of Diseases, Tenth Revision (ICD-10) codes as a primary diagnosis, and the adjusted hazard ratio (AHR) and 95% CI of all-cause dementia, Alzheimer disease, vascular dementia, and other dementia were estimated using multivariable Cox proportional hazards regression models. In the patients with type 2 diabetes with an age range between 42 and 84 years (M = 57.8, SD = 9.5), this study identified 2059 events of dementia during an average follow-up time of 5.7 years. In patients with type 2 diabetes, subjects with sleep disorders were associated with an increased risk of all-cause dementia (AHR, 1.46; 95% CI, 1.19-1.80), Alzheimer disease (AHR, 1.39; 95% CI, 1.02-1.88), and other dementia (AHR, 1.69; 95% CI, 1.23-2.31) compared to those without sleep disorders. Men (AHR, 1.93; 95% CI, 1.42-2.62) and older adults (AHR, 1.70; 95% CI, 1.35-2.15) with sleep disorders were associated with an increased risk of dementia than their counterparts without sleep disorders among patients with type 2 diabetes. These findings suggest that sleep disorders are significantly associated with an increased risk of dementia in patients with new-onset type 2 diabetes.

Growing evidence supports a strong and likely causal association between cardiovascular disease (CVD), and its risk factors, with incidence of cognitive decline and Alzheimer's disease. Individuals with subclinical CVD are at higher risk for dementia and Alzheimer's. Several cardiovascular risk factors are also risk factors for dementia, including hypertension, high LDL cholesterol, low HDL cholesterol and especially diabetes. Moderate alcohol appears to be protective for both CVD and dementia. In contrast, inflammatory markers predict cardiovascular risk, but not dementia, despite biological plausibility for such a link. The substantial overlap in risk factors points to new avenues for research and prevention.

Given the fear and stigma surrounding dementia

The "LIfestyle for BRAin health" (LIBRA) index was recently updated with three new modifiable factors: hearing impairment, social contact, and sleep (LIBRA2), but has not yet been validated. Comparison of the performance of both LIBRA versions in predicting dementia risk. Longitudinal data from the English Longitudinal Study of Ageing (ELSA) and the Maastricht Aging Study (MAAS) were used. The weighted LIBRA (11/12 factors available) and LIBRA2 (14/15 factors available) scores were calculated, with higher scores representing an unhealthier lifestyle. Dementia diagnoses were based on self- or informant reported physician diagnosis, an informant-based cognitive screening tool, registry data or test data. Cox-proportional hazards regression was used to investigate the association between LIBRA(2) scores and dementia risk. Model fit and predictive accuracy were determined using the Akaike information criterion and Harrell's C index. Over an average follow-up of 8.3 years in ELSA and 17.9 years in MAAS, 346 (4.6%) and 120 (8.5%) individuals developed dementia, respectively. In ELSA, a one-point increase in LIBRA2 was associated with an 8% (1.06-1.11) higher dementia risk (LIBRA: 13%, 1.09-1.16). In MAAS, a one-point increase in LIBRA2 was associated with a 6% (1.01-1.12) higher dementia risk (LIBRA: 8%, 0.99-1.16). In ELSA, LIBRA (Harrell's C = 0.68) and LIBRA2 (Harrell's C = 0.67) performed similarly. In MAAS, LIBRA2 (Harrell's C = 0.62) performed better compared to LIBRA (Harrell's C = 0.52). LIBRA2 is a better model for identifying individuals at increased dementia risk and for public health initiatives aimed at dementia risk reduction.

The study aimed to investigate the association between changes in sarcopenia and the risk of dementia, and whether cumulative levels of physical activity (PA) mediate the association of changes in sarcopenia with dementia. Our data are from the English Longitudinal Study of Aging (2004-2019). Robust, probable sarcopenia and sarcopenia were assessed according to European Working Group of Sarcopenia in Older People (EWGSOP2) criteria. Kaplan-Meier cumulative risk curves were used to explore the association between changes in sarcopenia and the risk of dementia. Cox proportional hazard models were used to calculate the hazard ratios (HR) and 95% confidence intervals (95% CI). Causal mediation analysis was used to assess the mediating effects of cumulative levels of PA. A total of 3610 participants were included in the analysis. At a median follow-up time of 9.83 years, 296 participants developed dementia. Compared with participants with stable robust, participants with robust to probable sarcopenia/sarcopenia had an increased risk of dementia (HR = 1.49, 95% CI = 1.05-2.10); conversely, compared with participants with stable sarcopenia, participants with sarcopenia to probable sarcopenia/robust did not have a reduced risk of dementia (HR = 0.79, 95% CI = 0.51-1.52). The cumulative levels of PA mediate the association with robust to probable sarcopenia/sarcopenia and the risk of dementia with a natural indirect effect HR (95% CI) of 1.06 (1.01-1.13), proportion mediated = 15.4%. Different changes in sarcopenia were associated with different dementia risks, with continued progression of sarcopenia, increased dementia risk, and cumulative levels of PA mediated the association between the progression of sarcopenia and the risk of dementia.

With the projected surge in global dementia cases and no curative treatment available, research is increasingly focusing on lifestyle factors as preventive measures. Social and cognitive leisure activities are promising targets, but it is unclear which types of activities are more beneficial. This study investigated the individual and joint contribution of cognitive and social leisure activities to dementia risk and whether they modify the risks associated with other potentially modifiable and non-modifiable risk factors. We used data from the English Longitudinal Study of Ageing (ELSA) from 7917 participants, followed up from 2008/2009 (Wave 4) until 2018/2019 (Wave 9) for incident dementia. Self-reported baseline cognitive activities (e.g. 'reading the newspaper'), the number of social memberships (e.g. being a member of a social club) and social participation (e.g. 'going to the cinema') were clustered into high and low based on a median split. Subsequently, their individual and joint contribution to dementia risk, as well as their interaction with other dementia risk factors, were assessed with Cox regression models, adjusting for age, sex, level of education, wealth and a composite score of 11 lifestyle-related dementia risk factors. After a median follow-up period of 9.8 years, the dementia incidence rate was 54.5 cases per 10.000 person-years (95% CI 49.0-60.8). Adjusting for demographic and other lifestyle-related risk factors, higher engagement in cognitive activities (HR = 0.58; 95% CI 0.40-0.84), a greater number of social memberships (HR = 0.65; 95% CI 0.51-0.84) and more social participation (HR = 0.71; 95% CI 0.54-0.95) were associated with lower dementia risk. In a joint model, only engagement in cognitive activities (HR = 0.60; 95% CI 0.40-0.91) and social memberships (HR = 0.75; 95% CI 0.56-0.99) independently explained dementia risk. We did not find any interaction with other modifiable and non-modifiable risk factors. Engagement in cognitive and social leisure activities may be beneficial for overall dementia risk, independent of each other and other risk factors. Both types of activities may be potential targets for dementia prevention measures and health advice initiatives.

BackgroundRestless leg syndrome (RLS) is associated with poor sleep quality, depression or anxiety, poor dietary patterns, microvasculopathy, and hypoxia, all of which are known risk factors for dementia. However, the relationship between RLS and incident dementia remains unclear. This retrospective cohort study aimed to explore the possibility that RLS could be deemed as a non-cognitive prodromal feature of dementia.MethodsThis was a retrospective cohort study using the Korean National Health Insurance Service-Elderly Cohort (aged ≥ 60). The subjects were observed for 12 years, from 2002 to 2013. Identifying patients with RLS and dementia was based on the 10th revised code of the International Classification of Diseases (ICD-10). We compared the risk of all-cause dementia, Alzheimer’s disease (AD), and vascular dementia (VaD) in 2501 subjects with newly diagnosed RLS and 9977 matched controls based on age, sex, and index date. The association between RLS and the risk of dementia was assessed using Cox regression hazard regression models. The effect of dopamine agonists on the risk of dementia among RLS patients was also explored.ResultsThe baseline mean age was 73.4, and the subjects were predominantly females (63.4%). The incidence of all-cause dementia was higher in the RLS group than that in the control group (10.4% vs 6.2%). A baseline diagnosis of RLS was associated with an increased risk of incident all-cause dementia (adjusted hazard ratio [aHR] 1.46, 95% confidence interval [CI] 1.24–1.72). The risk of developing VaD (aHR 1.81, 95% CI 1.30–2.53) was higher than that of AD (aHR 1.38, 95% CI 1.11–1.72). The use of dopamine agonists was not associated with the risk of subsequent dementia among patients with RLS (aHR 1.00, 95% CI 0.76–1.32).ConclusionsThis retrospective cohort study suggests that RLS is associated with an increased risk of incident all-cause dementia in older adults, providing some evidence that requires confirmation through prospective studies in the future. Awareness of cognitive decline in patients with RLS may have clinical implications for the early detection of dementia.

To determine the interrelationships between baseline Mini-Mental State Examination (MMSE) score and risk of overall dementia, post-recurrent stroke dementia, and dementia without recurrent stroke among patients with a history of stroke. Prospective cohort study among participants enrolled in the Perindopril Protection Against Recurrent Stroke Study (PROGRESS) for whom baseline MMSE score was available. Baseline MMSE score was divided into 4 categories: 30, 29-27, 26-24, and <24. Participants were followed for incident dementia and recurrent stroke. Logistic regression models were used to examine the association between MMSE score and dementia. Of the 6080 participants included in this analysis, 2493 had an MMSE score of 30, 1768 had a score of 29-28, 1369 had a score of 26-24, and 450 had a score of <24. Average follow-up time was 3.8 years. There were 407 cases of dementia, 106 of which were preceded by a recurrent stroke. The risk of overall dementia increased with decreasing MMSE score. However, the impact of MMSE score on the risk of dementia without recurrent stroke was much stronger than the impact of MMSE score on the risk of post-recurrent stroke dementia. For those with MMSE score <24, the risk of dementia without recurrent stroke was 47.89 (95% confidence interval, 28.57-80.26), whereas the risk of post-recurrent stroke dementia was only 7.17 (95% confidence interval, 3.70-13.89). Higher MMSE scores were even less strongly associated with the risk of post-recurrent stroke dementia. Patients with stroke with low MMSE scores are at high risk of dementia over time, even in the absence of a recurrent stroke, and should therefore be followed closely for further cognitive decline.

Physical activity attenuates the risk for dementia associated with aging in older adults with mild cognitive impairment. Findings from a population-based cohort study

Associations of socioeconomic status and healthy lifestyle with incident dementia and cognitive decline: two prospective cohort studies

Arterial hypertension in midlife may increase the risk of late-life dementia. Notably, there is conflicting data as to whether hypertension in the elderly (age 65 years and older) is a risk factor for dementia and Alzheimer's disease (AD). We determined whether drug-untreated hypertension was associated with a higher risk of incident dementia and AD. In a population-based study of older people in central Spain (NEDICES), non-demented participants were followed prospectively. Dementia at follow-up was diagnosed using DSM-IV criteria. Using Cox proportional hazards models, the risk of dementia was estimated in participants with drug-untreated hypertension and in participants with drug-treated hypertension versus controls. The 3,824 participants had a mean duration of follow-up of 3.2 years. Sixty-two (3.3%) of 1,870 participants without baseline hypertension developed incident dementia versus 78 (4.7%) of 1,657 with drug-treated, baseline hypertension and 19 (12.0%) with drug-untreated, baseline hypertension. In an unadjusted Cox model, risk of dementia was increased in participants with drug-untreated hypertension (relative risk [RR] =1.93, 95% confidence interval [CI]=1.15–3.23, p = 0.01) and in participants with drug-treated hypertension (RR =1.43, 95% CI= 1.02–2.0, p =0.035) versus participants without hypertension (reference group). In a fully adjusted Cox model, the risk of dementia remained increased in participants with drug-untreated hypertension (RR =2.38, 95% CI =1.32–4.29, p=0.004). Results were similar for risk of AD. Our results suggest that drug-untreated hypertension may be an independent risk factor for dementia and AD in the elderly.