Dataset Information

Investigation of antihypertensive class, dementia, and cognitive decline: A meta-analysis.

ABSTRACT:

Objective

High blood pressure is one of the main modifiable risk factors for dementia. However, there is conflicting evidence regarding the best antihypertensive class for optimizing cognition. Our objective was to determine whether any particular antihypertensive class was associated with a reduced risk of cognitive decline or dementia using comprehensive meta-analysis including reanalysis of original participant data.

Methods

To identify suitable studies, MEDLINE, Embase, and PsycINFO and preexisting study consortia were searched from inception to December 2017. Authors of prospective longitudinal human studies or trials of antihypertensives were contacted for data sharing and collaboration. Outcome measures were incident dementia or incident cognitive decline (classified using the reliable change index method). Data were separated into mid and late-life (>65 years) and each antihypertensive class was compared to no treatment and to treatment with other antihypertensives. Meta-analysis was used to synthesize data.

Results

Over 50,000 participants from 27 studies were included. Among those aged >65 years, with the exception of diuretics, we found no relationship by class with incident cognitive decline or dementia. Diuretic use was suggestive of benefit in some analyses but results were not consistent across follow-up time, comparator group, and outcome. Limited data precluded meaningful analyses in those ≤65 years of age.

Conclusion

Our findings, drawn from the current evidence base, support clinical freedom in the selection of antihypertensive regimens to achieve blood pressure goals.

Clinical trials registration

The review was registered with the international prospective register of systematic reviews (PROSPERO), registration number CRD42016045454.

SUBMITTER: Peters R

PROVIDER: S-EPMC7108807 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:Background: More people with cognitive dysfunction and dementia also fall into the category of high vascular risk, for which aspirin is one of the most frequently used drugs. However, previous studies reporting that aspirin buffers against mild cognitive decline (MCI) and dementia remain controversial. We thus conducted an updated systematic review and meta-analysis to evaluate the association of aspirin use with the risk of MCI and dementia in older adults. Methods: Data sources from PubMed, Embase, Web of Science, and the Cochrane Database for randomized controlled trails (RCTs) and cohort studies (published between January 1, 2000 and April 11, 2020). Relative risks (RRs) and 95% confidence intervals (95% CIs) were used to pool data on the occurrence of dementia and MCI with random-effects models. Results: Of 3,193 identified articles, 15 studies (12 cohort studies and three RCTs) were eligible and were included in our analysis, which involved a total of 100,909 participants without cognitive dysfunctions or dementia at baseline. In pooled cohort studies, aspirin use did not reduce the incidence of MCI and dementia (the pooled RR = 0.97; 95% CI = 0.85-1.11; Ifor heterogeneity2 = 65%) compared with non-users. However, low-dose aspirin (75-100 mg/day) was associated with a decreased likelihood of developing dementia or MCI (the pooled RR = 0.75; 95% CI = 0.63-0.9; Ifor heterogeneity2 = 50.5%). This association existed in studies including all-cause dementia (the pooled RR = 0.82; 95% CI = 0.71-0.96) and Alzheimer's disease (AD) (the pooled RR = 0.54; 95% CI = 0.33-0.89), but not in MCI (the pooled RR = 0.58; 95% CI = 0.31-1.08). In RCTs, low-dose aspirin use was not significantly associated with less prevalence of dementia or MCI (RR = 0.94; 95% CI = 0.84-1.05; Ifor heterogeneity2 = 0.0%). Conclusions: In cohort studies, we found that low-dose aspirin use had a higher likelihood of reducing the incidence of dementia, which was not supported by RCTs. The evidence was insufficient to fully evaluate the effect of aspirin on cognitive function and dementia. Well-designed studies and innovative approaches are therefore needed to clarify whether the use of aspirin improves cognitive function and reduces the risk of dementia.

Project description:BackgroundEmerging evidence indicates that poor periodontal health adversely impacts cognition. This review examined the available longitudinal evidence concerning the effect of poor periodontal health on cognitive decline and dementia.MethodsComprehensive literature search was conducted on five electronic databases for relevant studies published until April 2022. Longitudinal studies having periodontal health as exposure and cognitive decline and/or dementia as outcomes were considered. Random effects pooled estimates and 95% confidence intervals were generated (pooled odds ratio for cognitive decline and hazards ratio for dementia) to assess whether poor periodontal health increases the risk of cognitive decline and dementia. Heterogeneity between studies was estimated by I2 and the quality of available evidence was assessed through quality assessment criteria.ResultsAdopted search strategy produced 2132 studies for cognitive decline and 2023 for dementia, from which 47 studies (24 for cognitive decline and 23 for dementia) were included in this review. Poor periodontal health (reflected by having periodontitis, tooth loss, deep periodontal pockets, or alveolar bone loss) was associated with both cognitive decline (OR = 1.23; 1.05-1.44) and dementia (HR = 1.21; 1.07-1.38). Further analysis, based on measures of periodontal assessment, found tooth loss to independently increase the risk of both cognitive decline (OR = 1.23; 1.09-1.39) and dementia (HR = 1.13; 1.04-1.23). Stratified analysis based on the extent of tooth loss indicated partial tooth loss to be important for cognitive decline (OR = 1.50; 1.02-2.23) and complete tooth loss for dementia (HR = 1.23; 1.05-1.45). However, the overall quality of evidence was low, and associations were at least partly due to reverse causality.ConclusionsPoor periodontal health and tooth loss appear to increase the risk of both cognitive decline and dementia. However, the available evidence is limited (e.g., highly heterogenous, lacking robust methodology) to draw firm conclusions. Further well-designed studies involving standardized periodontal and cognitive health assessment and addressing reverse causality are highly warranted.

Project description:Preclinical prediction of Alzheimer disease (AD) is important and critical to effective intervention. Plasma levels of amyloid-? (A?) peptides have been a principal focus of the growing literature on blood-based biomarkers, but studies to date have varied in design, assay methods, and sample size, making it difficult to readily interpret the overall data.To conduct a systematic review and meta-analysis of relevant prospective studies to determine whether plasma amyloid-? levels may predict development of dementia, AD, and cognitive decline.We searched prospective studies published between 1995 and 2011 indexed in the MEDLINE, EMBASE, and PsycINFO databases. Selected studies included those measuring at least 1 relevant plasma amyloid-? species (A?(40), A?(42), or A?(42):A?(40) ratio) and reporting an effect estimate for dementia, AD, or cognitive change.Using a standardized extraction form, appropriate study parameters on subject information, exposure, and outcome were extracted. Random effects models were used to generate summary risk ratios and 95% confidence intervals comparing the bottom vs top quantiles for each plasma measure.Thirteen studies with a total of 10 303 subjects met inclusion criteria for meta-analysis. Lower A?(42):A?(40) ratios were significantly associated with development of AD (summary risk ratio, 1.60; 95% CI, 1.04-2.46; P = .03) and dementia (risk ratio, 1.67; 95% CI, 1.02-2.75; P = .04). Significant heterogeneity was found for both summary estimates, which could not be explained by participants' age, sex distribution, the study's follow-up time, or year of publication. Plasma levels of A?(40) and A?(42) alone were not significantly associated with either outcome.Overall, the literature indicates that plasma A?(42):A?(40) ratios predict development of AD and dementia. However, significant heterogeneity in the meta-analysis underlines the need for substantial further investigation of plasma amyloid-? levels as a preclinical biomarker.

Project description:BackgroundBy 2050, it has been estimated that approximately one-fifth of the population will be made up of older adults (aged ≥60 years). Old age often comes with cognitive decline and dementia. Physical activity may prevent cognitive decline and dementia.MethodsWe reviewed and synthesised prospective studies into physical activity and cognitive decline, and physical activity and dementia, published until January 2014. Forty-seven cohorts, derived from two previous systematic reviews and an updated database search, were used in the meta-analyses. Included participants were aged ≥40 years, in good health and/or randomly selected from the community. Studies were assessed for methodological quality.ResultsTwenty-one cohorts on physical activity and cognitive decline and twenty-six cohorts on physical activity and dementia were included. Meta-analysis, using the quality-effects model, suggests that participants with higher levels of physical activity, when compared to those with lower levels, are at reduced risk of cognitive decline, RR 0.65, 95% CI 0.55-0.76, and dementia, RR 0.86, 95% CI 0.76-0.97. Sensitivity analyses revealed a more conservative estimate of the impact of physical activity on cognitive decline and dementia for high quality studies, studies reporting effect sizes as ORs, greater number of adjustments (≥10), and longer follow-up time (≥10 years). When one heavily weighted study was excluded, physical activity was associated with an 18% reduction in the risk of dementia (RR 0.82; 0.73-0.91).ConclusionsLongitudinal observational studies show an association between higher levels of physical activity and a reduced risk of cognitive decline and dementia. A case can be made for a causal interpretation. Future research should use objective measures of physical activity, adjust for the full range of confounders and have adequate follow-up length. Ideally, randomised controlled trials will be conducted. Regardless of any effect on cognition, physical activity should be encouraged, as it has been shown to be beneficial on numerous levels.

Project description:BackgroundDecline in cognitive performance is associated with gait deterioration. Our objectives were: 1) to determine, from an original study in older community-dwellers without diagnosis of dementia, which gait parameters, among slower gait speed, higher stride time variability (STV) and Timed Up & Go test (TUG) delta time, were most strongly associated with lower performance in two cognitive domains (i.e., episodic memory and executive function); and 2) to quantitatively synthesize, with a systematic review and meta-analysis, the association between gait performance and cognitive decline (i.e., mild cognitive impairment (MCI) and dementia).MethodsBased on a cross-sectional design, 934 older community-dwellers without dementia (mean±standard deviation, 70.3±4.9years; 52.1% female) were recruited. A score at 5 on the Short Mini-Mental State Examination defined low episodic memory performance. Low executive performance was defined by clock-drawing test errors. STV and gait speed were measured using GAITRite system. TUG delta time was calculated as the difference between the times needed to perform and to imagine the TUG. Then, a systematic Medline search was conducted in November 2013 using the Medical Subject Heading terms "Delirium," "Dementia," "Amnestic," "Cognitive disorders" combined with "Gait" OR "Gait disorders, Neurologic" and "Variability."FindingsA total of 294 (31.5%) participants presented decline in cognitive performance. Higher STV, higher TUG delta time, and slower gait speed were associated with decline in episodic memory and executive performances (all P-values <0.001). The highest magnitude of association was found for higher STV (effect size = -0.74 [95% Confidence Interval (CI): -1.05;-0.43], among participants combining of decline in episodic memory and in executive performances). Meta-analysis underscored that higher STV represented a gait biomarker in patients with MCI (effect size = 0.48 [95% CI: 0.30;0.65]) and dementia (effect size = 1.06 [95% CI: 0.40;1.72]).ConclusionHigher STV appears to be a motor phenotype of cognitive decline.