Cognitive Reserve, Alzheimer's Neuropathology, and Risk of Dementia: A Systematic Review and Meta-Analysis.
Ontology highlight
ABSTRACT:
SUBMITTER: Nelson ME
PROVIDER: S-EPMC7790730 | biostudies-literature | 2021 Jan
REPOSITORIES: biostudies-literature
Publications
Cognitive Reserve, Alzheimer's Neuropathology, and Risk of Dementia: A Systematic Review and Meta-Analysis.
Nelson Monica E ME Jester Dylan J DJ Petkus Andrew J AJ Andel Ross R
Neuropsychology review 20210108 2
Cognitive reserve (CR) may reduce the risk of dementia. We summarized the effect of CR on progression to mild cognitive impairment (MCI) or dementia in studies accounting for Alzheimer's disease (AD)-related structural pathology and biomarkers. Literature search was conducted in Web of Science, PubMed, Embase, and PsycINFO. Relevant articles were longitudinal, in English, and investigating MCI or dementia incidence. Meta-analysis was conducted on nine articles, four measuring CR as cognitive res ...[more]
Similar Datasets
Project description:Substantial evidence supports that glaucoma and dementia share pathological mechanisms and pathogenic risk factors. However, the association between glaucoma, cognitive decline and dementia has yet to be elucidated. This study was aimed to assess whether glaucoma increase the risk of dementia or cognitive impairment. PubMed, Cochrane Library, Web of Science, and EMBASE databases for cohort or case-control studies were searched from inception to March 10, 2024. The Newcastle-Ottawa Quality Assessment Scale (NOS) was used to the risk of bias. Heterogeneity was rigorously evaluated using the I2 test, while publication bias was assessed by visual inspection of the funnel plot and by Egger' s regression asymmetry test. Subgroup analyses were applied to determine the sources of heterogeneity. Twenty-seven studies covering 9,061,675 individuals were included. Pooled analyses indicated that glaucoma increased the risk of all-cause dementia, Alzheimer's disease, vascular dementia, and cognitive impairment. Subgroup analysis showed that the prevalence of dementia was 2.90 (95% CI: 1.45-5.77) in age ≥ 65 years and 2.07 (95% CI: 1.18-3.62) in age<65 years; the incidence rates in female glaucoma patients was 1.46 (95% CI: 1.06-2.00), respectively, which was no statistical significance in male patients. Among glaucoma types, POAG was more likely to develop dementia and cognitive impairment. There were also differences in regional distribution, with the highest prevalence in the Asia region, while glaucoma was not associated with dementia in Europe and North America regions. Glaucoma increased the risk of subsequent cognitive impairment and dementia. The type of glaucoma, gender, age, and region composition of the study population may significantly affect the relationship between glaucoma and dementia.
| S-EPMC11335947 | biostudies-literature
Project description:Aims/hypothesisAccumulating evidence suggests an association between coronary heart disease and risk for cognitive impairment or dementia, but no study has systematically reviewed this association. Therefore, we summarized the available evidence on the association between coronary heart disease and risk for cognitive impairment or dementia.MethodsMedline, Embase, PsycINFO, and CINAHL were searched for all publications until 8th January 2016. Articles were included if they fulfilled the inclusion criteria: (1) myocardial infarction, angina pectoris or coronary heart disease (combination of both) as predictor variable; (2) cognition, cognitive impairment or dementia as outcome; (3) population-based study; (4) prospective (≥1 year follow-up), cross-sectional or case-control study design; (5) ≥100 participants; and (6) aged ≥45 years. Reference lists of publications and secondary literature were hand-searched for possible missing articles. Two reviewers independently screened all abstracts and extracted information from potential relevant full-text articles using a standardized data collection form. Study quality was assessed with the Newcastle-Ottawa Scale. We pooled estimates from the most fully adjusted model using random-effects meta-analysis.ResultsWe identified 6,132 abstracts, of which 24 studies were included. A meta-analysis of 10 prospective cohort studies showed that coronary heart disease was associated with increased risk of cognitive impairment or dementia (OR = 1.45, 95%CI = 1.21-1.74, p<0.001). Between-study heterogeneity was low (I2 = 25.7%, 95%CI = 0-64, p = 0.207). Similar significant associations were found in separate meta-analyses of prospective cohort studies for the individual predictors (myocardial infarction, angina pectoris). In contrast, meta-analyses of cross-sectional and case-control studies were inconclusive.Conclusion/interpretationThis meta-analysis suggests that coronary heart disease is prospectively associated with increased odds of developing cognitive impairment or dementia. Given the projected worldwide increase in the number of people affected by coronary heart disease and dementia, insight into causal mechanisms or common pathways underlying the heart-brain connection is needed.
| S-EPMC5590905 | biostudies-literature
Project description:BackgroundAtrial fibrillation (AF) is a risk factor for cognitive impairment and dementia in patients with stroke history. However, the association between AF and cognitive impairment in broader populations is less clear.ObjectiveTo systematically review and quantitatively synthesize the existing evidence regarding the association of AF with cognitive impairment of any severity and etiology and dementia.MethodsMedline, Scopus, and Cochrane Central were searched in order to identify studies investigating the association between AF and cognitive impairment (or dementia) cross-sectionally and longitudinally. Studies encompassing and analyzing exclusively patients with stroke history were excluded. A random-effects model meta-analysis was conducted. Potential sources of between-study heterogeneity were investigated via subgroup and meta-regression analyses. Sensitivity analyses including only studies reporting data on stroke-free patients, vascular dementia, and Alzheimer's disease were performed.ResultsIn total, 43 studies were included. In the pooled analysis, AF was significantly associated with dementia (adjusted OR, 1.6; 95% CI, 1.3 to 2.1; I2, 31%) and the combined endpoint of cognitive impairment or dementia (pooled adjusted OR, 1.5; 95% CI, 1.4 to 1.8; I2, 34%). The results were significant, even when studies including only stroke-free patients were pooled together (unadjusted OR, 2.2; 95% CI, 1.4 to 3.5; I2, 96%), but the heterogeneity rates were high. AF was significantly associated with increased risk of both vascular (adjusted OR, 1.7; 95% CI, 1.2 to 2.3; I2, 43%) and Alzheimer's dementia (adjusted HR, 1.4; 95% CI, 1.2 to 1.6; I2, 42%).ConclusionAF increases the risk of cognitive impairment, all-cause dementia, vascular dementia, and Alzheimer's disease. Future studies should employ interventions that may delay or even prevent cognitive decline in AF patients.
| S-EPMC8481403 | biostudies-literature
Project description:With an increasing focus on biomarkers in dementia research, illustrating the role of neuropsychological assessment in detecting mild cognitive impairment (MCI) and Alzheimer's dementia (AD) is important. This systematic review and meta-analysis, conducted in accordance with PRISMA (Preferred Reporting Items for Systematic reviews and Meta-Analyses) standards, summarizes the sensitivity and specificity of memory measures in individuals with MCI and AD. Both meta-analytic and qualitative examination of AD versus healthy control (HC) studies (n = 47) revealed generally high sensitivity and specificity (? 80% for AD comparisons) for measures of immediate (sensitivity = 87%, specificity = 88%) and delayed memory (sensitivity = 89%, specificity = 89%), especially those involving word-list recall. Examination of MCI versus HC studies (n = 38) revealed generally lower diagnostic accuracy for both immediate (sensitivity = 72%, specificity = 81%) and delayed memory (sensitivity = 75%, specificity = 81%). Measures that differentiated AD from other conditions (n = 10 studies) yielded mixed results, with generally high sensitivity in the context of low or variable specificity. Results confirm that memory measures have high diagnostic accuracy for identification of AD, are promising but require further refinement for identification of MCI, and provide support for ongoing investigation of neuropsychological assessment as a cognitive biomarker of preclinical AD. Emphasizing diagnostic test accuracy statistics over null hypothesis testing in future studies will promote the ongoing use of neuropsychological tests as Alzheimer's disease research and clinical criteria increasingly rely upon cerebrospinal fluid (CSF) and neuroimaging biomarkers.
| S-EPMC5886311 | biostudies-literature
Project description:The notion that procedural learning and memory is spared in Alzheimer's disease (AD) has important implications for interventions aiming to build on intact cognitive functions. However, despite these clinical implications, there are mixed findings in the literature about whether or not procedural learning remains intact. This meta-analysis examines the standard mean difference of all published studies regarding procedural learning in AD dementia or amnestic Mild Cognitive Impairment (aMCI) compared to cognitively healthy older adults. Additionally, we conducted statistical equivalence analyses. Our systematic review showed that only a limited number of studies (k = 17) have compared procedural learning between individuals with aMCI or AD dementia and healthy controls. Our meta-analysis, which synthesized these studies, demonstrated that while procedural learning performance was not statistically equivalent between individuals with aMCI or AD dementia, and healthy older adults, the difference was clinically and statistically trivial. Although larger studies are needed, the present findings suggest that procedural learning does appear to remain spared in aMCI and AD dementia.
| S-EPMC7889687 | biostudies-literature
Project description:The literature on repetition priming in Alzheimer's disease (AD) is inconsistent, with some findings supporting spared priming while others do not. Several factors may explain these inconsistencies, including AD severity (e.g., dementia vs. Mild Cognitive Impairment; MCI) and priming paradigm-related characteristics. This systematic review and meta-analysis provides a quantitative summary of repetition priming in AD. We examined the between-group standard mean difference comparing repetition priming in AD dementia or amnestic MCI (aMCI; presumably due to AD) to controls. Thirty-two studies were selected, including 590 individuals with AD dementia, 267 individuals with amnestic MCI, and 703 controls. Our results indicated that both individuals with aMCI and AD dementia perform worse on repetition priming tasks than cognitively older adults. Paradigm-related moderators suggested that the effect size between studies comparing the combined aMCI or AD dementia group to cognitively healthy older adults was the highest for paradigms that required participants to produce, rather than identify, primes during the test phase. Our results further suggested that priming in AD is impaired for both conceptual and perceptual priming tasks. Lastly, while our results suggested that priming in AD is impaired for priming tasks that require deep processing, we were unable to draw firm conclusions about whether priming is less impaired in aMCI or AD dementia for paradigms that require shallow processing.
| S-EPMC9090892 | biostudies-literature
Project description:Importance:Fear of dementia is pervasive in older people with cognitive concerns. Much research is devoted to finding prognostic markers for dementia risk. Studies suggest apathy in older people may be prodromal to dementia and could be a relevant, easily measurable predictor of increased dementia risk. However, evidence is fragmented and methods vary greatly between studies. Objective:To systematically review and quantitatively synthesize the evidence for an association between apathy in dementia-free older individuals and incident dementia. Data Sources:Two reviewers conducted a systematic search of Medline, Embase, and PsychINFO databases. Study Selection:Inclusion criteria were (1) prospective cohort studies, (2) in general populations or memory clinic patients without dementia, (3) with clear definitions of apathy and dementia, and (4) reporting on the association between apathy and incident dementia. Data Extraction and Synthesis:PRISMA and MOOSE guidelines were followed. Data were extracted by 1 reviewer and checked by a second. Main Outcomes and Measures:Main outcomes were pooled crude risk ratios, maximally adjusted reported hazard ratios (HR), and odds ratios (OR) using DerSimonian-Laird random effects models. Results:The mean age of the study populations ranged from 69.2 to 81.9 years (median, 71.6 years) and the percentage of women ranged from 35% to 70% (median, 53%). After screening 2031 titles and abstracts, 16 studies comprising 7365 participants were included. Apathy status was available for 7299 participants. Studies included populations with subjective cognitive concerns (n = 2), mild cognitive impairment (n = 11), cognitive impairment no dementia (n = 1), or mixed cognitive and no cognitive impairment (n = 2). Apathy was present in 1470 of 7299 participants (20.1%). Follow-up ranged from 1.2 to 5.4 years. In studies using validated apathy definitions (n = 12), the combined risk ratio of dementia for patients with apathy was 1.81 (95% CI, 1.32-2.50; I2 = 76%; n = 12), the hazard ratio was 2.39 (95% CI, 1.27-4.51; I2 = 90%; n = 7), and the odds ratio was 17.14 (95% CI, 1.91-154.0; I2 = 60%; n = 2). Subgroup analyses, meta-regression, and individual study results suggested the association between apathy and dementia weakened with increasing follow-up time, age, and cognitive impairment. Meta-regression adjusting for apathy definition and follow-up time explained 95% of heterogeneity in mild cognitive impairment. Conclusions and Relevance:Apathy was associated with an approximately 2-fold increased risk of dementia in memory clinic patients. Moderate publication bias may have inflated some of these estimates. Apathy deserves more attention as a relevant, cheap, noninvasive, and easily measureable marker of increased risk of incident dementia with high clinical relevance, particularly because these vulnerable patients may forgo health care.
| S-EPMC6233800 | biostudies-other
Project description:INTRODUCTION:Stroke is an established risk factor for all-cause dementia, though meta-analyses are needed to quantify this risk. METHODS:We searched Medline, PsycINFO, and Embase for studies assessing prevalent or incident stroke versus a no-stroke comparison group and the risk of all-cause dementia. Random effects meta-analysis was used to pool adjusted estimates across studies, and meta-regression was used to investigate potential effect modifiers. RESULTS:We identified 36 studies of prevalent stroke (1.9 million participants) and 12 studies of incident stroke (1.3 million participants). For prevalent stroke, the pooled hazard ratio for all-cause dementia was 1.69 (95% confidence interval: 1.49-1.92; P < .00001; I2 = 87%). For incident stroke, the pooled risk ratio was 2.18 (95% confidence interval: 1.90-2.50; P < .00001; I2 = 88%). Study characteristics did not modify these associations, with the exception of sex which explained 50.2% of between-study heterogeneity for prevalent stroke. DISCUSSION:Stroke is a strong, independent, and potentially modifiable risk factor for all-cause dementia.
| S-EPMC6231970 | biostudies-literature
Project description:Serum uric acid (sUA) level may be associated with cognitive impairment/dementia. It is possible this relationship varies with dementia subtype, particularly between vascular dementias (VaD) and Alzheimer's (AD) or Parkinson's disease (PDD)-related dementia. We aimed to present a synthesis of all published data on sUA and relationship with dementia/cognition through systematic review and meta-analysis. We included studies that assessed the association between sUA and any measure of cognitive function or a clinical diagnosis of dementia. We pre-defined subgroup analyses for patients with AD, VaD, PDD, mild cognitive impairment (MCI), and mixed or undifferentiated. We assessed risk of bias/generalizability, and where data allowed, we performed meta-analysis to describe pooled measures of association across studies. From 4811 titles, 46 papers (n?=?16,688 participants) met our selection criteria. Compared to controls, sUA was lower in dementia (SDM -0.33 (95%CI)). There were differences in association by dementia type with apparent association for AD (SDM -0.33 (95%CI)) and PDD (SDM -0.67 (95%CI)) but not in cases of mixed dementia (SDM 0.19 (95%CI)) or VaD (SDM -0.05 (95%CI)). There was no correlation between scores on Mini-Mental State Examination and sUA level (summary r 0.08, p?=?0.27), except in patients with PDD (r 0.16, p?=?0.003). Our conclusions are limited by clinical heterogeneity and risk of bias in studies. Accepting this caveat, the relationship between sUA and dementia/cognitive impairment is not consistent across all dementia groups and in particular may differ in patients with VaD compared to other dementia subtypes.
| S-EPMC5005871 | biostudies-other
Project description:ObjectiveTo examine the comparative efficacy and safety of cognitive enhancers by patient characteristics for managing Alzheimer's dementia (AD).DesignSystematic review and individual patient data (IPD) network meta-analysis (NMA) based on our previously published systematic review and aggregate data NMA.Data sourcesMEDLINE, Embase, Cochrane Methodology Register, CINAHL, AgeLine and Cochrane Central Register of Controlled Trials up to March 2016.Participants80 randomised controlled trials (RCTs) including 21 138 adults with AD, and 12 RCTs with IPD including 6906 patients.InterventionsCognitive enhancers (donepezil, rivastigmine, galantamine and memantine) alone or in any combination against other cognitive enhancers or placebo.Data extraction and synthesisWe requested IPD from authors, sponsors and data sharing platforms. When IPD were not available, we used aggregate data. We appraised study quality with the Cochrane risk-of-bias. We conducted a two-stage random-effects IPD-NMA, and assessed their findings using CINeMA (Confidence in Network Meta-Analysis).Primary and secondary outcomesWe included trials assessing cognition with the Mini-Mental State Examination (MMSE), and adverse events.ResultsOur IPD-NMA compared nine treatments (including placebo). Donepezil (mean difference (MD)=1.41, 95% CI: 0.51 to 2.32) and donepezil +memantine (MD=2.57, 95% CI: 0.07 to 5.07) improved MMSE score (56 RCTs, 11 619 participants; CINeMA score: moderate) compared with placebo. According to P-score, oral rivastigmine (OR=1.26, 95% CI: 0.82 to 1.94, P-score=16%) and donepezil (OR=1.08, 95% CI: 0.87 to 1.35, P-score=30%) had the least favourable safety profile, but none of the estimated treatment effects were sufficiently precise when compared with placebo (45 RCTs, 15 649 patients; CINeMA score: moderate to high). For moderate-to-severe impairment, donepezil, memantine and their combination performed best, but for mild-to-moderate impairment donepezil and transdermal rivastigmine ranked best. Adjusting for MMSE baseline differences, oral rivastigmine and galantamine improved MMSE score, whereas when adjusting for comorbidities only oral rivastigmine was effective.ConclusionsThe choice among the different cognitive enhancers may depend on patient's characteristics. The MDs of all cognitive enhancer regimens except for single-agent oral rivastigmine, galantamine and memantine, against placebo were clinically important for cognition (MD larger than 1.40 MMSE points), but results were quite imprecise. However, two-thirds of the published RCTs were associated with high risk of bias for incomplete outcome data, and IPD were only available for 15% of the included RCTs.Prospero registration numberCRD42015023507.
| S-EPMC9045061 | biostudies-literature