Vitamin and mineral supplementation for preventing dementia or delaying cognitive decline in people with mild cognitive impairment.
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ABSTRACT:
SUBMITTER: McCleery J
PROVIDER: S-EPMC6378925 | biostudies-literature | 2018 Nov
REPOSITORIES: biostudies-literature
Publications
Vitamin and mineral supplementation for preventing dementia or delaying cognitive decline in people with mild cognitive impairment.
McCleery Jenny J Abraham Rajesh P RP Denton David A DA Rutjes Anne Ws AW Chong Lee-Yee LY Al-Assaf Aalya S AS Griffith Daniel J DJ Rafeeq Shireen S Yaman Hakan H Malik Muzaffar A MA Di Nisio Marcello M Martínez Gabriel G Vernooij Robin Wm RW Tabet Naji N
The Cochrane database of systematic reviews 20181101
<h4>Background</h4>Vitamins and minerals have many functions in the nervous system which are important for brain health. It has been suggested that various different vitamin and mineral supplements might be useful in maintaining cognitive function and delaying the onset of dementia. In this review, we sought to examine the evidence for this in people who already had mild cognitive impairment (MCI).<h4>Objectives</h4>To evaluate the effects of vitamin and mineral supplementation on cognitive func ...[more]
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Project description:ImportanceMild cognitive impairment (MCI) is a transition state between normal cognitive aging and dementia that increases the risk for progressive cognitive decline. Preventing cognitive decline is a public health priority.ObjectiveTo determine whether behavioral activation prevents cognitive and functional decline over 2 years in black individuals with MCI.Design, setting, and participantsSingle-center, single-masked, attention-controlled randomized clinical trial. Participants were enrolled from June 21, 2011, to October 3, 2014, and follow-up ended December 13, 2016. Community-based recruitment and treatment of black individuals older than 65 years with amnestic MCI. Volunteer sample of 1390 persons with memory complaints were screened. Overall, 536 individuals had baseline assessment, and 315 (58.8%) were ineligible, most often owing to normal cognition (205 of 315 [65%]) or dementia (59 of 315 [18.7%]); 221 fully eligible participants were randomized. Analyses were intention to treat.InterventionsParticipants were randomized to behavioral activation, which aimed to increase cognitive, physical, and social activity (111 [50.2%]), or supportive therapy, an attention control treatment (110 [49.8%]).Main outcomes and measuresThe prespecified primary outcome was a decline of 6 or more recalled words on the total recall score of the Hopkins Verbal Learning Test-Revised assessed at 6, 12, 18, and 24 months. The secondary outcome was functional decline.ResultsOf 221 randomized participants (mean [SD] age, 75.8 [7.0] years, 175 women [79%]), 77 behavioral activation participants (69.4%) and 87 supportive therapy participants (79.1%) had 2-year outcome assessments. After baseline, behavioral activation participants engaged in significantly more cognitive activities than supportive therapy participants. The 2-year incidence of memory decline was 1.2% (95% CI, 0.2-6.4) for behavioral activation vs 9.3% (95% CI, 5.30-16.4) for supportive therapy (relative risk, 0.12; 95% CI, 0.02-0.74; P = .02). Behavioral activation was associated with stable everyday function, whereas supportive therapy was associated with decline (difference in slopes, 2.71; 95% CI, 0.12-5.30; P = .04). Rates of serious adverse events for behavioral activation and supportive therapy, respectively, were: falls (14 [13%] vs 28 [25%]), emergency department visits (24 [22%] vs 24 [22%]), hospitalizations (36 [32%] vs 31 [28%]), and deaths (7 [5%] vs 3 [4%]).Conclusions and relevanceBehavioral activation prevented cognitive and functional decline, but this finding requires further investigation. Black individuals have almost twice the rate of dementia as white individuals; behavioral activation may reduce this health disparity.Trial registrationClinicalTrials.gov Identifier: NCT01299766.
| S-EPMC6583200 | biostudies-literature
Project description:ObjectiveWe examined whether sarcopenia is associated with the occurrence of late-life cognitive impairment.MethodsNondemented older adults (N = 1175) underwent annual testing with 17 cognitive tests summarized as a global cognitive score. A composite sarcopenia score was constructed based on muscle mass measured with bioelectrical impedance and muscle function based on grip strength. Cox proportional hazard models were employed to examine associations of sarcopenia with incident Alzheimer's dementia (AD) and incident mild cognitive impairment (MCI). Linear mixed-effect models determined the association of sarcopenia with cognitive decline. All models controlled for age, sex, education, race, and height squared.ResultsAverage follow-up was 5.6 years. More severe sarcopenia at baseline was associated with a higher risk of incident AD (hazard ratio [HR], 1.50 [95% confidence interval 1.20-1.86]; p < 0.001) and of MCI (1.21 [1.01-1.45]; 0.04) and a faster rate of cognitive decline (estimate = -0.013; p = 0.01). Analyses of the individual components of sarcopenia showed that muscle function was associated with incident AD, incident MCI, and cognitive decline with and without a term for lean muscle mass in the model. In contrast, lean muscle mass was not associated with incident cognitive impairment or cognitive decline when a term for muscle function was included in the model.ConclusionsPoor muscle function, but not reduced lean muscle mass, drives the association of sarcopenia with late-life cognitive impairment. Further work is needed to identify features of muscle structure, which may increase the specificity of sarcopenia for identifying older adults at risk for late-life cognitive impairment.
| S-EPMC8286176 | biostudies-literature
Project description:To determine the relationship between psychological stress with cognitive outcomes in a multi-centre longitudinal study of people with amnestic mild cognitive impairment (aMCI) we assessed three parameters of psychological stress (Recent Life Changes Questionnaire (RLCQ); the Perceived Stress Scale (PSS) and salivary cortisol) and their relationship with rates of cognitive decline over an 18 month follow up period and conversion to dementia over a 5.5 year period. In 133 aMCI and 68 cognitively intact participants the PSS score was higher in the aMCI compared with control group but neither the RLCQ scores nor salivary cortisol measures were different between groups. In the aMCI group the RLCQ and the PSS showed no significant association with cognitive function at baseline, cognitive decline or with conversion rates to dementia but high salivary cortisol levels were associated with RLCQ scores and poorer cognitive function at baseline and lower rates of cognitive decline. No relationship was found between salivary cortisol levels and conversion rate to dementia. We conclude that psychological stress as measured by the RLCQ or PSS was not associated with adverse cognitive outcomes in an aMCI population and hypothesise that this may reflect diminished cortisol production to psychological stress as the disease progresses.
| S-EPMC7046646 | biostudies-literature
Project description:BackgroundSubjective cognitive decline (SCD) and anxiety symptoms both predict neurocognitive disorders, but the two correlate strongly with each other. It is unclear whether they reflect two independent disease processes in the development of neurocognitive disorders and hence deserve separate attention. This cohort study examined whether SCD and anxiety symptoms demonstrate independent risks of mild cognitive disorder and dementia (MCI/dementia).MethodsThe study included 14,066 participants aged ≥ 50 years and diagnosed with normal cognition at baseline, recruited from Alzheimer's Disease Centers across the USA. The participants were evaluated for SCD and anxiety symptoms at baseline and followed up almost annually for incident MCI/dementia (median follow-up 4.5 years; interquartile range 2.2-7.7 years). SCD and anxiety symptoms were included in Cox regression to investigate their independent risks of MCI/dementia.ResultsSCD and anxiety symptoms demonstrated independent risks of MCI/dementia, with HR 1.9 (95% CI 1.7-2.1) and 1.3 (95% CI 1.2-1.5), respectively. Co-occurring SCD and anxiety symptoms demonstrated the highest risk (HR 2.4, 95% CI 1.9-2.9)-participants in this group had a 25% probability of developing MCI/dementia by 3.1 years (95% 2.4-3.7), compared to 8.2 years among those without SCD or anxiety (95% CI 7.9-8.6). The results remained robust even in the sensitivity analyses that took into account symptom severity and consistency of symptoms in the first 2 annual visits.ConclusionsThe findings suggest that clinicians should not dismiss one over the other when patients present with both SCD and anxiety and that both constructs may potentially be useful to identify high-risk populations for preventive interventions and trials. The findings also point to the need for further research to clarify on the neurobiological distinctions between SCD and anxiety symptoms, which may potentially enrich our understanding on the pathogenesis of neurocognitive disorders.
| S-EPMC7488541 | biostudies-literature
Project description:Backgroundthe long-term effect of the use of drugs with anticholinergic activity on cognitive function remains unclear.Methodswe conducted a systematic review and meta-analysis of the relationship between anticholinergic drugs and risk of dementia, mild cognitive impairment (MCI) and cognitive decline in the older population. We identified studies published between January 2002 and April 2018 with ≥12 weeks follow-up between strongly anticholinergic drug exposure and the study outcome measurement. We pooled adjusted odds ratios (OR) for studies reporting any, and at least short-term (90+ days) or long-term (365+ days) anticholinergic use for dementia and MCI outcomes, and standardised mean differences (SMD) in global cognition test scores for cognitive decline outcomes. Statistical heterogeneity was measured using the I2 statistic and risk of bias using ROBINS-I.Resultstwenty-six studies (including 621,548 participants) met our inclusion criteria. 'Any' anticholinergic use was associated with incident dementia (OR 1.20, 95% confidence interval [CI] 1.09-1.32, I2 = 86%). Short-term and long-term use were also associated with incident dementia (OR 1.23, 95% CI 1.17-1.29, I2 = 2%; and OR 1.50, 95% CI 1.22-1.85, I2 = 90%). 'Any' anticholinergic use was associated with cognitive decline (SMD 0.15; 95% CI 0.09-0.21, I2 = 3%) but showed no statistically significant difference for MCI (OR 1.24, 95% CI 0.97-1.59, I2 = 0%).Conclusionsanticholinergic drug use is associated with increased dementia incidence and cognitive decline in observational studies. However, a causal link cannot yet be inferred, as studies were observational with considerable risk of bias. Stronger evidence from high-quality studies is needed to guide the management of long-term use.
| S-EPMC7583519 | biostudies-literature
Project description:BackgroundIn cognitively normal individuals, subjective cognitive decline (SCD) has been reported to predict MCI and dementia (MCI/dementia). However, prior studies mostly captured SCD at single time-points without considering the longitudinal course of SCD. This study examined whether the trajectories of SCD provide any added information-beyond one-time assessments of SCD-on the risk of MCI/dementia.MethodsThis cohort study included 5661 participants from the Alzheimer's Disease Centers across the USA, who were ≥ 50 years and had normal cognition in the first-four annual visits (year 1 to year 4). The participants were evaluated for SCD in the first-four annual visits (year 1 to year 4), and followed-up almost annually (year 4 up to year 14) for incident MCI/dementia. SCD trajectories (as identified from latent-class-growth-curve-analysis) were included in Cox regression to estimate their risks of MCI/dementia, with analyses further stratified by age (< 75 years versus ≥ 75 years; based on median-split).ResultsCompared to those without SCD (in the first-four annual visits), Intermittent SCD (i.e., reported in 1-2 of the first-four annual visits) predicted a higher risk (HR 1.4) and Persistent SCD (i.e., reported in 3-4 of the first-four annual visits) predicted the highest risk (HR 2.2), with the results remaining significant even after adjusting for baseline SCD. Age-stratified analysis revealed that the risk associated with Intermittent SCD was only present in older individuals, while risk related to Persistent SCD was consistently present across the younger and older age groups. Age compounded the effects of the trajectories, whereby older individuals with Persistent SCD had > 75% probability of developing MCI/dementia by 10 years, in contrast to < 25% probability by 10 years in younger individuals with No SCD.ConclusionsThe findings demonstrate the utility of SCD trajectories-especially when used in combination with age strata-in identifying high-risk populations for preventive interventions and trials. They also suggest a potential modification in the current SCD criteria, with the inclusion of "persistent SCD over several years" as a feature of SCD plus.
| S-EPMC7592368 | biostudies-literature
Project description:BackgroundWith no current cure for mild cognitive impairment (MCI), delaying its progression could significantly reduce the disease burden and improve the quality of life for patients with MCI. Computerized cognitive training (CCT) has recently become a potential instrument for improvement of cognition. However, the evidence for its effectiveness remains limited.ObjectiveThis systematic review aims to (1) analyze the efficacy of CCT on cognitive impairment or cognitive decline in patients with MCI and (2) analyze the relationship between the characteristics of CCT interventions and cognition-related health outcomes.MethodsA systematic search was performed using MEDLINE, Cochrane, Embase, Web of Science, and Google Scholar. Full texts of randomized controlled trials of CCT interventions in adults with MCI and published in English language journals between 2010 and 2021 were included. Overall global cognitive function and domain-specific cognition were pooled using a random-effects model. Sensitivity analyses were performed to determine the reasons for heterogeneity and to test the robustness of the results. Subgroup analyses were performed to identify the relationship between the characteristics of CCT interventions and cognition-related effectiveness.ResultsA total of 18 studies with 1059 participants were included in this review. According to the meta-analysis, CCT intervention provided a significant but small increase in global cognitive function compared to that in the global cognitive function of the control groups (standardized mean difference=0.54, 95% CI 0.35-0.73; I2=38%). CCT intervention also resulted in a marginal improvement in domain-specific cognition compared to that in the control groups, with moderate heterogeneity. Subgroup analyses showed consistent improvement in global cognitive behavior in the CCT intervention groups.ConclusionsThis systematic review suggests that CCT interventions could improve global cognitive function in patients with MCI. Considering the relatively small sample size and the short treatment duration in all the included studies, more comprehensive trials are needed to quantify both the impact of CCT on cognitive decline, especially in the longer term, and to establish whether CCT should be recommended for use in clinical practice.Trial registrationPROSPERO International Prospective Register of Systematic Reviews CRD42021278884; https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=278884.
| S-EPMC9650579 | biostudies-literature
Project description:Cerebral blood flow (CBF) measured with arterial spin labelling (ASL) magnetic resonance imaging (MRI) reflects cerebral perfusion, related to metabolism, and arterial transit time (ATT), related to vascular health. Our aim was to investigate the spatial coefficient of variation (sCoV) of CBF maps as a surrogate for ATT, in volunteers meeting criteria for subjective cognitive decline (SCD), amnestic mild cognitive impairment (MCI) and probable Alzheimer's dementia (AD). Whole-brain pseudo continuous ASL MRI was performed at 3 T in 122 participants (controls = 20, SCD = 44, MCI = 45 and AD = 13) across three sites in New Zealand. From CBF maps that included all grey matter, sCoV progressively increased across each group with increased cognitive deficit. A similar overall trend was found when examining sCoV solely in the temporal lobe. We conclude that sCoV, a simple to compute imaging metric derived from ASL MRI, is sensitive to varying degrees of cognitive changes and supports the view that vascular health contributes to cognitive decline associated with Alzheimer's disease.
| S-EPMC8639710 | biostudies-literature
Project description:IntroductionThis study examines the link between daytime and nighttime excessive sleep and cognition, cognitive decline, and dementia in individuals with existing mild cognitive impairment (MCI).MethodsUsing data from the Swedish longitudinal study Good Aging in Skåne, participants aged 60-102 years were retrospectively classified as MCI based on cognitive testing. The average follow-up time was 6.59 years. Mixed linear models assessed cross-sectional and longitudinal associations between excessive sleep patterns (napping ≥2 h or nighttime sleep ≥9 h) and multiple cognitive domains. Cox regressions estimated dementia risk for excessive sleep.ResultsOf 4930 participants, 2052 (41%) had MCI. Excessive daytime napping and nighttime sleep were associated with worse cognition and cognitive decline. Excessive napping and nighttime sleep were also linked to higher dementia risk (hazard ratios: 1.75 and 1.86, respectively).DiscussionThese findings suggest that excessive sleep in MCI is associated with further cognitive decline and dementia.HighlightsExcessive daytime napping and nighttime sleep are linked cognitive decline for those with MCI.Excessive sleep during the day or at night heighten dementia risk.Worse test scores across multiple cognitive domains were observed for excessive daytime nappers.Excessive sleep in MCI may be a warning sign for further cognitive decline.
| S-EPMC11848587 | biostudies-literature