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BACKGROUND: High cognitive reserve (CR) has been related to lower dementia risk, but its association with heart disease (HD) is unknown. We aimed to explore the relation of CR to HD and cardiac structure and function. METHODS AND RESULTS: Within the UK Biobank, 349 907 HD-free participants were followed up. A composite CR indicator involving education/occupation attainment/television viewing time/confiding frequency/social connection frequency/variety of leisure activities was generated, and further categorized into low/moderate/high levels. Incident HD, including coronary HD, cardiac arrhythmia, and heart failure, was ascertained on the basis of medical records. During the follow-up, a subsample (n=31 182) underwent cardiac magnetic resonance imaging to assess ventricular structure and function. Data were analyzed using Cox regression, Laplace regression, and linear regression. Compared with low CR, the hazard ratio and 95% CI of any HD for high CR was 0.78 (0.75-0.80) (including 0.68 [0.66-0.71] for coronary HD, 0.91 [0.87-0.95] for cardiac arrhythmia, and 0.63 [0.58-0.68] for heart failure). Furthermore, high CR was associated with delayed HD onset by 1.59 (95% CI, 1.37-1.82) years compared with low CR. In cardiac magnetic resonance imaging data analysis, compared with low CR, high CR was associated with larger left ventricular end-diastolic volume (ß, 0.13 [95% CI, 0.09-0.17]), left ventricular end-systolic volume (ß, 0.05 [95% CI, 0.01-0.10]), left ventricular stroke volume (ß, 0.16 [95% CI, 0.12-0.21]), and left ventricular ejection fraction (ß, 0.08 [95% CI, 0.03-0.13]). CONCLUSIONS: High CR is associated with favorable HD health. Our findings suggest that the beneficial effect of CR is not limited to dementia but also HD.

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Importance: Inflammation has been proposed as a mechanism linking cardiometabolic diseases (CMDs) to increased risk of dementia. However, whether an anti-inflammatory diet can support brain and cognitive health among people with CMDs is unclear. Objective: To examine CMD status and dietary inflammatory potential in association with dementia risk and brain magnetic resonance imaging (MRI) measures using joint effect analysis. Design, Setting, and Participants: The UK Biobank is an ongoing community-based cohort study with baseline assessments conducted between March 13, 2006, and October 1, 2010. The present study included 84 342 dementia-free older adults (≥60 years), who were followed up until January 20, 2022 (maximum, 15 years). A subsample (n = 8917) underwent brain MRI scans between May 2, 2014, and March 13, 2020. Exposures: Baseline CMDs (including type 2 diabetes, heart disease, and stroke) were ascertained from medical records. Dietary Inflammatory Index scores (anti-inflammatory [≤-1.5 points], neutral [>-1.5 to <0.5 points], or proinflammatory [≥0.5 points]) were calculated from participants' average intake of 31 nutrients, assessed up to 5 times using the Oxford WebQ, a web-based, 24-hour dietary assessment. Main Outcomes and Measures: Incident dementia was identified through linkage to medical records. Regional brain volumes were collected from brain MRI scans. Results: The study included 84 342 participants (mean [SD] age, 64.1 [2.9] years; 43 220 [51.2%] female). At baseline, 14 079 (16.7%) had at least 1 CMD. Over a median follow-up of 12.4 (IQR, 11.8-13.1) years, 1559 individuals (1.9%) developed dementia. With the use of joint effect analysis, the hazard ratio of dementia was 2.38 (95% CI, 1.93-2.93) for people with CMDs and a proinflammatory diet and 1.65 (95% CI, 1.36-2.00) for those with CMDs and an anti-inflammatory diet (reference: CMD-free, anti-inflammatory diet). Dementia risk was 31% lower (hazard ratio, 0.69; 95% CI, 0.55-0.88; P = .003) among people with CMDs and an anti-inflammatory diet. On brain MRI, participants with CMDs and an anti-inflammatory diet compared with a proinflammatory diet additionally had significantly larger gray matter volume (ß = -0.15; 95% CI, -0.24 to -0.06 vs ß = -0.27; 95% CI, -0.38 to -0.16) and smaller white matter hyperintensity volume (ß = 0.05; 95% CI, -0.04 to 0.14 vs ß = 0.16; 95% CI, 0.05-0.27). Conclusions and Relevance: In this cohort study, people with CMDs and an anti-inflammatory compared with proinflammatory diet had a significantly lower hazard ratio of dementia, larger gray matter volume, and smaller white matter hyperintensity volume.

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BACKGROUND: Poorer psychological well-being has been related to an increased dementia risk, but changes in psychological well-being along the dementia course are unclear. We explored psychological well-being trajectories before and after the diagnosis of mild cognitive impairment (MCI) and dementia. METHODS: Within the Rush Memory and Aging Project, 910 cognitively intact older adults were followed annually for up to 14 years to detect incident MCI and dementia. Psychological well-being and its six components (self-acceptance, autonomy, environmental mastery, purpose in life, positive relation with others, and personal growth) were annually measured based on Ryff's Scales of Psychological Well-Being. Data were analysed using mixed-effect models with a backward timescale. RESULTS: Compared with participants who remained cognitively intact, those who developed incident MCI had a faster decline in psychological well-being (ß -0.015, 95% CI -0.027 to -0.003), leading to lower well-being 2 years before MCI diagnosis (mean difference at year -2, -0.099, 95% CI -0.187 to -0.012). Considering different well-being components, those who developed MCI had lower levels of purpose in life and personal growth beginning 3 years (-0.126, 95% CI -0.251 to -0.001) and 6 years (-0.139, 95% CI -0.268 to -0.009) before MCI, respectively. The slope of psychological well-being decline was similar before and after MCI diagnosis for each component except for positive relation with others, which had an accelerated decline after MCI (ß -0.042, 95% CI-0.075 to -0.009). Well-being trajectories remained similar for individuals with MCI regardless of whether they later developed dementia. CONCLUSIONS: Psychological well-being (specifically purpose in life and personal growth) became significantly lower before MCI diagnosis.

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OBJECTIVE: Diabetes is a well-known risk factor for dementia. We investigated the association between (pre)diabetes and older brain age and whether this can be attenuated by modifiable lifestyle behaviors. RESEARCH DESIGN AND METHODS: The study included 31,229 dementia-free adults from the UK Biobank between the ages of 40 and 70. Glycemic status (normoglycemia, prediabetes, or diabetes) was ascertained based on medical history, medication use, and HbA1c measured at baseline. Information on cardiometabolic risk factors (obesity, hypertension, low HDL, and high triglycerides) and lifestyle behaviors (smoking, drinking, and physical activity) was also collected at baseline. Participants underwent up to two brain MRI scans over 11 years of follow-up. Brain age was estimated using a machine learning model based on 1,079 brain MRI phenotypes and used to calculate brain age gap (BAG; i.e., brain age minus chronological age). RESULTS: At baseline, 13,518 participants (43.3%) had prediabetes and 1,149 (3.7%) had diabetes. Prediabetes (ß = 0.22 [95% CI 0.10, 0.34]) and diabetes (2.01 [1.70, 2.32]) were both associated with significantly higher BAG, and diabetes was further associated with significant increase in BAG over time (0.27 [0.01, 0.53]). The association between (pre)diabetes and higher BAG was more pronounced in men and in people with two or more cardiometabolic risk factors. In joint exposure analysis, having a healthy lifestyle (i.e., no smoking, no heavy drinking, and high physical activity) significantly attenuated the diabetes-BAG association. CONCLUSIONS: Diabetes and even prediabetes are associated with accelerated brain aging, especially among men and people with poor cardiometabolic health. However, a healthy lifestyle may counteract this.

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BACKGROUND: Cardiometabolic diseases (CMDs) including type 2 diabetes, heart disease, and stroke have been linked to a higher risk of dementia. We examined whether high levels of cognitive reserve (CR) can attenuate the increased dementia risk and brain pathologies associated with CMDs. METHODS: Within the UK Biobank, 216,178 dementia-free participants aged ≥ 60 were followed for up to 15 years. Baseline CMDs and incident dementia were ascertained from medical records, medication use, and medical history. Latent class analysis was used to generate an indicator of CR (low, moderate, and high) based on education, occupational attainment, confiding in others, social contact, leisure activities, and television watching time. A subsample (n = 13,663) underwent brain MRI scans during follow-up. Volumes of total gray matter (GMV), hippocampus (HV), and white matter hyperintensities (WMHV) were ascertained, as well as mean diffusivity (MD) and fractional anisotropy (FA) in white matter tracts. RESULTS: At baseline, 43,402 (20.1%) participants had at least one CMD. Over a mean follow-up of 11.7 years, 6,600 (3.1%) developed dementia. The presence of CMDs was associated with 57% increased risk of dementia (HR 1.57 [95% CI 1.48, 1.67]). In joint effect analysis, the HRs of dementia for people with CMDs and moderate-to-high CR and low CR were 1.78 [1.66, 1.91] and 2.13 [1.97, 2.30]), respectively (reference: CMD-free, moderate-to-high CR). Dementia risk was 17% lower (HR 0.83 [0.77, 0.91], p < 0.001) among people with CMDs and moderate-to-high compared to low CR. On brain MRI, CMDs were associated with smaller GMV (ß -0.18 [-0.22, -0.13]) and HV (ß -0.13 [-0.18, -0.08]) as well as significantly larger WMHV (ß 0.06 [0.02, 0.11]) and MD (ß 0.08 [0.02, 0.13]). People with CMDs and moderate-to-high compared to low CR had significantly larger GMV and HV, but no differences in WMHV, MD, or FA. CONCLUSIONS: Among people with CMDs, having a higher level of CR was associated with lower dementia risk and larger gray matter and hippocampal volumes. The results highlight a mentally and socially active life as a modifiable factor that may support cognitive and brain health among people with CMDs.

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BACKGROUND: Cognitive reserve (CR) has been linked to dementia, yet its influence on the risk of depression and related outcomes remains unknown. We aimed to examine the association of CR with depression and subsequent dementia or death, and to assess the extent to which CR is related to depression-free survival. METHODS: Within the UK Biobank, 436,232 participants free of depression and dementia were followed. A comprehensive CR indicator (low, moderate, and high) was created using latent class analysis based on information on education, occupation, mentally passive sedentary behavior, social connection, confiding with others, and leisure activities. Depression, dementia, and survival status were ascertained through self-reported medical history and/or linkages to medical records. Data were analyzed using multi-state Markov model and Laplace regression. RESULTS: Over a median follow-up of 12.96 years, 16,560 individuals developed depression (including 617 with subsequent dementia) and 28,655 died. In multivariable multi-state models, compared with low CR, high CR was associated with lower risk of depression (hazard ratio 0.53 [95% confidence interval 0.51-0.56]) and lower risk of post-depression dementia (0.55 [0.34-0.88]) or death (0.69 [0.55-0.88]) in middle-aged adults (aged <60 years). In Laplace regression, the depression-free survival time was prolonged by 2.77 (2.58-2.96) years in participants with high compared to low CR. CONCLUSIONS: High CR is associated with lower risks of depression and subsequent transitions to dementia and death, particularly in middle age. High CR may prolong depression-free survival. Our findings highlight the importance of enhancing CR in the prevention and prognosis of depression.

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BACKGROUND: This article aimed to develop and validate a simple-to-use nomogram to predict 15-year disability-free survival among older adults. METHODS: A cohort of 1878 disability-free participants aged ≥60 was followed for 15 years. Participants were randomly divided into a training cohort for nomogram development (n = 1314 [70 %]) and validation cohort to confirm the model's performance (n = 564 [30 %]). Information on socio-demographic, lifestyle factors, the Life Satisfaction Index A (LSI-A), chronic diseases, and Mini-Mental State Examination (MMSE) score, and biomarkers were collected through interviews, clinical and neuropsychological examinations, and medical records. Disability-free survival was defined as survival in the absence of dementia and physical disability, and the composite endpoint is first occurrence of events of death, dementia and physical disability. We developed a nomogram summing the number of risk points corresponding to weighted covariates to predict disability-free survival. Validation of the nomogram using C statistic, calibration plots, and Kaplan-Meier curves. RESULTS: In the multivariate-adjusted model, factors associated with composite end point were younger age, high MMSE (hazard ratio [HR], 0.93; [95 % CI, 0.87-0.99]), high LSI-A (0.78, [0.64-0.97]), non-smoking (0.74, [0.59-0.94]), engagement in physical leisure activity (0.62, [0.48-0.78]), and absence of chronic diseases (0.78, [0.66-0.91]). Incorporating these 6 factors, the nomogram achieved C-statistics of 0.78 (95 % CI, 0.75-0.81) and 0.77 (95 % CI, 0.74-0.80) in predicting disability-free survival in the training and validation cohorts, respectively, and had good calibration curves. CONCLUSION: The nomogram was able to predict long-term of disability-free survival and performed well on internal validation, and may be considered for use in effective surveillance, promote, management of clinical and public health ageing.

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BACKGROUND AND OBJECTIVES: Cardiovascular health (CVH) has been associated with cognitive decline and dementia, but the extent to which CVH affects brain health remains unclear. We investigated the association of CVH, assessed using Life's Essential 8 (LE8), with neuroimaging-based brain age and brain-predicted age difference (brain-PAD). METHODS: This longitudinal community-based study was based on UK Biobank participants aged 40-69 years who were free from dementia and other neurologic diseases at baseline. LE8 score at baseline was assessed with 8 measures and tertiled as low, moderate, and high CVH. Structural and functional brain MRI scans were performed approximately 9 years after baseline, and 1,079 measures from 6 neuroimaging modalities were used to model brain age. A Least Absolute Shrinkage and Selection Operator regression model was trained in 4,355 healthy participants and then used to calculate brain age and brain-PAD in the whole population. Data were analyzed using linear regression models. RESULTS: The study included 32,646 participants (mean age at baseline 54.74 years; 53.44% female; mean LE8 score: 71.90). In multivariable-adjusted linear regression, higher LE8 score was associated with younger brain age (ß [95% CI] -0.037 [-0.043 to -0.031]) and more negative brain-PAD (ß [95% CI] -0.043 [-0.048 to -0.038]) (brain looks younger for chronological age). Compared with high CVH, low/moderate CVH was associated with older brain age (ß [95% CI] 1.030 [0.852-1.208]/0.475 [0.303-0.647]) and increased brain-PAD (ß [95% CI] 1.193 [1.029-1.357]/0.528 [0.370-0.686]). The associations between low CVH and older brain age/brain-PAD remained similar and significant in both middle-aged (ß [95% CI] 1.199 [0.992-1.405]/1.351 [1.159-1.542]) and older adults (ß [95% CI] 0.764 [0.417-1.110]/0.948 [0.632-1.263]). DISCUSSION: Low CVH is associated with older brain age and greater brain-PAD, even among middle-aged adults. Our findings suggest that optimizing CVH could support brain health. The main limitation of our study is that the study sample was healthier than the general population, thus caution is required when generalizing our findings to other populations.

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OBJECTIVE: This study aimed to examine the association between past/current sleep duration and macro-/micro-structural brain outcomes and explore whether hypertension or social activity plays a role in such association. METHODS: Within the UK Biobank, 40 436 dementia-free participants (age 40-70 years) underwent a baseline assessment followed by a brain magnetic resonance imaging (MRI) scan 9 years later. Past (baseline) and current (MRI scans) sleep duration (hours/day) were recorded and classified as short (≤5), intermediate (6-8), and long (≥9). Brain structural volumes and diffusion markers were assessed by MRI scans. RESULTS: Compared with past intermediate sleep, past short sleep was related to smaller cortex volumes (standardized ß [95 % CI]: -0.04 [-0.07, -0.02]) and lower regional fractional anisotropy (FA) (-0.08 [-0.13, -0.03]), while past long sleep was related to smaller regional subcortical volumes (standardized ß: -0.04 to -0.07 for thalamus, accumbens, and hippocampus). Compared to current intermediate sleep, current short sleep was associated with smaller cortex volumes (-0.03 [-0.05, -0.01]), greater white matter hyperintensities (WMH) volumes (0.04 [0.01, 0.08]), and lower regional FA (-0.07 [-0.11, -0.02]). However, current long sleep was related to smaller total brain (-0.03 [-0.05, -0.02]), grey matter (-0.05 [-0.07, -0.03]), cortex (-0.05 [-0.07, -0.03]), regional subcortical volumes [standardized ß: -0.05 to -0.09 for putamen, thalamus, hippocampus, and accumbens]), greater WMH volumes (0.06 [0.03, 0.09]), as well as lower regional FA (-0.05 [-0.09, -0.02]). The association between current long sleep duration and poor brain health was stronger among people with hypertension or low frequency of social activity (all Pinteraction <0.05). CONCLUSIONS: Both past and current short/long sleep are associated with smaller brain volume and poorer white matter health in the brain, especially in individuals with hypertension and low frequency of social activity. Our findings highlight the need to maintain 6-8 h' sleep duration for healthy brain aging.

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BACKGROUND: The recruitment of patients to emergency research studies without the requirement for prior informed consent has furthered the conduct of randomised studies in cardiac arrest. Frameworks enabling this vary around the world depending on local legal or ethical requirements. When an enrolled patient does not survive, researchers may take one of three approaches to inform relatives of their enrolment: a direct (active) approach, providing information indirectly (passively) and inviting relatives to seek further information if they choose, or providing no information about the trial (no attempt). Previous studies have described experiences of US researchers' active approach but there is little known about approaches elsewhere.We aimed to conduct a structured investigation of methods used in cardiac arrest trials to provide information about trial enrolment to relatives of non-surviving patients. METHODS: We systematically searched trial registries to identify randomised clinical trials that recruited cardiac arrest patients. Trials were eligible for inclusion if they recruited adults during cardiac arrest (or within 1 hour of return of spontaneous circulation) between 2010 and 2022 (in the decade prior to study conception). We extracted data from trial registries and, where relevant, published papers and protocols. Investigators were contacted and asked to describe the style, rationale and timing of approach to relatives of non-surviving patients. We present descriptive statistics. RESULTS: Our trial registry search identified 710 unique trials, of which 108 were eligible for inclusion. We obtained information from investigators for 64 (62%) trials. Approximately equal numbers of trials attempted to actively inform relatives of non-survivors (n=28 (44% (95% CI; 31% to 57%))), or made no attempt (n=25 (39% (95% CI; 27% to 52%))). The remaining studies provided general information about the trial to relatives but did not actively inform them (n=11 (17% (95% CI; 8% to 29%))). CONCLUSIONS: There is wide variability in the approach taken to informing relatives of non-surviving patients enrolled in cardiac arrest randomised clinical trials.

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INTRODUCTION: The presence of multiple cardiometabolic diseases (CMDs) has been linked to increased dementia risk, but the combined influence of CMDs on cognition and brain structure across the life course is unclear. METHODS: In the UK Biobank, 46,562 dementia-free participants completed a cognitive test battery at baseline and a follow-up visit 9 years later, at which point 39,306 also underwent brain magnetic resonance imaging. CMDs (diabetes, heart disease, and stroke) were ascertained from medical records. Data were analyzed using age-stratified (middle age [< 60] versus older [≥ 60]) mixed-effects models and linear regression. RESULTS: A higher number of CMDs was associated with significantly steeper global cognitive decline in older (ß = -0.008; 95% confidence interval: -0.012, -0.005) but not middle age. Additionally, the presence of multiple CMDs was related to smaller total brain volume, gray matter volume, white matter volume, and hippocampal volume and larger white matter hyperintensity volume, even in middle age. DISCUSSION: CMDs are associated with cognitive decline in older age and poorer brain structural health beginning already in middle age. Highlights: We explored the association of CMDs with cognitive decline and brain MRI measures.CMDs accelerated cognitive decline in older (≥60y) but not middle (<60) age.CMDs were associated with poorer brain MRI parameters in both middle and older age.Results highlight the connection between CMDs and cognitive/brain aging.

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BACKGROUND: It remains unclear whether cognitive reserve can attenuate dementia risk among people with different genetic predispositions. AIMS: We aimed to examine the association between cognitive reserve and dementia, and further to explore whether and to what extent cognitive reserve may modify the risk effect of genetic factors on dementia. METHOD: Within the UK Biobank, 210 631 dementia-free participants aged ≥60 years were followed to detect incident dementia. Dementia was ascertained through medical and death records. A composite cognitive reserve indicator encompassing education, occupation and multiple cognitively loaded activities was created using latent class analysis, categorised as low, moderate and high level. Polygenic risk scores for Alzheimer's disease were constructed to evaluate genetic risk for dementia, categorised by tertiles (high, moderate and low). Data were analysed using Cox models and Laplace regression. RESULTS: In multi-adjusted Cox models, the hazard ratio (HR) of dementia was 0.66 (95% confidence interval (CI) 0.61-0.70) for high cognitive reserve compared with low cognitive reserve. In Laplace regression, participants with high cognitive reserve developed dementia 1.62 (95% CI 1.35-1.88) years later than those with low cognitive reserve. In stratified analysis by genetic risk, high cognitive reserve was related to more than 30% lower dementia risk compared with low cognitive reserve in each stratum. There was an additive interaction between low cognitive reserve and high genetic risk on dementia (attributable proportion 0.24, 95% CI 0.17-0.31). CONCLUSIONS: High cognitive reserve is associated with reduced risk of dementia and may delay dementia onset. Genetic risk for dementia may be mitigated by high cognitive reserve. Our findings underscore the importance of enhancing cognitive reserve in dementia prevention.

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BACKGROUND: The association between kidney function and dementia risk and the mechanisms underlying this relationship remain unclear. METHODS: Within the UK Biobank, 191 970 dementia-free participants aged ≥60 (mean age: 64.1 ± 2.9 years) were followed for 16 years to detect incident dementia. Serum creatinine and Cystatin C were measured at baseline to calculate estimated glomerular filtration rate (eGFR, mL/min/1.73 m2). Kidney function was categorized as normal (eGFR ≥ 90), mildly impaired (60 ≤ eGFR < 90), or moderately to severely impaired (eGFR < 60). Dementia was assessed based on self-reported medical history and medical records. During the follow-up, a subsample of 12 637 participants underwent brain MRI scans. Volumes of total brain, gray matter, white matter, hippocampus, and white matter hyperintensities were assessed. RESULTS: Over the follow-up, 5 327 (2.8%) participants developed dementia. Compared to normal kidney function, there was an increased risk of dementia with moderate to severely impaired kidney function (hazard ratio = 1.53, 95% confidence interval [CI]: 1.32-1.76) but not mildly impaired kidney function. In Laplace regression, dementia onset among people with moderate to severely impaired kidney function occurred 1.53 (95% CI: 0.98-2.08) years earlier than those with normal kidney function. Moderate to severely impaired kidney function was related to significantly lower gray matter volume (ß = -0.11, 95% CI: -0.19 to -0.03), but not to other brain magnetic resonance imaging measures. CONCLUSIONS: Impaired kidney function is associated with about 50% increased risk of dementia and anticipates dementia onset by more than 1.5 years. Brain neurodegeneration may underlie the kidney function-dementia association.

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BACKGROUND: Some studies have linked late-life overweight to a reduced mortality risk compared to normal body mass index (BMI). However, the impact of late-life overweight and its combination with mid-life BMI status on healthy survival remains unclear. We aimed to investigate whether and to what extent mid- and/or late-life overweight are associated with chronic disease-free survival. METHODS: Within the Swedish Twin Registry, 11 597 chronic disease-free twins aged 60-79 years at baseline were followed up for 18 years. BMI (kg/m2) was recorded at baseline and 25-35 years before baseline (ie, midlife) and divided as underweight (<20), normal (≥20-25), overweight (≥25-30), and obese (≥30). Incident chronic diseases (cardiovascular diseases, type 2 diabetes, and cancer) and deaths were ascertained via registries. Chronic disease-free survival was defined as years lived until the occurrence of any chronic diseases or death. Data were analyzed using multistate survival analysis. RESULTS: Of all participants, 5 640 (48.6%) were overweight/obese at baseline. During the follow-up, 8 772 (75.6%) participants developed at least 1 chronic disease or died. Compared to normal BMI, late-life overweight and obesity were associated with 1.1 (95% CI, 0.3, 2.0) and 2.6 (1.6, 3.5) years shorter chronic disease-free survival. Compared to normal BMI through mid- to late life, consistent overweight/obesity and overweight/obesity only in mid-life led to 2.2 (1.0, 3.4) and 2.6 (0.7, 4.4) years shorter disease-free survival, respectively. CONCLUSIONS: Late-life overweight and obesity may shorten disease-free survival. Further research is needed to determine whether preventing overweight/obesity from mid- to late life might favor longer and healthier survival.

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BACKGROUND: The association of anemia with cognitive function and dementia remains unclear. OBJECTIVE: We aimed to investigate the association of anemia with cognitive function and dementia risk and to explore the role of inflammation in these associations. METHODS: Within the UK Biobank, 207,203 dementia-free participants aged 60+ were followed for up to 16 years. Hemoglobin (HGB) and C-creative protein (CRP) were measured from blood samples taken at baseline. Anemia was defined as HGB <13 g/dL for males and <12 g/dL for females. Inflammation was categorized as low or high according to the median CRP level (1.50 mg/L). A subset of 18,211 participants underwent cognitive assessments (including global and domain-specific cognitive). Data were analyzed using linear mixed-effects model, Cox regression, and Laplace regression. RESULTS: Anemia was associated with faster declines in global cognition (ß= -0.08, 95% confidence interval [CI]: -0.14, -0.01) and processing speed (ß= -0.10, 95% CI: -0.19, -0.01). During the follow-up of 9.76 years (interquartile range 7.55 to 11.39), 6,272 developed dementia. The hazard ratio of dementia was 1.57 (95% CI: 1.38, 1.78) for people with anemia, and anemia accelerated dementia onset by 1.53 (95% CI: 1.08, 1.97) years. The risk of dementia tended to be higher in people with both anemia and high CRP (1.89, 95% CI: 1.60, 2.22). There was a statistically significant interaction between anemia and CRP on dementia risk (p-interaction = 0.032). CONCLUSIONS: Anemia is associated with cognitive decline (specifically for processing speed) and increased risk of dementia, especially in people with high inflammation.

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BACKGROUND AND OBJECTIVES: The association of motor function with cognitive health remains controversial, and the mechanisms underlying this relationship are unclear. We aimed to examine the association between motor function and long-term cognitive trajectories and further explore the underlying mechanisms using brain MRI. METHODS: In the Rush Memory and Aging Project, a prospective cohort study, a total of 2,192 volunteers were recruited from the communities in northeastern Illinois and followed up for up to 22 years (from 1997 to 2020). Individuals with dementia, disability, missing data on motor function at baseline, and missing follow-up data on cognitive function were excluded. At baseline, global motor function was evaluated using the averaged z scores of 10 motor tests covering dexterity, gait, and hand strength; the composite score was tertiled as low, moderate, or high. Global and domain-specific cognitive functions-including episodic memory, semantic memory, working memory, visuospatial ability, and perceptual speed-were measured annually through 19 cognitive tests. A subsample (n = 401) underwent brain MRI scans and regional brain volumes were measured. Data were analyzed using linear mixed-effects models and linear regression. RESULTS: Among the 1,618 participants (mean age 79.45 ± 7.32 years) included in this study, baseline global motor function score ranged from 0.36 to 1.82 (mean 1.03 ± 0.22). Over the follow-up (median 6.03 years, interquartile range 3.00-10.01 years), low global motor function and its subcomponents were related to significantly faster declines in global cognitive function (ß = -0.005, 95% CI -0.006 to -0.005) and each of the 5 cognitive domains. Of the 344 participants with available MRI data, low motor function was also associated with smaller total brain (ß = -25.848, 95% CI -44.902 to -6.795), total white matter (ß = -18.252, 95% CI -33.277 to -3.226), and cortical white matter (ß = -17.503, 95% CI -32.215 to -2.792) volumes, but a larger volume of white matter hyperintensities (ß = 0.257, 95% CI 0.118-0.397). DISCUSSION: Low motor function is associated with an accelerated decline in global and domain-specific cognitive functions. Both neurodegenerative and cerebrovascular pathologies might contribute to this association.

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OBJECTIVE: To examine the association between reproductive duration and postmenopausal depression (taking the use of hormone replacement therapy [HRT] into account). METHODS: In this population-based cohort study, 11 320 postmenopausal women (mean age 63.6 years) were followed for up to 18 years. Reproductive duration was categorized into three groups: short (≤34 years), average (35-39 years), and long (≥40 years). Depression was ascertained from the Sweden National Patient Registry. RESULTS: During the follow up, 593 (5.24%) women developed depression. In the multi-adjusted generalized estimating equation model, the odds ratios (ORs) of depression were 1.28 (95% confidence interval [CI] 1.05-1.55) and 1.25 (95% CI 1.01-1.55) for women with short and long reproductive durations, respectively, compared with those women with average reproductive duration. Women with a non-typical reproductive duration (≤34 or ≥40 years) who received HRT were at a higher risk of depression (OR 1.82, 95% CI 1.42-2.33). There was a significant additive interaction between non-typical reproductive duration and the use of HRT on depression (attributable proportion 0.26, 95% CI 0.03-0.50). CONCLUSION: Women with a short or long reproductive duration, especially those with a history of HRT use, have a higher risk of depression after menopause compared with those with an average reproductive duration.

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INTRODUCTION: The association between cognitive reserve (CR) and survival with independence is unknown. We examined whether lifelong CR accumulation is associated with disability-free survival and explored the extent to which cognitive function mediates this association. METHODS: Within the Rush Memory and Aging Project, 1633 dementia- and disability-free participants were followed annually for up to 22 years. Lifelong CR including education, early-/mid-/late-life cognitive activities, and late-life social activity was assessed and tertiled. RESULTS: CR score was dose-dependently associated with disability/death (hazard ratio [HR] 0.96, 95% confidence interval [CI] 0.93-0.99). Compared to low CR, the HR (95% CI) of disability/death was 0.82 (0.70-0.95) for high CR. The median disability-free survival time was prolonged by 0.99 (95% CI 0.28-1.71) years for participants with high CR. Cognitive function mediated 35.7% of the association between CR and disability-free survival. DISCUSSION: High lifelong CR was associated with prolonged disability-free survival. Cognitive function mediates about one-third of this association. Our findings underscore the importance of CR for healthy aging.

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INTRODUCTION: The impact of life-course traumatic brain injury (TBI) on dementia is unclear. METHODS: Within the Swedish Twin Registry (STR), 35,312 dementia-free twins were followed for up to 18 years. TBI history was identified via medical records. Data were analyzed using generalized estimating equation (GEE) and conditional logistic regression. RESULTS: In multi-adjusted GEE models, the odds ratio (OR, 95% confidence interval [CI]) of dementia was 1.27 (1.03-1.57) for TBI at any age, 1.55 (1.04-2.31) for TBI at 50 to 59 years, and 1.67 (1.12-2.49) for TBI at 60 to 69 years. Cardiometabolic diseases (CMDs) increased dementia risk associated with TBI at age 50 to 69 years. The ORs in GEE and conditional logistic regression did not differ significantly (P = .37). DISCUSSION: TBI, especially between ages 50 and 69 years, is associated with an increased risk of dementia, and this is exacerbated among people with CMDs. Genetic and early-life environmental factors may not account for the TBI-dementia association.

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