Association of Aortic Stiffness and Cognitive Decline: A Systematic Review and Meta-Analysis.
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ABSTRACT:
SUBMITTER: Liu Q
PROVIDER: S-EPMC8261283 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Aortic stiffness is associated with an increased risk of cardio- and cerebrovascular disease and mortality and may increase risk of dementia. The aim of the present study is to examine the association between arterial stiffness and cognitive decline in a large prospective cohort study with three repeated cognitive assessment over 7 years of follow-up. Aortic pulse wave velocity (PWV) was measured among 4300 participants (mean ± standard deviation age 65.1 ± 5.2 years) in 2007-2009 and categorized based on the tertiles: (lowest third: < 7.41 m/s), (middle third: 7.41-8.91 m/s), and (highest third: > 8.91 m/s). A global cognitive score was calculated in 2007-2009, 2012-2013, and 2015-2016 based on responses to memory, reasoning and fluency tests. Standardized global cognitive score (mean = 0, SD = 1) in highest third versus lowest third of PWV category was lower at baseline (- 0.12, 95% CI - 0.18, - 0.06). Accelerated 7-year cognitive decline was observed among individuals with the highest PWV [difference in 7-year cognitive change for highest third versus lowest third PWV: - 0.06, 95% CI - 0.11, - 0.01, P < 0.01]. Higher aortic stiffness was associated with faster cognitive decline. Clinicians may be able to use arterial stiffness severity as an indicator to administer prompt treatments to prevent or delay the onset of cognitive decline or dementia. Future studies need to determine whether early intervention of vascular stiffness is effective in delaying these outcomes.
| S-EPMC7441227 | biostudies-literature
Project description:ObjectivesThis review provides a broad overview of the effectiveness of interventions for subjective cognitive decline (SCD) in improving psychological well-being, metacognition and objective cognitive performance.MethodsDatabases including PubMed, Web of Science and Cochrane Systematic Reviews were searched up to August 2017 to identify randomised controlled trials evaluating interventions for SCD. Interventions were categorised as psychological, cognitive, lifestyle or pharmacological. Outcomes of interest included psychological well-being, metacognitive ability and objective cognitive performance. To assess the risk of bias, three authors independently rated study validity using criteria based on the Critical Appraisal Skills Programme. Random-effects meta-analyses were undertaken where three or more studies investigated similar interventions and reported comparable outcomes.ResultsTwenty studies met inclusion criteria and 16 had sufficient data for inclusion in the meta-analyses. Of these, only seven were rated as being high quality. Group psychological interventions significantly improved psychological well-being (g=0.40, 95% CI 0.03 to 0.76; p=0.03) but the improvement they conferred on metacognitive ability was not statistically significant (g=0.26, 95% CI -0.22 to 0.73; p=0.28). Overall, cognitive training interventions led to a small, statistically significant improvement in objective cognitive performance (g=0.13, 95% CI 0.01 to 0.25; p=0.03). However, the pooled effect sizes of studies using active control groups (g=0.02, 95% CI -0.19 to 0.22; p=0.85) or reporting global cognitive measures (g=0.06, 95% CI -0.19 to 0.31; p=0.66) were non-significant.ConclusionsThere is a lack of high-quality research in this field. Group psychological interventions improve psychological well-being and may also improve metacognition. A large, high-quality study is indicated to investigate this further. There is no evidence to suggest that cognitive interventions improve global cognitive performance and the clinical utility of small improvements in specific cognitive domains is questionable. There is a lack of research considering lifestyle interventions and poor quality evidence for pharmacological interventions.Prospero registration numberCRD42017079391.
| S-EPMC6059327 | biostudies-literature
Project description:Arterial stiffness may be a cause of cerebral small vessel disease and cognitive impairment. We therefore performed a systematic review and meta-analysis of studies on the association between stiffness, cerebral small vessel disease and cognitive impairment. For the associations between stiffness (i.e. carotid-femoral pulse wave velocity (cfPWV), brachial-ankle PWV (baPWV), carotid stiffness and pulse pressure) on the one hand and cerebral small vessel disease and cognitive impairment on the other, we identified 23 (n=15,666/20 cross-sectional; 1 longitudinal; 2 combined cross-sectional/longitudinal) and 41 studies (n=57,671/26 cross-sectional; 11 longitudinal; 4 combined cross-sectional/longitudinal), respectively. Pooled analyses of cross-sectional studies showed that greater stiffness was associated with markers of cerebral small vessel disease with odds ratios, per +1 SD, of 1.29-1.32 (P<.001). Studies on cognitive impairment could not be pooled due to large heterogeneity. Some (but not all) studies showed an association between greater stiffness and cognitive impairment, and the strength of this association was relatively weak. The present study supports the hypothesis that greater arterial stiffness is a contributor to microvascular brain disease.
| S-EPMC5314721 | biostudies-literature
Project description:ObjectiveHearing loss has been pointed out as a potential predictor for cognitive decline. This study conducted a systematic review to evaluate the scientific evidence on the association between hearing loss in the elderly and cognitive decline, as well as whether race/color influences this relationship.MethodThe search for studies was performed in the following electronic databases: MedLine/PubMed Web of Science, Scopus and Virtual Health Library, and MedRkiv up to August 2022. Studies with epidemiological designs that assess the association between hearing loss and cognitive decline in the elderly were eligible for inclusion. Three independent reviewers performed the selection, data extraction and evaluation of the quality of the studies using the Newcastle-Ottawa Scale. A meta-analysis using a random effects model estimated the global association measurements (Beta coefficient: β) and their 95% confidence intervals (95%CI), and the Higgins and Thompson indicator (I2) was also estimated to assess statistical heterogeneity among the studies.Results5,207 records were identified in the database surveys, of which only 18 were eligible studies, totaling 19,551 individuals. Hearing loss was associated with cognitive decline in the elderly, with statistical significance: β = -0.13; 95%CI = -0.23 to -0.04; I2 = 98.70%). For black individuals, the magnitude of the association increased: β = -0.64; 95%CI = -3.36 to 2.07; I2 = 95.65%, but it was not statistically significant.ConclusionThe findings of this systematic review showed the existence of a significant relationship between hearing loss and cognitive decline in the elderly, as well as signaling that among black individuals the magnitude of the association can be increased.
| S-EPMC10635537 | biostudies-literature
Project description:At present, prevention is particularly important when there is no effective treatment for cognitive decline. Since the adverse events of pharmacological interventions counterbalance the benefits, nonpharmacological approaches seem desirable to prevent cognitive decline. To our knowledge, no meta-analyses have been published on nonpharmacological interventions preventing cognitive decline. To investigate whether nonpharmacological interventions play a role in preventing cognitive decline among older people, we searched related trials up to March 31, 2019, in MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials (CENTRAL), ClinicalTrials and the Cochrane library databases. Randomized controlled trials (RCTs) were included if they enrolled participants older than 60 years of age who had a risk of cognitive decline, and the interventions were nonpharmacological. Two reviewers independently extracted data and assessed study quality. The Grading of Recommendations Assessment Development and Evaluation (GRADE) approach was used to rate the quality of evidence. Heterogeneity was quantified with I2. Subgroup analysis and meta-regression were used to research the sources of heterogeneity. Influence analyses were used to detect and remove extreme effect sizes (outliers) in our meta-analysis. Publication bias was assessed with funnel plots and Egger test. Primary outcomes were the incidence of mild cognitive impairment (MCI) or dementia and Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-Cog) scores. Second outcomes were activities of daily living (ADL) and Mini-Mental State Examination (MMSE) scores. A total of 22 studies with 13,264 participants were identified for analysis. In terms of prevention, nonpharmacological interventions appeared to be more effective than control conditions, as assessed by the incidence of MCI or dementia (RR, 0.73; CI, 0.55-0.96; moderate-certainty evidence), while the results of ADAS-Cog suggested no significant differences between two groups (MD, -0.69; CI, -1.52-0.14; very low-certainty evidence). Second outcomes revealed a significant improvement from nonpharmacological interventions versus control in terms of the change in ADL (MD, 0.73; CI, 0.65-0.80) and MMSE scores (posttreatment scores: MD, 0.25; CI, 0.02-0.47; difference scores: MD, 0.59, CI, 0.29-0.88). Univariable meta-regression showed association between lower case of MCI or dementia and two subgroup factors (P = 0.013 for sample size; P = 0.037 for area). Multiple meta-regression suggested that these four subgroup factors were not associated with decreased incidence of MCI (P > 0.05 for interaction). The Naive RR estimate was calculated as 0.73. When the three studies that detected by outlier and influence analysis were left out, the Robust RR was 0.66. In conclusion, nonpharmacological therapy could have an indicative role in reducing the case of MCI or dementia. However, given the heterogeneity of the included RCTs, more preregistered trials are needed that explicitly examine the association between nonpharmacological therapy and cognitive decline prevention, and consider relevant moderators.
| S-EPMC7026127 | biostudies-literature
Project description:Evidence suggests that affective problems, such as depression and anxiety, increase risk for late-life dementia. However, the extent to which affective problems influence cognitive decline, even many years prior to clinical diagnosis of dementia, is not clear. The present study systematically reviews and synthesises the evidence for the association between affective problems and decline in cognitive state (i.e., decline in non-specific cognitive function) in older adults. An electronic search of PubMed, PsycInfo, Cochrane, and ScienceDirect was conducted to identify studies of the association between depression and anxiety separately and decline in cognitive state. Key inclusion criteria were prospective, longitudinal designs with a minimum follow-up period of 1 year. Data extraction and methodological quality assessment using the STROBE checklist were conducted independently by two raters. A total of 34 studies (n = 71 244) met eligibility criteria, with 32 studies measuring depression (n = 68 793), and five measuring anxiety (n = 4698). A multi-level meta-analysis revealed that depression assessed as a binary predictor (OR 1.36, 95% CI 1.05-1.76, p = 0.02) or a continuous predictor (B = -0.008, 95% CI -0.015 to -0.002, p = 0.012; OR 0.992, 95% CI 0.985-0.998) was significantly associated with decline in cognitive state. The number of anxiety studies was insufficient for meta-analysis, and they are described in a narrative review. Results of the present study improve current understanding of the temporal nature of the association between affective problems and decline in cognitive state. They also suggest that cognitive function may need to be monitored closely in individuals with affective disorders, as these individuals may be at particular risk of greater cognitive decline.
| S-EPMC6331688 | biostudies-other
Project description:BACKGROUND:Development of cognitive decline represents substantial issues in today's society, steadily gaining importance with increasing life expectancy. One potential approach to preventing cognitive decline is to lower homocysteine by administering vitamin B. In this systematic review and meta-analysis, we address this topic and investigate whether oral supplementation of vitamin B can successfully prevent cognitive decline in cognitively unimpaired individuals. METHODS:A computerized systematic literature search was conducted using the electronic databases PubMed, Embase, and the Cochrane Library. Eligibility criteria included oral supplementation with vitamin B (B1, B6, folic acid, and B12) and the absence of cognitive impairment. A meta-analysis was conducted with "global cognition" as the primary outcome of this review. Secondary outcomes were changes in cognitive function in other cognitive domains reported in the included studies. Risk of bias was assessed according to the Cochrane Risk of Bias tool and the GRADE approach to establish the overall certainty of the evidence. RESULTS:The meta-analysis did not yield a significant overall effect of supplementation with vitamin B on cognitive function (Z = 0.87; p = 0.39; SMD, 0.02; 95% CI, -?0.034, 0.08). A sensitivity analysis focusing on specific risk factors did not alter this result. Some studies reported isolated significant effects of the intervention on secondary outcomes. However, these findings were outnumbered by the number of cognitive tests that did not yield significant effects. DISCUSSION:We found no overall evidence that oral vitamin B supplementation prevented cognitive decline. The isolated significant effects that were reported could be attributed to methodological issues. The results of this review do not provide evidence that population groups with certain risk factors would profit more from the intervention than others. Our findings do not apply to forms of administration other than oral supplementation nor do they offer information regarding the treatment of cognitively impaired individuals via the administration of vitamin B. SYSTEMATIC REVIEW REGISTRATION:PROSPERO CRD42017071692.
| S-EPMC7229605 | biostudies-literature
Project description:Background: People with chronic pain (CP) sometimes report impaired cognitive function, including a deficit of attention, memory, executive planning, and information processing. However, the association between CP and cognitive decline was still not clear. Our study aimed to assess the association of CP as a risk factor with cognitive decline among adults. Methods: We included data from clinical studies. Publications were identified using a systematic search strategy from PubMed, Embase, and Cochrane Library databases from inception to October 10, 2020. We used the mean cognitive outcome data and the standard deviations from each group. The standardized mean difference (SMD) or odds ratio (OR), and 95% confidence intervals (CI) were performed for each cognitive decline outcome. I 2-values were assessed to quantify the heterogeneities. Results: We included 37 studies with a total of 52,373 patients with CP and 80,434 healthy control participants. Because these studies used different evaluative methods, we analyzed these studies. The results showed CP was associated with cognitive decline when the short-form 36 health survey questionnaire (SF-36) mental component summary (SMD = -1.50, 95% CI = -2.19 to -0.81), the Montreal cognitive assessment (SMD = -1.11, 95% CI = -1.60 to -0.61), performance validity testing (SMD = 3.05, 95% CI = 1.74 to 4.37), or operation span (SMD = -1.83, 95% CI = -2.98 to -0.68) were used. However, we got opposite results when the studies using International Classification of Diseases and Related Health Problems classification (OR = 1.58, 95% CI = 0.97 to 2.56), the Mini-Mental State Examination (SMD = -0.42, 95% CI = -0.94 to 0.10; OR = 1.14, 95% CI = 0.91 to 1.42), and Repeatable Battery for the Assessment of Neuropsychological Status memory component (SMD = -0.06, 95% CI = -0.37 to 0.25). Conclusion: There may be an association between CP and the incidence of cognitive decline when some cognitive, evaluative methods were used, such as short-form 36 health survey questionnaire, Montreal cognitive assessment, performance validity testing, and operation span.
| S-EPMC8492915 | biostudies-literature
Project description:BackgroundIt is well known that atrial fibrillation (AF) carried a high risk of cognitive decline, which is independent of stroke or transient ischemic attack (TIA). Whether anticoagulation is associated with reduced risk of cognitive decline in participants with AF still remains controversial. We conducted a systematic review and meta-analysis to explore the effect of anticoagulation on the risk of cognitive decline in patients with AF.MethodsWe systematically searched the PubMed, Embase and the Cochrane Database for eligible studies published up to January 2018. Risk ratios (RR) with 95% confidence interval (CI) for cognitive decline were extracted, and pooled estimations were calculated using the fixed effects model. Subgroup analyses were further performed.ResultsEight relevant articles involved 454,273 patients were ultimately included in this meta-analysis. We found that anticoagulation was associated with reduced risk of cognitive impairment as compared with nonanticoagulation (RR 0.72, 95% CI 0.69-0.75, I 11.5%). This reduction was still significant after adjustment for stroke and TIA (RR 0.72, 95% CI 0.69-0.74, I 0.0%). In the subgroup analyses, the incidence of cognitive decline was significantly decreased in those treated with anticoagulation compared to no treatment (RR 0.72, 95% CI 0.69-0.75, I 0.0%), but the cognitive benefit showed no significant difference between anticoagulant and antiplatelet treatment (RR 1.01, 95% CI 0.68-1.50, I 46.8%).ConclusionAnticoagulation is associated with cognitive benefit in participants with AF independent of stroke and TIA, but it was not superior to antiplatelet drugs in reducing the risk of cognitive decline.
| S-EPMC6408007 | biostudies-literature
Project description:BackgroundNo clear evidence is available for the influence of napping on cognitive function in older adults. This systematic review and meta-analysis aimed to elucidate the cross-sectional and longitudinal relationships between napping and cognitive function (global cognition and memory) and to explore whether some individual characteristics and sleep characteristics can modify this relationship.MethodsWe systematically searched Medline (via PubMed), Web of Science, and Scopus. DerSimonian and Lair and Hartung-Knapp-Sidik-Jonkman random effects methods were used to compute pooled estimates of odds ratios (ORs) and their respective 95% confidence intervals (95% CIs) for the association of global cognition and memory with napping. The mean age, the night sleep time (hours), and the percentage of women, no nappers, and people in the less night-time sleep duration category were used for meta-regressions.ResultsTwenty-five studies were included in this systematic review and meta-analysis, 18 cross-sectional and seven longitudinal studies, including 95,719 participants older than 60 years. The pooled ORs from the cross-sectional analyses were 1.03 (95% CI: 1.01 to 1.06) for global cognition and 1.06 (95%: 0.90 to 1.26) for memory. The pooled ORs from the longitudinal analyses were 1.00 (95% 0.85 to 1.18) for global cognition and 1.08 (95% 0.98 to 1.19) for memory. These associations were not modified by individual or sleep characteristics.ConclusionOur data confirm the absence of association between napping and global cognition and memory regardless of the characteristics of the population. This information might be considered when providing lifestyle recommendations to adults with and without cognitive complaints.
| S-EPMC9479293 | biostudies-literature