ORCID Profile
0000-0002-4143-8485
Current Organisations
Paul Scherrer Institut PSI
,
Monash University
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Harvard University
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Framingham Heart Study
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Pattern Recognition and Data Mining | Psychology | Computer-Human Interaction | Developmental Psychology and Ageing
Expanding Knowledge in Psychology and Cognitive Sciences | Expanding Knowledge in the Medical and Health Sciences | Expanding Knowledge in Technology |
Publisher: Cambridge University Press (CUP)
Date: 30-09-2014
DOI: 10.1017/S0954422414000158
Abstract: Cognitive outcomes are frequently implemented as endpoints in nutrition research. To reduce the number of statistical comparisons it is commonplace for nutrition researchers to combine cognitive test results into a smaller number of broad cognitive abilities. However, there is a clear lack of understanding and consensus as to how best execute this practice. The present paper reviews contemporary models of human cognition and proposes a standardised, evidence-based method for grouping cognitive test data into broader cognitive abilities. Both Carroll's model of human cognitive ability and the Cattell–Horn–Carroll (CHC) model of intelligence provide empirically based taxonomies of human cognition. These models provide a cognitive ‘map’ that can be used to guide the handling and analysis of cognitive outcomes in nutrition research. Making use of a valid cognitive nomenclature can provide the field of clinical nutrition with a common cognitive language enabling efficient comparisons of cognitive outcomes across studies. This will make it easier for researchers, policymakers and readers to interpret and compare cognitive outcomes for different interventions. Using an empirically derived cognitive nomenclature to guide the creation of cognitive composite scores will ensure that cognitive endpoints are theoretically valid and meaningful. This will increase the generalisability of trial results to the general population. The present review also discusses how the CHC model of cognition can also guide the synthesis of cognitive outcomes in systematic reviews and meta-analysis.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 02-10-2017
Publisher: Elsevier BV
Date: 05-2014
DOI: 10.1016/J.PHYSBEH.2014.03.015
Abstract: Low cerebral blood flow velocity is associated with cognitive decline. However, the association between pulsatile brain blood flow velocity and cognition has not been investigated. High pulsatile hemodynamic stress in the brain may impair cognitive function through damage to small cerebral vessels. The current objective was to examine the cross-sectional association of pulsatile and mean cerebral blood flow velocity with age and neuropsychological performance. We also examined whether cerebral blood flow velocity was associated with aortic pulse pressure, a measure of arterial ageing and aortic stiffness. Cerebral blood flow velocity was measured in the middle cerebral artery using Transcranial Doppler Ultrasonography (TDU) while neuropsychological performance was measured using a computerized cognitive test battery. Aortic pulse pressure was non-invasively derived from applanation tonometry of the radial artery. The s le comprised 160 healthy adults aged 50-70 years. Results indicated that increasing age correlated with lower mean (r=-0.23, p<0.01) and higher pulsatile (r=0.27, p<0.01) brain blood flow velocity. In multivariate adjusted models, both peripheral (β=0.28, p<0.05) and aortic (β=0.24, p<0.05) pulse pressure were associated with higher pulsatile flow velocity through the middle cerebral artery. In adjusted models, neither mean nor pulsatile cerebral blood flow velocity was associated with performance on any cognitive task. In conclusion, arterial ageing was associated with increased pulsatile hemodynamic stress in the brain. However, this was not associated with impaired neuropsychological performance.
Publisher: SAGE Publications
Date: 06-09-2013
Abstract: Central (aortic) blood pressures differ from brachial pressures and may be more relevant to the study of cognitive function, given that blood is delivered to the brain through the central large arteries. Pulse-pressure lification reflects the augmentation of blood pressure between the central and peripheral arteries, which diminishes with aging. We aimed to determine the association between central blood pressure and cognitive function in independently living adults aged 20 to 82 years ( N = 493). In adjusted regression models, higher central systolic pressure and higher central pulse pressure were each associated with poorer processing speed, Stroop processing, and recognition memory. Lower lification was associated with poorer Stroop processing, working memory, and recognition memory. Higher brachial systolic pressure and brachial pulse pressure were both associated with poorer Stroop processing. In summary, central pressures and lification were sensitive indicators of cognitive aging, predicting aspects of cognitive performance not predicted by brachial blood pressure.
Publisher: Public Library of Science (PLoS)
Date: 18-02-2015
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 06-2017
DOI: 10.1161/STROKEAHA.116.016321
Abstract: Previous reports from the Framingham Heart Study have identified cross-sectional associations of arterial stiffness, as reflected by carotid–femoral pulse wave velocity (CFPWV) and systolic blood pressure with vascular brain injury. The purpose of this study is to examine free water (FW), fractional anisotropy (FA), and white matter hyperintensities (WMH) in relation to arterial stiffness among subjects of the Framingham Offspring and Third-Generation cohorts. In 2422 participants aged 51.3±11.6 years, FA, FW, and WMH were related to CFPWV using voxel-based linear and generalized linear regressions, adjusting for relevant covariables. Mean FW, mean FA, and WMH burden (log transformed) were computed within white matter (WM) region and related to systolic blood pressure and CFPWV using multiple mediation analyses. CFPWV was found to be associated with higher FW, lower FA, and higher WMH incidence in WM areas covering, respectively, 356.1, 211.8, and 10.9 mL of the WM mask. Mediation analyses revealed that the effect of systolic blood pressure on FW was mediated by CFPWV (direct and indirect effects: a=0.040 P .001, and a′=0.020 P .05). Moreover, the effect of CFPWV on FA was mediated by FW (direct and indirect effects: b=−0.092 P .001, and b′=0.012 P .05), whose effect on WMH was, in turn, mediated by FA (direct and indirect effects: c=0.246 P .001, and c′=0.116 P .05). From these data, we propose a biomechanical hypothesis designed for future research experiments to explain how hemodynamic alteration may lead to WM injury by impacting cerebral water content and more subtly WM integrity, to finally lead to WMH development.
Publisher: SAGE Publications
Date: 06-2015
Abstract: With increasing life expectancies in most Western populations, the number of people experiencing age-associated cognitive impairment is increasing. Research is needed to identify factors that may help the elderly maintain or even improve cognitive function in the face of advancing age. This review evaluates whether dietary supplementation with natural pharmaceuticals can be used as a means to improve cognitive function or limit cognitive decline. The evidence surrounding popular supplements such as Ginkgo biloba, fish oils, Bacopa monnieri, polyphenol extracts, and vitamins is reviewed briefly. Potential mechanisms of action are also highlighted. This review also discusses challenges surrounding cognitive testing in psychopharmacological research, highlighting discrepancies between the domains of human cognition as described by contemporary models and as measured in clinical trials.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 08-2010
Publisher: Wiley
Date: 02-11-2015
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 05-03-2018
Publisher: Elsevier BV
Date: 02-2012
DOI: 10.1016/J.PHYSBEH.2011.11.013
Abstract: In a randomized, double-blind placebo controlled trial, 63 middle-aged volunteers aged between 40 and 65 years were administered a daily chocolate drink containing 250 mg or 500 mg cocoa flavanols versus a low cocoa flavanol (placebo) drink over a 30-day period. Participants were tested at baseline as well as at the end of the treatment period on a test of Spatial Working Memory. Steady State Probe Topography (SST) was used to assess neurocognitive changes associated with cocoa flavanol supplementation during the completion of the Spatial Working Memory task. SST is an electrophysiological technique which utilizes a 13 Hz diffuse visual flicker in order to generate a steady state visually evoked potential (SSVEP). Changes in the litude and phase of the SSVEP response after 30 days were compared between treatment groups. Behavioral measures of accuracy and reaction time were not found to be significantly different between treatment groups, while average SSVEP litude and phase differences at a number of posterior parietal and centro-frontal sites were found to be significantly different between groups during memory encoding, the working memory hold period and retrieval. In the absence of significant behavioral effects, these differences in brain activation can be interpreted as evidence of increased neural efficiency in spatial working memory function associated with chronic cocoa flavanol consumption.
Publisher: American Psychological Association (APA)
Date: 07-2023
DOI: 10.1037/NEU0000900
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 02-10-2017
Publisher: Elsevier BV
Date: 02-2011
Abstract: Although dietary and nutrient interventions have been extensively studied as a means of improving arterial stiffness, to our knowledge no systematic analysis of the data has been conducted. The aim of the current study was to systematically review the human clinical trial data and qualitatively examine the efficacy of dietary and nutrient interventions in the treatment of arterial stiffness. We systematically searched multiple databases until July 2010 for relevant randomized controlled human clinical trials of common dietary and nutrient interventions in the treatment of arterial stiffness. Located studies were subject to strict inclusion criteria and objectively assessed for scientific quality. Of the 75 relevant studies located, we considered 38 studies to be appropriate for review. Results revealed support for intakes of omega-3 (n-3) fish oils (Cohen's d = 0.21-0.81) and soy isoflavones (Cohen's d = 0.35-0.39) in the treatment of arterial stiffness. There was limited but consistent evidence to suggest that salt restriction (Cohen's d = 0.28-0.37) as well as consumption of fermented-milk products (Cohen's d = 0.15-0.33) that contain bioactive peptides improved arterial stiffness. The evidentiary support for intakes of vitamins, micronutrients, and herbal medicines was insufficient. Limited but consistent evidence suggested that caffeine intake acutely increased arterial stiffness (Cohen's d = 0.34-0.51). Current evidence from several small studies suggests that omega-3 and soy isoflavone supplementation provides an effective means of reducing arterial stiffness. There was little research that explored intakes of herbal medicines or micronutrients in the treatment of arterial stiffness, and this remains an area of potential research.
Publisher: Elsevier BV
Date: 2020
Publisher: Cambridge University Press (CUP)
Date: 23-08-2021
DOI: 10.1017/S000711452100324X
Abstract: Flavonoids have shown anti-hypertensive and anti-atherosclerotic properties: the impact of habitual flavonoid intake on vascular function, central haemodynamics and arterial stiffness may be important. We investigated the relationship between habitual flavonoid consumption and measures of central blood pressure and arterial stiffness. We performed cross-sectional analysis of 381 non-smoking healthy older adults (mean age 66·0 ( sd 4·1) years BMI, 26·4 ( sd 4·41) kg/m 2 41 % male) recruited as part of the Australian Research Council Longevity Intervention study. Flavonoid intake (i.e. flavonols, flavones, flavanones, anthocyanins, isoflavones, flavan-3-ol monomers, proanthocyanidins, theaflavins/thearubigins and total consumption) was estimated from FFQ using the US Department of Agriculture food composition databases. Measures of central haemodynamics and arterial stiffness included systolic blood pressure (cSBP), diastolic blood pressure (cDBP), mean arterial pressure (cMAP) and augmentation index (cAIx). After adjusting for demographic and lifestyle confounders, each sd /d higher intake of anthocyanins (( sd 44·3) mg/d) was associated with significantly lower cDBP (−1·56 mmHg, 95 % CI −2·65, −0·48) and cMAP (−1·62 mmHg, 95 % CI −2·82, −0·41). Similarly, each sd /d higher intake of flavanones (( sd 19·5) mg/d) was associated with ~1 % lower cAIx (−0·93 %, 95 % CI −1·77, −0·09). These associations remained significant after additional adjustment for (1) a dietary quality score and (2) other major nutrients that may affect blood pressure or arterial stiffness (i.e. Na, K, Ca, Mg, n -3, total protein and fibre). This study suggests a possible benefit of dietary anthocyanin and flavanone intake on central haemodynamics and arterial stiffness these findings require corroboration in further research.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 08-2017
Publisher: Elsevier
Date: 2016
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 10-2018
Publisher: Elsevier BV
Date: 06-2018
Publisher: Springer Science and Business Media LLC
Date: 02-12-2022
DOI: 10.1007/S11065-022-09567-Y
Abstract: Psychological stress is a potential modifiable risk factor for cognitive decline. However, the extent to which self-reported psychological stress is differentially associated with decline in specific cognitive domains remains unclear. Differences may be due to heterogeneity in the aspects of psychological stress investigated, for ex le, neuroticism (which is linked to vulnerability to stress), perceived stress, or exposure to stressful life events. This review aims to establish the associations between these aspects of self-reported psychological stress and cognitive decline. PsychINFO, Embase and MEDLINE were searched from database inception to September 2021. Studies were included if they were observational, prospective, and if they investigated the association between self-reported psychological stress and cognitive decline in adults with a minimum mean age of 40 years at baseline. Thirty studies satisfied the inclusion criteria, with most examining neuroticism (n = 17) as a predictor of cognitive decline. Fewer examined perceived stress (n = 7) or stressful life events (n = 6). There was evidence of an association between neuroticism and cognitive decline, particularly in the domain of memory. Similarly, across studies, perceived stress was also associated with memory decline. Research investigating the relationship between stressful life events and cognitive decline had fewer outcomes to interpret. Overall, the findings highlight that memory may be particularly susceptible to high levels of neuroticism and perceived stress. We identified a lack of research into some cognitive domains, such as executive function, which should be addressed by future studies.
Publisher: Elsevier BV
Date: 02-2013
Abstract: Multivitamins are the most commonly used supplement in the developed world. Recent epidemiologic findings suggest that multivitamin use increases the risk of mortality. We aimed to determine whether multivitamin-multimineral treatment, used for primary or secondary prevention, increases the risk of mortality in independently living adults. We performed a meta-analysis of randomized controlled trials. Multiple electronic databases were systematically searched from March to October 2012. Randomized controlled primary or secondary prevention trials were considered for inclusion. Eligible trials investigated daily multivitamin-multimineral supplementation for ≥1 y. Cohorts described as institutionalized or as having terminal illness (tertiary prevention) were excluded. The number of deaths and the s le size of each study arm were extracted independently by 2 researchers. Twenty-one articles were included in the analysis, which generated a total pooled s le of 91,074 people and 8794 deaths. These trials were pooled in a meta-analysis, and the outcomes were expressed as RRs and 95% CIs. The average age of the pooled s le was 62 y, and the average duration of supplementation was 43 mo. Across all studies, no effect of multivitamin-multimineral treatment on all-cause mortality (RR: 0.98 95% CI: 0.94, 1.02) was observed. There was a trend for a reduced risk of all-cause mortality across primary prevention trials (RR: 0.94 95% CI: 0.89, 1.00). Multivitamin-multimineral treatment had no effect on mortality due to vascular causes (RR: 1.01 95% CI: 0.93, 1.09) or cancer (RR: 0.96 95% CI: 0.88, 1.04). No statistical evidence of heterogeneity or publication bias was observed. Multivitamin-multimineral treatment has no effect on mortality risk.
Publisher: Wiley
Date: 29-07-2019
DOI: 10.1002/ANA.25542
Abstract: Higher plasma total‐tau level is associated with incident dementia, but its relationship with stroke risk is unknown. In this prospective community‐based study, we evaluated plasma total‐tau level as a biomarker of stroke risk in 2,794 Framingham Heart Study participants. Persons with plasma total‐tau levels in the top quintile, versus the bottom 4, had an increased risk of incident stroke over a mean follow‐up of 8.3 years (hazard ratio = 2.01 95% confidence interval = 1.32–3.08) following adjustments for age, sex, and stroke risk factors. Our findings demonstrate that plasma total‐tau relates to the risk of stroke in a community s le. ANN NEUROL 2019 :463–467
Publisher: American Academy of Sleep Medicine (AASM)
Date: 15-03-2016
DOI: 10.5664/JCSM.5598
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 05-2016
DOI: 10.1161/STROKEAHA.115.012608
Abstract: The American Heart Association developed the ideal cardiovascular health (CVH) index as a simple tool to promote CVH yet, its association with brain atrophy and dementia remains unexamined. Our aim was to investigate the prospective association of ideal CVH with vascular brain injury, including the 10-year risks of incident stroke and dementia, as well as cognitive decline and brain atrophy on magnetic resonance imaging, measured for ≈7 years. We studied 2750 stroke- and dementia-free Framingham Heart Study Offspring cohort participants (mean age, 62±9 years 45% men). Ideal CVH was quantified on a 7-point scale with 1 point awarded for each of the following: nonsmoking status, ideal body mass index, regular physical activity, healthy diet, as well as optimum blood pressure, cholesterol, and fasting blood glucose. Both recent (baseline) and remote (6.9 years earlier) ideal CVH scores were examined. Recent ideal CVH was associated with stroke (hazard ratio, 0.80 95% confidence interval, 0.67–0.95), vascular dementia (hazard ratio, 0.49 95% confidence interval, 0.30–0.81), frontal brain atrophy ( P =0.003), and cognitive decline on tasks measuring visual memory and reasoning ( P .05). In addition to predicting stroke, vascular dementia, whole-brain atrophy, and cognitive decline, remote ideal CVH was associated with the incidence of all-cause dementia (hazard ratio, 0.80 95% confidence interval, 0.67–0.97) and Alzheimer disease (hazard ratio, 0.79 95% confidence interval, 0.64–0.98). Adherence to the American Heart Association’s ideal CVH factors and behaviors, particularly in midlife, may protect against cerebrovascular disease and dementia.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 09-03-2021
DOI: 10.1212/WNL.0000000000011377
Abstract: To test the hypothesis that reduced slow-wave sleep, or N3 sleep, which is thought to underlie the restorative functions of sleep, is associated with MRI markers of brain aging, we evaluated this relationship in the community-based Framingham Heart Study Offspring cohort using polysomnography and brain MRI. We studied 492 participants (age 58.8 ± 8.8 years, 49.4% male) free of neurological diseases who completed a brain MRI scan and in-home overnight polysomnography to assess slow-wave sleep (absolute duration and percentage of total sleep). Volumes of total brain, total cortical, frontal cortical, subcortical gray matter, hippoc us, and white matter hyperintensities were investigated as a percentage of intracranial volume, and the presence of covert brain infarcts was evaluated. Linear and logistic regression models were adjusted for age, age squared, sex, time interval between polysomnography and MRI (3.3 ± 1.0 years), APOE ε4 carrier status, stroke risk factors, sleeping pill use, body mass index, and depression. Less slow-wave sleep was associated with lower cortical brain volume (absolute duration, β [standard error] = 0.20 [0.08], p = 0.015 percentage, 0.16 [0.08], p = 0.044), lower subcortical brain volume (percentage, 0.03 [0.02], p = 0.034), and higher white matter hyperintensities volume (absolute duration, −0.12 [0.05], p = 0.010 percentage, −0.10 [0.04], p = 0.033). Slow-wave sleep duration was not associated with hippoc al volume or the presence of covert brain infarcts. Loss of slow-wave sleep might facilitate accelerated brain aging, as evidence by its association with MRI markers suggestive of brain atrophy and injury. Alternatively, subtle injuries and accelerated aging might reduce the ability of the brain to produce slow-wave sleep.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 06-2019
DOI: 10.1161/STROKEAHA.119.025171
Abstract: Stroke at midlife has a disproportionately large impact on disability-adjusted life-years lost. Ischemic stroke incidence may be increasing at this age. We investigated long-term trends in ischemic stroke incidence and changes in stroke risk factors in a community s le stratified by stroke onset at middle and older age. In the Framingham Study, surveillance for incident stroke is ongoing since 1948. We examined age-adjusted and sex-adjusted 10-year incidence of ischemic stroke using Cox models in persons aged 35 to 54 and ≥55 years at start of follow-up. Tests for linear trend were performed over 4 epochs, controlling for the distance in time between intervals. Further, we calculated the mean 10-year risk of stroke at each epoch and for both age groups, based on vascular risk factors from the Framingham Stroke Risk Profile. There were 153, 197, 176, and 165 incident ischemic strokes within each epoch beginning in 1962 (n=3966), 1971 (n=5779), 1987 (n=5133), and 1998 (n=6964). Most ischemic strokes at midlife (n=71) were because of atherosclerotic brain infarction (n=50) or cardioembolism (n=19). Using the risk in the 1962 epoch as the reference, the risk of ischemic stroke at midlife did not significantly decline (hazard ratio, 0.87 95% CI, 0.74–1.02 P trend =0.09). Incidence of ischemic stroke declined in the older group (hazard ratio, 0.82 95% CI, 0.77–0.88 P trend .001). Between epochs 1 and 4, the average 10-year risk of stroke, as estimated by the Framingham Stroke Risk Profile, declined by 0.7% at midlife and 1.1% at older age. Long-term rates of ischemic stroke declined in our community s le the decline was greater in older as compared with younger adults. Early prevention, focused on modification of cardiovascular risk factors, is important to see sustained declines in stroke incidence and mortality at midlife.
Publisher: Oxford University Press (OUP)
Date: 29-08-2020
Abstract: To determine whether C-reactive protein (CRP), a marker of systemic inflammation, moderates the association between sleep and incident dementia. We studied Framingham Heart Study participants who completed at baseline a serum CRP assessment and in-home polysomnography to measure sleep duration, sleep efficiency, sleep latency, wake after sleep onset (WASO), number of awakenings, arousal index, and apnea–hypopnea index. Participants were ided into groups according to their CRP level: low (& mg/L), average (1–3 mg/L), and high inflammation (& mg/L). Surveillance for outcomes (incident all-cause and Alzheimer’s disease [AD] dementia) commenced at baseline and continued up to 22.5 years. In 291 participants (mean age 67.5 ± 4.9 years, 51.6% men) followed for 13.4 ± 5.4 years, we observed 43 cases of all-cause dementia, 33 of which were clinically consistent with AD. Whereas no direct association between CRP or sleep exposures was observed with incident dementia, CRP levels interacted with nighttime wakefulness when predicting both incident all-cause and AD dementia. In the high CRP group, longer WASO (hazard ratio [HR], 2.89 95% CI, 1.31–6.34) and more nighttime awakenings (HR, 4.55 95% CI, 1.19–17.38) were associated with higher risk of incident dementia. In the low CRP group, fewer nighttime awakenings were associated with a higher risk of incident dementia (HR, 0.07 95% CI, 0.01–0.68). Our findings suggest that inflammation moderates the association between sleep, particularly nighttime wakefulness, and dementia risk. The presence of inflammation may be an important determinant in evaluating how sleep disturbances relate to neurodegeneration.
Publisher: Elsevier BV
Date: 2023
DOI: 10.1016/J.SLEEP.2022.10.021
Abstract: This meta-analysis of randomized controlled trials (RCTs) evaluates if treating sleep disturbances improves cognitive function over at least 12 weeks. Multiple data sources were searched until November 1, 2021. RCTs were included if they examined the effect of an intervention (behavioral or medical) on sleep and cognition in an adult s le with sleep disturbances and had an intervention duration and follow-up of at least 12 weeks. Two independent reviewers located 3784 studies 16 satisfied the inclusion criteria. Primary outcomes included the broad cognitive domains of visual processing, short-term memory, long-term storage and retrieval, processing speed, and reaction time. Most trials were conducted in participants with obstructive sleep apnea (OSA N = 13) the most studied intervention was continuous positive airway pressure (CPAP N = 10). All RCTs were 12 months in duration or less. The estimates of mean pooled effects were not indicative of significant treatment effect for any primary outcome. Although the interventions reduced daytime sleepiness (Hedge's g, 0.51 95% confidence interval, 0.29-0.74 p < 0.01), this did not lead to cognitive enhancement. Overall, there was insufficient evidence to suggest that treating sleep dysfunction can improve cognition. Further studies with longer follow-up duration and supporting biomarkers are needed.
Publisher: Springer Science and Business Media LLC
Date: 06-03-2012
Publisher: American Geophysical Union (AGU)
Date: 18-03-2019
DOI: 10.1029/2018GL081784
Publisher: Wiley
Date: 2020
DOI: 10.1002/TRC2.12043
Abstract: Web‐based platforms are used increasingly to assess cognitive function in unsupervised settings. The utility of cognitive data arising from unsupervised assessments remains unclear. We examined the acceptability, usability, and validity of unsupervised cognitive testing in middle‐aged adults enrolled in the Healthy Brain Project. A total of 1594 participants completed unsupervised assessments of the Cogstate Brief Battery. Acceptability was defined by the amount of missing data, and usability by examining error of test performance and the time taken to read task instructions and complete tests (learnability). Overall, we observed high acceptability (98% complete data) and high usability (95% met criteria for low error rates and high learnability). Test validity was confirmed by observation of expected inverse relationships between performance and increasing test difficulty and age. Consideration of test design paired with acceptability and usability criteria can provide valid indices of cognition in the unsupervised settings used to develop registries of in iduals at risk for Alzheimer's disease.
Publisher: Springer International Publishing
Date: 2016
Publisher: American Medical Association (AMA)
Date: 16-08-2021
Publisher: Wiley
Date: 14-11-2020
DOI: 10.1111/RESP.13728
Abstract: The burden of dementia is increasing globally. In the absence of curative treatment, preventive strategies to delay or reduce progression of dementia are crucial. This relies on the identification of modifiable risk factors. The effects of dementia on sleep are well recognized however, there is now growing evidence suggesting a bidirectional relationship between sleep pathologies and dementia. SDB, poor quality sleep and extremes of sleep duration are commonly experienced by both middle-aged and older populations. All have been associated with increased risk of dementia and cognitive decline in a number of observational studies, albeit inconsistently. The mechanisms by which these sleep disorders may contribute to neurodegeneration are manifold, and include impacts of fragmented sleep on the clearance of neurotoxins, and in SDB by the additive effects of intermittent hypoxia on beta-amyloid production, hypoxic cell death, neuroinflammation and damage to cerebral vasculature. Untangling the mechanisms by which sleep pathologies may impact risk of dementia is a challenge. Many insights into the pathophysiology of these relationships have been derived from animal- and population-based studies. Neuroimaging modalities offer important opportunities to further understand the link between sleep pathologies and dementia risk in vivo, especially in the critical preclinical phase of AD. In this review, we canvas updates in dementia pathophysiology, the evidence linking sleep pathologies with dementia and outline the advances in determining this potential pathophysiological link that have eventuated from the application of neuroimaging.
Publisher: eLife Sciences Publications, Ltd
Date: 03-07-2023
DOI: 10.7554/ELIFE.88359
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 22-02-2017
DOI: 10.1212/WNL.0000000000003732
Abstract: To evaluate the association between sleep duration and the risk of incident dementia and brain aging. Self-reported total hours of sleep were examined in the Framingham Heart Study (n = 2,457, mean age 72 ± 6 years, 57% women) as a 3-level variable: hours (short), 6–9 hours (reference), and hours (long), and was related to the risk of incident dementia over 10 years, and cross-sectionally to total cerebral brain volume (TCBV) and cognitive performance. We observed 234 cases of all-cause dementia over 10 years of follow-up. In multivariable analyses, prolonged sleep duration was associated with an increased risk of incident dementia (hazard ratio [HR] 2.01 95% confidence interval [CI] 1.24–3.26). These findings were driven by persons with baseline mild cognitive impairment (HR 2.83 95% CI 1.06–7.55) and persons without a high school degree (HR 6.05 95% CI 3.00–12.18). Transitioning to sleeping hours over a mean period of 13 years before baseline was associated with an increased risk of all-cause dementia (HR 2.43 95% CI 1.44–4.11) and clinical Alzheimer disease (HR 2.20 95% CI 1.17–4.13). Relative to sleeping 6–9 hours, long sleep duration was also associated cross-sectionally with smaller TCBV (β ± SE, −1.08 ± 0.41 mean units of TCBV difference) and poorer executive function (β ± SE, −0.41 ± 0.13 SD units of Trail Making Test B minus A score difference). Prolonged sleep duration may be a marker of early neurodegeneration and hence a useful clinical tool to identify those at a higher risk of progressing to clinical dementia within 10 years.
Publisher: Hindawi Limited
Date: 2015
DOI: 10.1155/2015/615384
Abstract: The detrimental effect of neuronal cell death due to oxidative stress and mitochondrial dysfunction has been implicated in age-related cognitive decline and neurodegenerative disorders such as Alzheimer’s disease. The Indian herb Bacopa monnieri is a dietary antioxidant, with animal and in vitro studies indicating several modes of action that may protect the brain against oxidative damage. In parallel, several studies using the CDRI08 extract have shown that extracts of Bacopa monnieri improve cognitive function in humans. The biological mechanisms of this cognitive enhancement are unknown. In this review we discuss the animal studies and in vivo evidence for Bacopa monnieri as a potential therapeutic antioxidant to reduce oxidative stress and improve cognitive function. We suggest that future studies incorporate neuroimaging particularly magnetic resonance spectroscopy into their randomized controlled trials to better understand whether changes in antioxidant status in vivo cause improvements in cognitive function.
Publisher: Mary Ann Liebert Inc
Date: 07-2012
Abstract: Traditional knowledge suggests that Bacopa monnieri enhances cognitive performance. Such traditional beliefs have now been scientifically tested through a handful of randomized, controlled human clinical trials. The current systematic review aimed to examine the scientific evidence as to whether Bacopa can enhance cognitive performance in humans. A systematic review of randomized controlled trials is presented. Multiple databases were systematically searched by multiple authors. Relevant trials were objectively assessed for methodological quality. The subjects studied were adult humans without dementia or significant cognitive impairment. B. monnieri, including Bacopa extracts, were administered over long-term supplementation periods. Any validated cognitive test, whether a primary or secondary outcome. Six (6) studies met the final inclusion criteria and were included in review. Trials were all conducted over 12 weeks. Across trials, three different Bacopa extracts were used at dosages of 300-450 mg extract per day. All reviewed trials examined the effects of Bacopa on memory, while other cognitive domains were less well studied. There were no cognitive tests in the areas of auditory perceptual abilities or idea production and only a paucity of research in the domains of reasoning, number facility, and language behavior. Across studies, Bacopa improved performance on 9 of 17 tests in the domain of memory free recall. There was little evidence of enhancement in any other cognitive domains. There is some evidence to suggest that Bacopa improves memory free recall with evidence for enhancement in other cognitive abilities currently lacking perhaps due to inconsistent measures employed by studies across these cognitive domains. Research into the nootropic effects of Bacopa is in its infancy, with research still yet to investigate the effects of Bacopa across all human cognitive abilities. Similarly, future research should examine the nootropic effects of Bacopa at varied dosages and across different extracts.
Publisher: Wiley
Date: 03-09-2022
DOI: 10.1002/ACN3.51652
Abstract: Expression of glial fibrillary acidic protein (GFAP), a marker of reactive astrocytosis, colocalizes with neuropathology in the brain. Blood levels of GFAP have been associated with cognitive decline and dementia status. However, further examinations at a population‐based level are necessary to broaden generalizability to community settings. Circulating GFAP levels were assayed using a Simoa HD‐1 analyzer in 4338 adults without prevalent dementia from four longitudinal community‐based cohort studies. The associations between GFAP levels with general cognition, total brain volume, and hippoc al volume were evaluated with separate linear regression models in each cohort with adjustment for age, sex, education, race, diabetes, systolic blood pressure, antihypertensive medication, body mass index, apolipoprotein E ε4 status, site, and time between GFAP blood draw and the outcome. Associations with incident all‐cause and Alzheimer's disease dementia were evaluated with adjusted Cox proportional hazard models. Meta‐analysis was performed on the estimates derived from each cohort using random‐effects models. Meta‐analyses indicated that higher circulating GFAP associated with lower general cognition ( ß = −0.09, [95% confidence interval [CI]: −0.15 to −0.03], p = 0.005), but not with total brain or hippoc al volume ( p 0.05). However, each standard deviation unit increase in log‐transformed GFAP levels was significantly associated with a 2.5‐fold higher risk of incident all‐cause dementia (Hazard Ratio [HR]: 2.47 (95% CI: 1.52–4.01)) and Alzheimer's disease dementia (HR: 2.54 [95% CI: 1.42–4.53]) over up to 15‐years of follow‐up. Results support the potential role of circulating GFAP levels for aiding dementia risk prediction and improving clinical trial stratification in community settings.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 19-09-2018
DOI: 10.1212/WNL.0000000000006360
Abstract: Given the potential therapeutic effect of vascular disease control timing to reduce dementia risk, we investigated the age-related influences of vascular risk factor burden on brain structure throughout the lifespan. We studied participants from the community-based prospective Framingham Heart Study. Overall vascular risk factor burden was calculated according to the Framingham Stroke Risk Profile, a validated algorithm that predicts stroke risk. Brain volume was estimated by MRI. We used cross-sectional data to examine how the strength of association between vascular risk factor burden and brain volume changed across each age decade from age 45–54 years through to 85–94 years (N = 2,887). Second, we leveraged up to 40 years of longitudinal data to determine how the strength of association between vascular risk factor burden and brain volume changed when vascular risk factors were examined at progressively earlier ages (N = 7,868). In both cross-sectional and longitudinal analyses, higher vascular risk factor burden was associated with lower brain volume across each age decade. In the cross-sectional analysis, the strength of this association decreased with each decade of advancing age ( p for trend 0.0001). In longitudinal analysis, the strength of association between vascular risk factor burden and brain volume was stronger when vascular risk factors were measured at younger ages. For ex le, vascular risk factor burden was most strongly associated with lower brain volume in later life when vascular risk factors were measured at age 45 years. Vascular risk factors at younger ages appear to have detrimental effects on current and future brain volume.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 07-2017
Publisher: Elsevier BV
Date: 2015
DOI: 10.1016/J.APPET.2014.09.019
Abstract: Despite a common perception that fruit juice is healthy, fruit juice contains high amounts of naturally occurring sugar without the fibre content of the whole fruit. Frequent fruit juice consumption may therefore contribute to excessive sugar consumption typical of the Western society. Although excess sugar intake is associated with high blood pressure (BP), the association between habitual fruit juice consumption and BP is unclear. The present study investigated the association of fruit juice consumption with brachial and central (aortic) BP in 160 community dwelling adults. Habitual fruit juice consumption was measured using a 12 month dietary recall questionnaire. On the same day, brachial BP was measured and central (aortic) BP was estimated through radial artery applanation. Frequency of fruit juice consumption was classified as rare, occasional or daily. Those who consumed fruit juice daily, versus rarely or occasionally, had significantly higher central systolic BP (F (2, 134) = 6.09, p <0.01), central pulse pressure (F (2, 134) = 4.16, p <0.05), central augmentation pressure (F (2, 134) = 5.98, p <0.01) and central augmentation index (F (2, 134) = 3.29, p <0.05) as well as lower pulse pressure lification (F (2, 134) = 4.36, p <0.05). There were no differences in brachial BP. Central systolic BP was 3-4 mmHg higher for those who consumed fruit juice daily rather than rarely or occasionally. In conclusion, more frequent fruit juice consumption was associated with higher central BPs.
Publisher: Elsevier BV
Date: 12-2015
Publisher: Public Library of Science (PLoS)
Date: 04-03-2019
Publisher: Cambridge University Press (CUP)
Date: 06-07-2011
DOI: 10.1017/S0007114511002819
Abstract: Fish oils, rich in long-chain n -3 PUFA, are known to reduce various risk factors for CVD. However, conclusive evidence regarding the benefits of n -3 on arterial stiffness, a risk factor for CVD, has not yet been established. Consequently, we conducted the first study aimed to quantify the effects of n -3 supplementation on arterial stiffness through meta-analysis. Multiple databases and clinical trial registries were systematically searched up until September 2010 for randomised and controlled adult human clinical trials to investigate the effects of long-chain n -3 fatty acids on arterial stiffness. No limits were set on dosage sizes or s le characteristics. A total of ten n -3 trials met the final inclusion criteria four using pulse wave velocity (PWV) and six using arterial compliance, measured as capacitive compliance or systemic arterial compliance, as respective outcome measures. Meta-analysis revealed that n -3 was statistically significant in effectively improving both PWV ( g = 0·33 95 % CI 0·12, 0·56 P 0·01) and arterial compliance ( g = 0·48 95 % CI 0·24, 0·72 P 0·001). There was no evidence of heterogeneity or publication bias. Results were not influenced by changes in blood pressure, heart rate or BMI. The findings of the present study reveal that supplementation with n -3 offers a scientifically supported means of reducing arterial stiffness. Reduction in arterial stiffness by n -3 may account for some of its purported cardioprotective effects.
Publisher: Springer Science and Business Media LLC
Date: 24-12-2022
Publisher: American Academy of Sleep Medicine (AASM)
Date: 02-2021
DOI: 10.5664/JCSM.8812
Publisher: Wiley
Date: 05-11-2019
DOI: 10.1002/ACN3.50936
Publisher: SAGE Publications
Date: 29-01-2013
Abstract: This study aimed to examine the acute and sub-chronic effects of cocoa polyphenols on cognition and mood. In a randomized, double-blind study, healthy middle-aged participants received a dark chocolate drink mix standardized to contain 500 mg, 250 mg or 0 mg of polyphenols (placebo) in a parallel-groups design. Participants consumed their assigned treatment once daily for 30 days. Cognition was measured with the Cognitive Drug Research system and self-rated mood with the Bond–Lader Visual Analogue Scale. Participants were tested at baseline, at 1, 2.5 and 4 h after a single acute dose and again after receiving 30 days of treatment. In total, 72 participants completed the trial. After 30 days, the high dose of treatment significantly increased self-rated calmness and contentedness relative to placebo. Mood was unchanged by treatment acutely while cognition was unaffected by treatment at all time points. This randomized controlled trial is perhaps the first to demonstrate the positive effects of cocoa polyphenols on mood in healthy participants. This provides a rationale for exploring whether cocoa polyphenols can ameliorate the symptoms associated with clinical anxiety or depression.
Publisher: Oxford University Press (OUP)
Date: 28-03-2020
Abstract: Sleep–wake disruption is a key modifiable risk factor and sequela of stroke. The pathogenesis of poststroke sleep dysfunction is unclear. It is not known whether poststroke sleep pathology is due to focal infarction to sleep–wake hubs or to accelerated poststroke neurodegeneration in subcortical structures after stroke. We characterize the first prospective poststroke regional brain volumetric and whole-brain, fiber-specific, white matter markers of objectively measured sleep–wake dysfunction. We hypothesized that excessively long sleep (& h) duration and poor sleep efficiency (& %) measured using the SenseWear Armband 3-months poststroke (n = 112) would be associated with reduced regional brain volumes of a priori-selected sleep–wake regions of interest when compared to healthy controls with optimal sleep characteristics (n = 35). We utilized a novel technique known as a whole-brain fixel-based analysis to investigate the fiber-specific white matter differences in participants with long sleep duration. Stroke participants with long sleep (n = 24) duration exhibited reduced regional volumes of the ipsilesional thalamus and contralesional amygdala when compared with controls. Poor sleep efficiency after stroke (n = 29) was associated with reduced ipsilesional thalamus, contralesional hippoc us, and contralesional amygdala volumes. Whole-brain fixel-based analyses revealed widespread macrostructural degeneration to the corticopontocerebellar tract in stroke participants with long sleep duration, with fiber reductions of up to 40%. Neurodegeneration to subcortical structures, which appear to be vulnerable to accelerated brain volume loss after stroke, may drive sleep–wake deficiencies poststroke, independent of lesion characteristics and confounding comorbidities. We discuss these findings in the context of the clinicopathological implications of sleep-related neurodegeneration and attempt to corroborate previous mechanistic-neuroanatomical findings.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 23-08-2017
DOI: 10.1212/WNL.0000000000004373
Abstract: Sleep disturbance is common in dementia, although it is unclear whether differences in sleep architecture precede dementia onset. We examined the associations between sleep architecture and the prospective risk of incident dementia in the community-based Framingham Heart Study (FHS). Our s le comprised a subset of 321 FHS Offspring participants who participated in the Sleep Heart Health Study between 1995 and 1998 and who were aged over 60 years at the time of sleep assessment (mean age 67 ± 5 years, 50% male). Stages of sleep were quantified using home-based polysomnography. Participants were followed for a maximum of 19 years for incident dementia (mean follow-up 12 ± 5 years). We observed 32 cases of incident dementia 24 were consistent with Alzheimer disease dementia. After adjustments for age and sex, lower REM sleep percentage and longer REM sleep latency were both associated with a higher risk of incident dementia. Each percentage reduction in REM sleep was associated with approximately a 9% increase in the risk of incident dementia (hazard ratio 0.91 95% confidence interval 0.86, 0.97). The magnitude of association between REM sleep percentage and dementia was similar following adjustments for multiple covariates including vascular risk factors, depressive symptoms, and medication use, following exclusions for persons with mild cognitive impairment at baseline and following exclusions for early converters to dementia. Stages of non-REM sleep were not associated with dementia risk. Despite contemporary interest in slow-wave sleep and dementia pathology, our findings implicate REM sleep mechanisms as predictors of clinical dementia.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 06-10-2020
Abstract: GDF15 (growth differentiation factor 15) and NT‐proBNP (N‐terminal pro‐B‐type natriuretic peptide) may offer promise as biomarkers for cognitive outcomes, including dementia. We determined the association of these biomarkers with cognitive outcomes in a community‐based cohort. Plasma GDF15 (n=1603) and NT‐proBNP levels (n=1590) (53% women mean age, 68.7 years) were measured in dementia‐free Framingham Offspring cohort participants at examination 7 (1998–2001). Participants were followed up for incident dementia. Secondary outcomes included Alzheimer disease dementia, magnetic resonance imaging structural brain measures, and neurocognitive performance. During a median 11.8‐year follow‐up, 131 participants developed dementia. On multivariable Cox proportional‐hazards analysis, higher circulating GDF15 was associated with an increased risk of incident all‐cause and Alzheimer disease dementia (hazard ratio [HR] per SD increment in natural log‐transformed biomarker value, 1.54 [95% CI, 1.22–1.95] and 1.37 [95% CI, 1.03–1.81], respectively), whereas higher plasma NT‐proBNP was also associated with an increased risk of all‐cause dementia (HR, 1.32 95% CI, 1.05–1.65). Elevated GDF15 was associated with lower total brain and hippoc al volumes, greater white matter hyperintensity volume, and poorer cognitive performance. Elevated NT‐proBNP was associated with greater white matter hyperintensity volume and poorer cognitive performance. Addition of both biomarkers to a conventional risk factor model improved dementia risk classification (net reclassification improvement index, 0.25 95% CI, 0.05–0.45). Elevated plasma GDF15 and NT‐proBNP were associated with vascular brain injury on magnetic resonance imaging, poorer neurocognitive performance, and increased risk of incident dementia in in iduals aged years. Both biomarkers improved dementia risk classification beyond that of traditional clinical risk factors, indicating their potential value in predicting incident dementia.
Publisher: Wiley
Date: 16-01-2020
DOI: 10.1002/ACN3.50973
Publisher: Wiley
Date: 02-08-2019
DOI: 10.1002/ACN3.50854
Publisher: Elsevier
Date: 2015
Publisher: Wiley
Date: 19-12-2012
DOI: 10.1002/PTR.4864
Abstract: Standardized extracts of the traditional Ayurvedic medicine Bacopa monnieri (BM) (Brahmi) have been recently shown to have cognitive enhancing effects in chronic administration studies. Pre-clinical work has also identified a number of acute anxiolytic, nootropic, and cardiovascular effects of BM. There has, however, been little research on the acute effects of BM on cognitive function. The current study aimed to assess the acute effects of a specific extract of BM (KeenMind®-CDRI 08) in a double-blind, placebo-controlled study in normal healthy participants who completed a cognitively demanding series of tests. Twenty-four healthy volunteers completed six repetitions of the Cognitive Demand Battery (CDB) after consuming a placebo, 320 mg BM or 640 mg of BM in a cross-over design and provided cardiovascular and mood assessments before and after treatment. Change from baseline scores indicated that the 320 mg dose of BM improved performance at the first, second, and fourth repetition post-dosing on the CDB, and the treatments had no effect upon cardiovascular activity or in attenuating task-induced ratings of stress and fatigue. It was concluded that assessment of an earlier pharmacological window and use of less memory-specific cognitive tests together with more temporally sensitive measures of brain activity may improve our understanding of the acute neurocognitive properties of BM.
Publisher: Frontiers Media SA
Date: 29-05-2019
Publisher: American Medical Association (AMA)
Date: 19-04-2019
Publisher: Wiley
Date: 14-08-2015
DOI: 10.1002/PTR.5440
Publisher: Informa UK Limited
Date: 02-01-2015
DOI: 10.1080/07315724.2014.880660
Abstract: Fish oils and multivitamins are two of the most commonly used dietary supplements. Fish oil use may reduce vascular risk factors associated with cognitive decline, thus providing benefits to both heart and brain health. Multivitamins may also have direct effects on brain function. The present study investigated the effects of fish oil, with and without the addition of a multivitamin, on cognitive and cardiovascular function. In a randomized, placebo-controlled, double-blind fashion, 160 healthy adults aged 50-70 years were randomized to receive either 3 g of fish oil (240 mg eicosapentaenoic acid [EPA] + 240 mg docosahexaenoic acid [DHA]) with a multivitamin, 6 g of fish oil (480 mg EPA + 480 mg DHA) with a multivitamin, or 6 g of fish oil without a multivitamin or a placebo. Cognitive performance, brachial blood pressure, and aortic (central) blood pressure were measured at baseline, 6 weeks, and 16 weeks. Treatment allocation had no effect on the primary cognitive outcomes at endpoint. Absolute increases in the red blood cell omega-3/6 ratio were associated with improvements in spatial working memory. The group receiving 6 g fish oil without the multivitamin displayed a significant decrease in aortic pulse pressure and aortic augmentation pressure, two measures of aortic blood pressure and aortic stiffness. Fish oil decreased aortic pulse pressure and augmentation pressure. Reductions in aortic blood pressure were not accompanied by consistent improvements in cognition.
Publisher: Elsevier
Date: 2015
Publisher: CRC Press
Date: 10-01-2013
DOI: 10.1201/B13736
Publisher: SAGE Publications
Date: 04-01-2021
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 07-2020
DOI: 10.1212/WNL.0000000000010022
Abstract: To determine changes in the incidence of dementia between 1988 and 2015. This analysis was performed in aggregated data from in iduals years of age in 7 population-based cohort studies in the United States and Europe from the Alzheimer Cohort Consortium. First, we calculated age- and sex-specific incidence rates for all-cause dementia, and then defined nonoverlapping 5-year epochs within each study to determine trends in incidence. Estimates of change per 10-year interval were pooled and results are presented combined and stratified by sex. Of 49,202 in iduals, 4,253 (8.6%) developed dementia. The incidence rate of dementia increased with age, similarly for women and men, ranging from about 4 per 1,000 person-years in in iduals aged 65–69 years to 65 per 1,000 person-years for those aged 85–89 years. The incidence rate of dementia declined by 13% per calendar decade (95% confidence interval [CI], 7%–19%), consistently across studies, and somewhat more pronouncedly in men than in women (24% [95% CI 14%–32%] vs 8% [0%–15%]). The incidence rate of dementia in Europe and North America has declined by 13% per decade over the past 25 years, consistently across studies. Incidence is similar for men and women, although declines were somewhat more profound in men. These observations call for sustained efforts to finding the causes for this decline, as well as determining their validity in geographically and ethnically erse populations.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 09-2017
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 04-2016
DOI: 10.1161/STROKEAHA.116.012949
Abstract: Previous work from the Framingham Heart Study suggests that brain changes because of arterial aging may begin in young adulthood and that such changes precede cognitive deficits. The objective of this study was to determine the association of arterial stiffness with measures of white matter and gray matter (GM) integrity in young adults. One thousand nine hundred three participants from the Framingham Heart Study Third Generation (mean age, 46±8.7 years) had complete tonometry measurements and brain magnetic resonance imaging (T1-weighted and diffusion tensor imaging). Tonometry measures included carotid-femoral pulse wave velocity, augmentation index, carotid-brachial pressure lification, and central pulse pressure. Fractional anisotropy and GM density images were computed from diffusion tensor imaging and T1 images. Registration to a common anatomic template enabled voxel-based linear regressions relating measures of fractional anisotropy and GM to tonometry measures, adjusting for relevant covariables. Higher carotid-femoral pulse wave velocity was associated with lower regional fractional anisotropy, including the corpus callosum and the corona radiata (8.7 and 8.6 cc, respectively, P .001), as well as lower GM density in the thalamus region (0.9 cc, P .001). Analyses did not reveal significant associations between other tonometry measures and fractional anisotropy or GM. Among young healthy adults, higher aortic stiffness was associated with measures of reduced white matter and GM integrity in areas implicated in cognitive decline and Alzheimer’s disease. Greater aortic stiffness may result in subclinical vascular brain injury at ages much younger than previously described.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 10-2012
DOI: 10.1161/STROKEAHA.112.666727
Abstract: Cardiovascular disease risk predicts cognitive decline although the mechanisms underpinning this association remain unclear. Increasing cardiovascular risk may impair cerebral blood flow predisposing to cerebrovascular damage, cognitive decline, and dementia. This study examined the association between the Framingham General Cardiovascular Risk Profile and cerebral blood flow velocity in 160 healthy middle-aged adults. Blood flow velocity was assessed in both the common carotid and middle cerebral arteries using Doppler. In adjusted linear regression models, cardiovascular risk predicted higher pulsatile (common carotid artery β=0.56, Δ R 2 =0.19, P .001 middle cerebral artery β=0.40, Δ R 2 =0.09, P .001) and lower mean flow velocity (common carotid artery β=−0.49, Δ R 2 =0.14, P .001 middle cerebral artery β=−0.27, Δ R 2 =0.04, P .05). Cardiovascular risk predicted common carotid artery mean and pulsatile flow over and above the effects of age (Δ R 2 =0.11–0.19, P .001) and sex (Δ R 2 =0.03–0.03, P .05). In contrast, cardiovascular risk remained a significant predictor of middle cerebral artery pulsatile, but not mean flow velocity, when controlling for age (Δ R 2 =0.05, P .05) and sex (Δ R 2 =0.06, P .01). Cardiovascular risk has ergent effects on mean and pulsatile blood flow velocity, each of which may independently contribute to cerebral pathology and cognitive impairment.
Publisher: Elsevier BV
Date: 07-2021
Publisher: Elsevier BV
Date: 08-2013
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 20-07-2020
DOI: 10.1212/WNL.0000000000010306
Abstract: To determine the joint role of ideal cardiovascular health (CVH) and genetic risk on risk of dementia. We categorized CVH on the basis of the American Heart Association Ideal CVH Index and genetic risk through a genetic risk score (GRS) of common genetic variants and the APOE ε4 genotype in 1,211 Framingham Heart Study (FHS) offspring cohort participants. We used multivariable Cox proportional hazards regression models to examine the association between CVH, genetic risk, and incident all-cause dementia with up to 10 years of follow-up (mean 8.4 years, 96 incident dementia cases), adjusting for age, sex, and education. We observed that a high GRS ( th percentile) was associated with a 2.6-fold risk of dementia (95% confidence interval [CI] of hazard ratio [HR] 1.23–5.29 p = 0.012) compared with having a low GRS ( th percentile) carrying at least 1 APOE ε4 allele was associated with a 2.3-fold risk of dementia compared with not carrying an APOE ε4 allele (95% CI of HR 1.49–3.53 p = 0.0002), and having a favorable CVH showed a 0.45-fold lower risk of dementia (95% CI of HR 0.20–1.01 p = 0.0527) compared to having an unfavorable CVH when all 3 components were included in the model. We did not observe an interaction between CVH and GRS ( p = 0.99) or APOE ε4 ( p = 0.16). We observed that both genetic risk and CVH contribute additively to dementia risk.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 03-2016
DOI: 10.1161/HYPERTENSIONAHA.115.06610
Abstract: Aortic stiffness is associated with cognitive decline and cerebrovascular disease late in life, although these associations have not been examined in young adults. Understanding the effects of aortic stiffness on the brain at a young age is important both from a pathophysiological and public health perspective. The aim of this study was to examine the cross-sectional associations of aortic stiffness with cognitive function and brain aging in the Framingham Heart Study Third Generation cohort (47% men mean age, 46 years). Participants completed the assessment of aortic stiffness (carotid–femoral pulse wave velocity), a neuropsychological test battery assessing multiple domains of cognitive performance and magnetic resonance imaging to examine subclinical markers of brain injury. In adjusted regression models, higher aortic stiffness was associated with poorer processing speed and executive function (Trail Making B–A β±SE, −0.08±0.03 P .01), larger lateral ventricular volumes (β±SE, 0.09±0.03 P .01) and a greater burden of white-matter hyperintensities (β±SE, 0.09±0.03 P .001). When stratifying by age, aortic stiffness was associated with lateral ventricular volume in young adults (30–45 years), whereas aortic stiffness was associated with white-matter injury and cognition in midlife (45–65 years). In conclusion, aortic stiffness was associated with cognitive function and markers of subclinical brain injury in young to middle-aged adults. Prospective studies are needed to examine whether aortic stiffening in young adulthood is associated with vascular cognitive impairment later in life.
Publisher: Wiley
Date: 07-2012
DOI: 10.1111/J.1445-5994.2011.02645.X
Abstract: Although arterial stiffness has recently been confirmed as a predictor of cardiovascular disease, the association between arterial stiffness and cognitive decline is less clear. We performed a systematic review and meta-analysis to examine the evidence for large artery stiffness as a cause of cognitive decline and dementia. Electronic databases were systematically searched until September 2011 for studies reporting on the longitudinal relationship between any validated measure of large artery stiffness and cognitive decline or dementia. Meta-analysis was performed on four studies investigating the association between aortic pulse wave velocity and a decline in Mini-Mental State Examination scores. Six relevant longitudinal studies were located, conducted over an average of 5 years follow up. Arterial stiffness was predictive of cognitive decline in five/six studies. In meta-analysis, higher aortic stiffness predicted lower Mini-Mental State Examination scores within the s le (β=-0.03, 95% confidence interval (CI): -0.06 to 0.01, n= 3947), although studies were not all homogeneous, and statistical heterogeneity was present (I(2) = 71.9%, P= 0.01). Removal of one study with a relatively younger cohort and lower median aortic stiffness found higher aortic stiffness to significantly predict cognitive decline (β=-0.04, 95% CI: -0.07 to -0.01, n= 3687) without evidence of heterogeneity (I(2) = 9.5%, P= 0.33). There was little research investigating the effects of aortic stiffness on the development of dementia. Aortic stiffness was found to predict cognitive decline in both qualitative review and quantitative analysis.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 07-2017
Publisher: MDPI AG
Date: 14-05-2014
DOI: 10.3390/NU6051956
Publisher: Hindawi Limited
Date: 2012
DOI: 10.1155/2012/809653
Abstract: Use of complementary medicines and therapies (CAM) and modification of lifestyle factors such as physical activity, exercise, and diet are being increasingly considered as potential therapeutic options for anxiety disorders. The objective of this metareview was to examine evidence across a broad range of CAM and lifestyle interventions in the treatment of anxiety disorders. In early 2012 we conducted a literature search of PubMed, Scopus, CINAHL, Web of Science, PsycInfo, and the Cochrane Library, for key studies, systematic reviews, and metaanalyses in the area. Our paper found that in respect to treatment of generalized anxiety or specific disorders, CAM evidence revealed current support for the herbal medicine Kava. One isolated study shows benefit for naturopathic medicine, whereas acupuncture, yoga, and Tai chi have tentative supportive evidence, which is h ered by overall poor methodology. The breadth of evidence does not support homeopathy for treating anxiety. Strong support exists for lifestyle modifications including adoption of moderate exercise and mindfulness meditation, whereas dietary improvement, avoidance of caffeine, alcohol, and nicotine offer encouraging preliminary data. In conclusion, certain lifestyle modifications and some CAMs may provide a beneficial role in the treatment of anxiety disorders.
Publisher: Elsevier BV
Date: 2021
DOI: 10.1016/J.JAD.2021.10.007
Abstract: In older adults, depressive and anxiety symptoms are associated with dementia risk, and represent a manifestation of the dementia prodrome. Understanding how these symptoms are related to cognition in midlife may inform risk models of dementia. This study examined the relationship between depressive and anxiety symptoms, and cognition, in a s le (n= 2,657) of participants enrolled in the Healthy Brain Project. Depressive and Anxiety symptoms were assessed using the Depression Anxiety and Stress Scale, Hospital Anxiety and Depression Scale, and centre for Epidemiological Studies Depression Scale. Objective cognition was assessed using the Cogstate Brief Battery and subjective cognition assessed using the Alzheimer's disease Cooperative Study Cognitive Function Instrument. Somatic- and panic-related anxiety symptoms were associated significantly with poorer attention while tension- and panic-related anxiety were associated significantly with poorer memory. Having clinically meaningful anxiety or depressive symptoms was associated with increased subjective cognitive concerns (d=-0.37). This was further increased for those with clinically meaningful anxiety and depressive symptoms (d = -1.07). This study reports cross-sectional data, and uses a s le enriched with in iduals with a family history of dementia who are therefore at a higher risk of developing dementia compared to the general population. Additionally, biological markers such as cortisol, Aβ, and tau were unavailable. The results support the hypothesis that depressive and anxiety symptoms may increase risk of cognitive decline. Further, they suggest that using depression and anxiety as clinical markers may be helpful in identifying the earliest signs of cognitive decline.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 29-10-2018
Publisher: Wiley
Date: 26-07-2021
DOI: 10.1002/ALZ.12405
Abstract: We evaluated whether insomnia symptom severity was associated with cognitive function, and whether this relationship was modified by biomarkers associated with Alzheimer's disease risk. We examined insomnia symptoms and neuropsychological performance 3.4 years later in 511 dementia‐free Framingham Heart Study participants (62.65 ± 8.7 years, 50.9% male). Additionally, we explored insomnia symptoms combined with self‐reported short habitual sleep duration and effect modification by apolipoprotein E ( APOE ) ε4 allele status. More severe insomnia symptoms were associated with lower performance on global cognition, and immediate and delayed Logical Memory recall, especially when insomnia symptoms were combined with short sleep duration. The association between insomnia symptoms and poorer memory recall was more pronounced in APOE ε4 allele carriers. Insomnia symptom severity was associated with worse subsequent global cognitive and memory performance, which was especially apparent in APOE ε4 allele carriers, suggesting that poor sleep might be particularly detrimental when the brain is already vulnerable to neurodegeneration.
Publisher: Elsevier BV
Date: 05-2015
DOI: 10.1016/J.NUT.2014.10.008
Abstract: Even short-term adherence to a Mediterranean-style diet may benefit aspects of psychological functioning. The aim of the present study was to assess the effects of switching to a 10-d Mediterranean-style diet on mood, cognition, and cardiovascular measures. Using a crossover design, 24 women were randomly assigned to either the diet change (where they switched to a Mediterranean-style diet) or no diet change (normal diet) condition for 10 days before switching to the other condition for the same duration. Mood, cognition, and cardiovascular measures of blood pressure, blood flow velocity, and arterial stiffness were assessed at baseline and at the completion of the two diets (days 11 and 22). Independent of whether the Mediterranean-style diet was undertaken before or after the crossover, it was associated with significantly elevated contentment and alertness, and significantly reduced confusion. Additionally, aspects of cognition, such as memory recall, improved significantly as a result of switching to the Mediterranean-style diet. Regarding cardiovascular measures, there was a significant reduction in augmentation pressure associated with the Mediterranean-style diet intervention, but blood flow velocity through the common carotid artery did not change. This Mediterranean-style diet has the potential to enhance aspects of mood, cognition, and cardiovascular function in a young, healthy adult s le.
Publisher: Springer Science and Business Media LLC
Date: 08-04-2022
DOI: 10.1038/S42003-022-03287-Y
Abstract: Circulating total-tau levels can be used as an endophenotype to identify genetic risk factors for tauopathies and related neurological disorders. Here, we confirmed and better characterized the association of the 17q21 MAPT locus with circulating total-tau in 14,721 European participants and identified three novel loci in 953 African American participants (4q31, 5p13, and 6q25) at P 5 × 10 −8 . We additionally detected 14 novel loci at P 5 × 10 −7 , specific to either Europeans or African Americans. Using whole-exome sequence data in 2,279 European participants, we identified ten genes associated with circulating total-tau when aggregating rare variants. Our genetic study sheds light on genes reported to be associated with neurological diseases including stroke, Alzheimer’s, and Parkinson’s ( F 5, MAP1B , and BCAS3 ), with Alzheimer’s pathological hallmarks ( ADAMTS12 , IL15 , and FHIT ), or with an important function in the brain ( PARD3 , ELFN2 , UBASH3B , SLIT3 , and NSD3 ), and suggests that the genetic architecture of circulating total-tau may differ according to ancestry.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 09-12-2019
DOI: 10.1212/WNL.0000000000008682
Abstract: To test the hypothesis that the inflammatory marker plasma soluble CD14 (sCD14) associates with incident dementia and related endophenotypes in 2 community-based cohorts. Our s les included the prospective community-based Framingham Heart Study (FHS) and Cardiovascular Health Study (CHS) cohorts. Plasma sCD14 was measured at baseline and related to the incidence of dementia, domains of cognitive function, and MRI-defined brain volumes. Follow-up for dementia occurred over a mean of 10 years (SD 4) in the FHS and a mean of 6 years (SD 3) in the CHS. We studied 1,588 participants from the FHS (mean age 69 ± 6 years, 47% male, 131 incident events) and 3,129 participants from the CHS (mean age 72 ± 5 years, 41% male, 724 incident events) for the risk of incident dementia. Meta-analysis across the 2 cohorts showed that each SD unit increase in sCD14 was associated with a 12% increase in the risk of incident dementia (95% confidence interval 1.03–1.23 p = 0.01) following adjustments for age, sex, APOE ε4 status, and vascular risk factors. Higher levels of sCD14 were associated with various cognitive and MRI markers of accelerated brain aging in both cohorts and with a greater progression of brain atrophy and a decline in executive function in the FHS. sCD14 is an inflammatory marker related to brain atrophy, cognitive decline, and incident dementia.
Publisher: Frontiers Media SA
Date: 20-05-2015
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 12-2018
DOI: 10.1161/STROKEAHA.118.022132
Abstract: The role of dietary fat on cardiovascular health and mortality remains under debate. Because the APOE is central to the transport and metabolism of lipids, we examined associations between plasma fatty acids and the risk of stroke, coronary heart disease, and mortality by APOE-ε4 genotype. We included 943 FHS (Framingham Heart Study) and 1406 3C (Three-City) Bordeaux Study participants. Plasma docosahexaenoic, linoleic, arachidonic, and palmitic fatty acids were measured at baseline by gas chromatography. All-cause stroke, ischemic stroke, coronary heart disease, and all-cause mortality events were identified prospectively using standardized protocols. Each cohort used Cox models to separately relate fatty acid levels to the risk of developing each event during ≤10 years of follow-up adjusting for potential confounders and stratifying by APOE genotype (ε4 carriers versus noncarriers). We then meta-analyzed summary statistics using random-effects models. On average, participants had a mean age of 74 years, 61% were women, and 21% (n=483) were APOE-ε4 carriers. Meta-analysis results showed that, only among APOE-ε4 carriers, every SD unit increase in linoleic acid was associated with a reduced risk of all-cause stroke (hazard ratio [HR], 0.54 [95% CI, 0.38–0.78]), ischemic stroke (HR, 0.48 [95% CI, 0.33–0.71]), and all-cause mortality (HR, 0.70 [95% CI, 0.57–0.85]). In contrast, every SD unit increase in palmitic acid was related to an increased risk of all-cause stroke (HR, 1.58 [95% CI, 1.16–2.17]), ischemic stroke (HR, 1.76 [95% CI, 1.26–2.45]), and coronary heart disease (HR, 1.48 [95% CI, 1.09–2.01]), also in APOE-ε4 carriers only. Results for docosahexaenoic acid and arachidonic acid were heterogeneous between cohorts. These exploratory results suggest that APOE-ε4 carriers may be more susceptible to the beneficial or adverse impact of fatty acids on cardiovascular disease and mortality. In this subgroup, higher linoleic acid was protective for stroke and mortality, whereas palmitic acid was a risk factor for stroke and coronary heart disease. The mechanisms underlying these novel findings warrant further investigation.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 09-2016
DOI: 10.1161/STROKEAHA.116.013508
Abstract: Aortic stiffening increases the transfers of high pressure and flow pulsatility to small cerebral vessels potentially causing the accumulation of vascular brain injury. Our aim was to investigate the prospective association of aortic stiffness with the risks of incident mild cognitive impairment and dementia. We studied 1101 dementia-free Framingham Offspring study participants (mean age, 69±6 years 54% women). Aortic stiffness was measured as carotid–femoral pulse wave velocity using applanation tonometry and modeled as a linear variable and the top 2 quintiles ( .4 m/s). Outcomes were the 10-year risk of incident mild cognitive impairment and dementia, including clinically characterized Alzheimer disease. We observed 106, 77, and 59 events of mild cognitive impairment, all-cause dementia, and clinical Alzheimer disease, respectively. After adjustment for age and sex, higher continuous aortic stiffness predicted an increased risk of mild cognitive impairment (hazard ratio, 1.40 [95% confidence interval, 1.13–1.73]), all-cause dementia (hazard ratio, 1.45 [95% confidence interval, 1.13–1.87]), and Alzheimer disease (hazard ratio, 1.41 [95% confidence interval, 1.06–1.87]). In risk factor–adjusted statistical models, aortic stiffness remained a significant predictor of mild cognitive impairment but not incident dementia. In nondiabetic patients, the top 2 quintiles of aortic stiffness were associated with a higher risk of incident all-cause dementia across all statistical models. Aortic stiffness was an independent predictor of incident mild cognitive impairment in the whole s le and with incident dementia in nondiabetic patients. Our findings suggest aortic stiffness as a potentially modifiable risk factor for clinical cognitive impairment and dementia.
Publisher: American Medical Association (AMA)
Date: 05-2019
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 11-2017
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 02-08-2017
Abstract: Relations of orthostatic change in blood pressure with brain structure and function have not been studied thoroughly, particularly in younger, healthier in iduals. Elucidation of factors that contribute to early changes in brain integrity may lead to development of interventions that delay or prevent cognitive impairment. In a s le of the Framingham Heart Study Third Generation (N=2119 53% women mean age±SD, 47±8 years), we assessed orthostatic change in mean arterial pressure ( MAP ), aortic stiffness (carotid‐femoral pulse wave velocity), neuropsychological function, and markers of subclinical brain injury on magnetic resonance imaging. Multivariable regression analyses were used to assess relations between orthostatic change in MAP and brain structural and neuropsychological outcomes. Greater orthostatic increase in MAP on standing was related to better Trails B‐A performance among participants aged years (β± SE , 0.062±0.029 P =0.031) and among participants with carotid‐femoral pulse wave velocity .9 m/s (β± SE , 0.063±0.026 P =0.016). This relation was not significant among participants who were older or had stiffer aortas. Conversely, greater orthostatic increase in MAP was related to larger total brain volume among older participants (β± SE , 0.065±0.029 P =0.023) and among participants with carotid‐femoral pulse wave velocity ≥6.9 m/s (β± SE , 0.078±0.031 P =0.011). Blunted orthostatic increase in MAP was associated with smaller brain volume among participants who were older or had stiffer aortas and with poorer executive function among persons who were younger or who had more‐elastic aortas. Our findings suggest that the brain is sensitive to orthostatic change in MAP , with results dependent on age and aortic stiffness.
Location: United States of America
Location: Australia
Start Date: 2020
End Date: 2020
Funder: National Institute on Aging
View Funded ActivityStart Date: 2015
End Date: 2018
Funder: National Health and Medical Research Council
View Funded ActivityStart Date: 2019
End Date: 2020
Funder: National Stroke Foundation
View Funded ActivityStart Date: 2019
End Date: 2020
Funder: Bethlehem Griffiths Research Foundation
View Funded ActivityStart Date: 2019
End Date: 2022
Funder: National Heart Foundation of Australia
View Funded ActivityStart Date: 2019
End Date: 2021
Funder: Alzheimer's Association
View Funded ActivityStart Date: 2019
End Date: 2023
Funder: National Health and Medical Research Council
View Funded ActivityStart Date: 05-2023
End Date: 05-2028
Amount: $4,583,816.00
Funder: Australian Research Council
View Funded Activity