Objective: Our aim was to test the association of vascular risk factor exposure in midlife with progression of MRI markers of brain aging and measures of cognitive decline. Methods: A total of 1,352 participants without dementia from the prospective Framingham Offspring Cohort Study were examined. Multivariable linear and logistic regressions were implemented to study the association of midlife vascular risk factor exposure with longitudinal change in white matter hyperintensity volume (WMHV), total brain volume (TBV), temporal horn volume, logical memory delayed recall, visual reproductions delayed-recall (VR-d), and Trail-Making Test B-A (TrB-A) performance a decade later. Results: Hypertension in midlife was associated with accelerated WMHV progression ( p p = 0.012). Midlife diabetes and smoking were associated with a more rapid increase in temporal horn volume, a surrogate marker of accelerated hippocampal atrophy ( p = 0.017 and p = 0.008, respectively). Midlife smoking also predicted a more marked decrease in total brain volume ( p = 0.025) and increased risk of extensive change in WMHV (odds ratio = 1.58 [95%confidence interval 1.07–2.33], p = 0.021). Obesity in midlife was associated with an increased risk of being in the top quartile of change in executive function (1.39 [1.02–1.88], p = 0.035) and increasing waist-to-hip ratio was associated with marked decline in TBV (10.81 [1.44–81.01], p = 0.021). Longitudinal changes in brain structure were significantly correlated with decline in memory and executive function. Conclusions: Midlife hypertension, diabetes, smoking, and obesity were associated with an increased rate of progression of vascular brain injury, global and hippocampal atrophy, and decline in executive function a decade later.

Midlife vascular risk factor exposure accelerates structural brain aging and cognitive decline

A decade has passed since we published a comprehensive review in this journal addressing the topic of promoting successful cognitive aging, making this a good time to take stock of the field. Because there have been limited large-scale, randomized controlled trials, especially following individuals from middle age to late life, some experts have questioned whether recommendations can be legitimately offered about reducing the risk of cognitive decline and dementia. Despite uncertainties, clinicians often need to at least make provisional recommendations to patients based on the highest quality data available. Converging lines of evidence from epidemiological/cohort studies, animal/basic science studies, human proof-of-concept studies, and human intervention studies can provide guidance, highlighting strategies for enhancing cognitive reserve and preventing loss of cognitive capacity. Many of the suggestions made in 2010 have been supported by additional research. Importantly, there is a growing consensus among major health organizations about recommendations to mitigate cognitive decline and promote healthy cognitive aging. Regular physical activity and treatment of cardiovascular risk factors have been supported by all of these organizations. Most organizations have also embraced cognitively stimulating activities, a heart-healthy diet, smoking cessation, and countering metabolic syndrome. Other behaviors like regular social engagement, limiting alcohol use, stress management, getting adequate sleep, avoiding anticholinergic medications, addressing sensory deficits, and protecting the brain against physical and toxic damage also have been endorsed, although less consistently. In this update, we review the evidence for each of these recommendations and offer practical advice about behavior-change techniques to help patients adopt brain-healthy behaviors.

Promoting Successful Cognitive Aging: A Ten-Year Update.

Adiposity impacts cognitive function in Asian populations: an epidemiological and Mendelian Randomization study

Abstract Background and aims Observational studies have linked elevated blood pressure (BP) to impaired cognitive function. However, the functional and structural changes in the brain that mediate the relationship between BP elevation and cognitive impairment remain unknown. Using observational and genetic data from large consortia, this study aimed to identify brain structures potentially associated with BP values and cognitive function. Methods and results Data on BP were integrated with 3935 brain magnetic resonance imaging-derived phenotypes (IDPs) and cognitive function defined by fluid intelligence score. Observational analyses were performed in the UK Biobank and a prospective validation cohort. Mendelian randomisation (MR) analyses used genetic data derived from the UK Biobank, International Consortium for Blood Pressure, and COGENT consortium. Mendelian randomisation analysis identified a potentially adverse causal effect of higher systolic BP on cognitive function [−0.044 standard deviation (SD); 95% confidence interval (CI) −0.066, −0.021] with the MR estimate strengthening (−0.087 SD; 95% CI −0.132, −0.042), when further adjusted for diastolic BP. Mendelian randomisation analysis found 242, 168, and 68 IDPs showing significant (false discovery rate P < 0.05) association with systolic BP, diastolic BP, and pulse pressure, respectively. Most of these IDPs were inversely associated with cognitive function in observational analysis in the UK Biobank and showed concordant effects in the validation cohort. Mendelian randomisation analysis identified relationships between cognitive function and the nine of the systolic BP-associated IDPs, including the anterior thalamic radiation, anterior corona radiata, or external capsule. Conclusion Complementary MR and observational analyses identify brain structures associated with BP, which may be responsible for the adverse effects of hypertension on cognitive performance.

/pdf/genetic-analyses-identify-brain-structures-related-to-93qd8hkh.pdf

Genetic analyses identify brain structures related to cognitive impairment associated with elevated blood pressure

Background Clinical practice guidelines recommend early identification of cognitive impairment in individuals with hypertension with the help of risk prediction tools based on risk factors. Objective The aim of this study was to develop a superior machine learning model based on easily collected variables to predict the risk of early cognitive impairment in hypertensive individuals, which could be used to optimize early cognitive impairment risk assessment strategies. Methods For this cross-sectional study, 733 patients with hypertension (aged 30–85, 48.98% male) enrolled in multi-center hospitals in China were divided into a training group (70%) and a validation group (30%). After least absolute shrinkage and selection operator (LASSO) regression analysis with 5-fold cross-validation determined the modeling variables, three machine learning classifiers, logistic regression (LR), XGBoost (XGB), and gaussian naive bayes (GNB), were developed. The area under the ROC curve (AUC), accuracy, sensitivity, specificity, and F1 score were used to evaluate the model performance. Shape Additive explanation (SHAP) analysis was performed to rank feature importance. Further decision curve analysis (DCA) assessed the clinical performance of the established model and visualized it by nomogram. Results Hip circumference, age, education levels, and physical activity were considered significant predictors of early cognitive impairment in hypertension. The AUC (0.88), F1 score (0.59), accuracy (0.81), sensitivity (0.84), and specificity (0.80) of the XGB model were superior to LR and GNB classifiers. Conclusion The XGB model based on hip circumference, age, educational level, and physical activity has superior predictive performance and it shows promise in predicting the risk of cognitive impairment in hypertensive clinical settings.

/pdf/a-risk-prediction-model-based-on-machine-learning-for-early-q8hq3iyo.pdf

A risk prediction model based on machine learning for early cognitive impairment in hypertension: Development and validation study

Whether high blood pressure has a causal effect on cognitive function as early as middle age is unclear. We investigated whether high blood pressure (BP) causally impairs cognitive function at midlife using Mendelian Randomization (MR). We applied a two-sample MR approach to investigate the causal relationship between BP and midlife cognitive performance measured by the Digit Symbol Substitution Test (DSST), Rey Auditory Verbal Learning Test (RAVLT), and Stroop Interference test. We used a total of 109 genetic polymorphisms with established associations with BP as instrumental variables and estimated gene-cognitive function association in 1369 middle-aged adults (Mean age (SD): 50.8 (3.3), 54.0% women) from the CARDIA study. A 10 mmHg increment in genetically-predicted systolic, diastolic, or pulse pressure was associated with a 4.9 to 7.7-point lower DSST score (P = 0.002, SBP; P = 0.005, DBP and P = 0.008, PP), while a 10 mmHg increment in genetically-predicted SBP was associated with a 0.7 point lower RAVLT and a 2.3 point higher Stroop (P = 0.046 and 0.011, respectively). This MR analysis shows that high BP, especially SBP, is causally associated with poorer processing speed, verbal memory, and executive function during midlife. These findings emphasize the need for further investigation of the role and mechanisms of BP dysregulation on cognitive health in middle age and perhaps, more broadly, across the lifespan.

/pdf/association-of-blood-pressure-with-cognitive-function-at-24zazs422o.pdf

Association of blood pressure with cognitive function at midlife: a Mendelian randomization study

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Association of blood pressure with cognitive function at midlife: a Mendelian randomization study