scholarly journals Physical inactivity, cardiometabolic disease, and risk of dementia: an individual-participant meta-analysis

BMJ ◽  
2019 ◽  
pp. l1495 ◽  
Author(s):  
Mika Kivimäki ◽  
Archana Singh-Manoux ◽  
Jaana Pentti ◽  
Séverine Sabia ◽  
Solja T Nyberg ◽  
...  
Keyword(s):  
Physical Activity ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Physical Inactivity ◽  
Meta Analysis ◽  
Hazard Ratio ◽  
Cardiometabolic Disease ◽  
Reverse Causation ◽  
Individual Participant ◽  
Incident Cases

AbstractObjectiveTo examine whether physical inactivity is a risk factor for dementia, with attention to the role of cardiometabolic disease in this association and reverse causation bias that arises from changes in physical activity in the preclinical (prodromal) phase of dementia.DesignMeta-analysis of 19 prospective observational cohort studies.Data sourcesThe Individual-Participant-Data Meta-analysis in Working Populations Consortium, the Inter-University Consortium for Political and Social Research, and the UK Data Service, including a total of 19 of a potential 9741 studies.Review methodThe search strategy was designed to retrieve individual-participant data from prospective cohort studies. Exposure was physical inactivity; primary outcomes were incident all-cause dementia and Alzheimer’s disease; and the secondary outcome was incident cardiometabolic disease (that is, diabetes, coronary heart disease, and stroke). Summary estimates were obtained using random effects meta-analysis.ResultsStudy population included 404 840 people (mean age 45.5 years, 57.7% women) who were initially free of dementia, had a measurement of physical inactivity at study entry, and were linked to electronic health records. In 6.0 million person-years at risk, we recorded 2044 incident cases of all-cause dementia. In studies with data on dementia subtype, the number of incident cases of Alzheimer’s disease was 1602 in 5.2 million person-years. When measured <10 years before dementia diagnosis (that is, the preclinical stage of dementia), physical inactivity was associated with increased incidence of all-cause dementia (hazard ratio 1.40, 95% confidence interval 1.23 to 1.71) and Alzheimer’s disease (1.36, 1.12 to 1.65). When reverse causation was minimised by assessing physical activity ≥10 years before dementia onset, no difference in dementia risk between physically active and inactive participants was observed (hazard ratios 1.01 (0.89 to 1.14) and 0.96 (0.85 to 1.08) for the two outcomes). Physical inactivity was consistently associated with increased risk of incident diabetes (hazard ratio 1.42, 1.25 to 1.61), coronary heart disease (1.24, 1.13 to 1.36), and stroke (1.16, 1.05 to 1.27). Among people in whom cardiometabolic disease preceded dementia, physical inactivity was non-significantly associated with dementia (hazard ratio for physical activity assessed >10 before dementia onset 1.30, 0.79 to 2.14).ConclusionsIn analyses that addressed bias due to reverse causation, physical inactivity was not associated with all-cause dementia or Alzheimer’s disease, although an indication of excess dementia risk was observed in a subgroup of physically inactive individuals who developed cardiometabolic disease.

scholarly journals Impact of Physical Activity on Cognitive Decline, Dementia, and Its Subtypes: Meta-Analysis of Prospective Studies

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Chris B. Guure ◽  
Noor A. Ibrahim ◽  
Mohd B. Adam ◽  
Salmiah Md Said
Keyword(s):  
Physical Activity ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Protective Effect ◽  
Cognitive Decline ◽  
Vascular Dementia ◽  
Prospective Studies ◽  
Odds Ratio ◽  
Meta Analysis ◽  
Nonparametric Models

The association of physical activity with dementia and its subtypes has remained controversial in the literature and has continued to be a subject of debate among researchers. A systematic review and meta-analysis of longitudinal studies on the relationship between physical activity and the risk of cognitive decline, all-cause dementia, Alzheimer’s disease, and vascular dementia among nondemented subjects are considered. A comprehensive literature search in all available databases was conducted up until April 2016. Well-defined inclusion and exclusion criteria were developed with focus on prospective studies ≥ 12 months. The overall sample from all studies is 117410 with the highest follow-up of 28 years. The analyses are performed with both Bayesian parametric and nonparametric models. Our analysis reveals a protective effect for high physical activity on all-cause dementia, odds ratio of 0.79, 95% CI (0.69, 0.88), a higher and better protective effect for Alzheimer’s disease, odds ratio of 0.62, 95% CI (0.49, 0.75), cognitive decline odds ratio of 0.67, 95% CI (0.55, 0.78), and a nonprotective effect for vascular dementia of 0.92, 95% CI (0.62, 1.30). Our findings suggest that physical activity is more protective against Alzheimer’s disease than it is for all-cause dementia, vascular dementia, and cognitive decline.

Physical activity in Alzheimer's disease: research in its infancy or why we need more randomized controlled trials

2013 ◽  
Vol 26 (1) ◽  
pp. 7-7 ◽  
Author(s):  
Nicola T. Lautenschlager
Keyword(s):  
Physical Activity ◽  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Randomized Controlled Trials ◽  
Physical Inactivity ◽  
Significant Risk ◽  
Controlled Trials ◽  
Randomized Controlled

With the global aging of our societies and predicted increase of cognitive impairment and dementia, it is no surprise that there is an increasing interest in the research community, but also among clinicians and the general population to learn more about how to focus on modifiable protective factors and how to avoid modifiable risk factors. A recent review of systematic reviews and meta-analyses on significant risk factors for Alzheimer's disease (AD) highlighted the importance of diabetes, hypertension, obesity, smoking, depression, cognitive inactivity, and physical inactivity (Barnes and Yaffe, 2011). For physical inactivity, for example, the authors reported that up to one million cases of AD could be prevented globally if a physical inactivity could be reduced by 25%. However, we should not forget about the various stages of prevention, and especially in the field of psychogeriatrics should also ask what preventative measures might be effective for older adults who have already experienced cognitive impairment. So we could focus on a secondary prevention approach for individuals with mild cognitive impairment (MCI) or on a tertiary preventative approach for patients with dementia. The number of randomized controlled trials (RCT) investigating the effectiveness of physical activity on cognition is limited for healthy participants and those with MCI, but is even more sparse for those with dementia. Even with the limited number of studies it often is difficult to compare RCTs due to the huge variation in inclusion and exclusion criteria, methodology, instruments used and outcomes, intervention and duration of interventions, and observations.

539 Interactions Between Cardiorespiratory Fitness and Sleep Apnea in Predicting Risk of Alzheimer’s Disease

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A212-A213
Author(s):  
Erika Hagen ◽  
Jodi Barnet ◽  
Laurel Ravelo ◽  
David Plante ◽  
Ira Driscoll ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Sleep Apnea ◽  
Cardiorespiratory Fitness ◽  
Hazard Ratio ◽  
Apnea Hypopnea Index ◽  
Fitness Level ◽  
Obstructive Sleep ◽  
Incident Cases ◽  
Fitness Levels

Abstract Introduction Several studies suggest a link between obstructive sleep apnea (OSA) and Alzheimer’s disease (AD). Additionally, frequent exercise is associated with more favorable AD biomarker profiles, and emerging evidence suggests greater cardiorespiratory fitness levels may be associated with lower risk of cognitive decline. We investigated whether cardiorespiratory fitness modifies the association of OSA and risk of AD. Methods A subset of the Wisconsin Sleep Cohort study participants with study visits starting in 2000 (n=1182, 46% female, mean [range] age at baseline=57 [37–82] years) completed multiple [range, 1–5] in-laboratory protocols that included overnight polysomnography, anthropometric measurements, and questionnaires. Additionally, the National Death Index was searched to determine cause of death among decedents. Cox proportional hazards models estimated relative hazards of AD (self-reported physician diagnosis or indication of AD on the death certificate) associated with the joint effects and the interaction of OSA – characterized by the base 10 logarithm of the apnea-hypopnea index (log10(AHI+1)) – and cardiorespiratory fitness (an index based on age, sex, BMI, self-reported physical activity, and resting heart rate). Additionally, the sample was stratified by fitness level at the 3rd quartile (&gt;75th percentile compared to &lt;75th percentile) and the hazard ratio for log10(AHI+1) was estimated for the lower and higher fitness-level groups. Results were adjusted for age, sex, BMI, and education. Results There were 10 incident cases of AD. The mean [range] fitness level was 7.1 [0–12.3]. 28% of the sample had moderate OSA (AHI 5–15); and 26% had severe OSA (AHI&gt;15). Higher log10(AHI+1) was associated with greater hazards (p=0.03) of AD and there was a significant interaction between log10(AHI) and fitness (p=0.04), such that at greater fitness levels, the effect of log10(AHI) on AD was mitigated. In stratified analysis, among the less fit, the hazard ratio for an increment of 1 in log10(AHI) was 12.8 (95% CI, 1.1–153.8, p=0.04); among those who were more fit, the hazard ratio was not significant. Conclusion More severe OSA is associated with higher risk of AD, and this risk is greater among those with lower levels of cardiorespiratory fitness. Support (if any) This work was supported by US NIH grants R01AG058680, R01AG062167, R01HL62252, 1R01AG036838 and 1UL1RR025011.

Effect of antihypertensive drugs on cognition and behavioral symptoms of patients with Alzheimer’s disease: A meta-analysis

2020 ◽  
Vol 21 ◽  
Author(s):  
Roja Rahimi ◽  
Shekoufeh Nikfar ◽  
Masoud Sadeghi ◽  
Mohammad Abdollahi ◽  
Reza Heidary Moghaddam ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Randomized Clinical Trials ◽  
Antihypertensive Drugs ◽  
Meta Analysis ◽  
Behavioral Symptoms ◽  
Cochrane Library ◽  
Mean Differences ◽  
Global Impression Of Change ◽  
State Examination

Background: It has been found that there is a link between hypertension and elevated risk of Alzheimer’s disease (AD). Herein, a meta-analysis based on randomized clinical trials (RCTs) was used to assess the effect of antihypertensive drugs on cognition and behavioral symptoms of AD patients. Method: The three databases – PubMed/Medline, Scopus, and Cochrane Library- were searched up to March 2020. The quality of the studies included in the meta-analysis was evaluated by the Jadad score. Clinical Global Impression of Change (CGIC) included in two studies, Mini-Mental State Examination (MMSE) included in three studies, and Neuropsychiatric Inventory (NPI) in three studies were the main outcomes in this systematic review. Results: Out of 1506 studies retrieved in the databases, 5 RCTs included and analyzed in the meta-analysis. The pooled mean differences of CGIC, MMSE, and NPI in patients with AD receiving antihypertensive drugs compared to placebo was -1.76 with (95% CI = -2.66 to -0.86; P=0.0001), 0.74 (95% CI = 0.20 to 1.28; P= 0.007), and -9.49 (95% CI = -19.76 to 0.79; P = 0.07), respectively. Conclusion: The findings of the present meta-analysis show that antihypertensive drugs may improve cognition and behavioral symptoms of patients with AD. However, more well-designed RCTs with similar drugs are needed to achieve more conclusive results.

Characteristics of Insulin-degrading Enzyme in Alzheimer's Disease: A Meta-Analysis

2018 ◽  
Vol 15 (7) ◽  
pp. 610-617 ◽  
Author(s):  
Huifeng Zhang ◽  
Dan Liu ◽  
Huanhuan Huang ◽  
Yujia Zhao ◽  
Hui Zhou
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Enzyme Activity ◽  
Protein Level ◽  
Senile Plaque ◽  
Meta Analysis ◽  
Cochrane Library ◽  
Insulin Degrading Enzyme ◽  
Degrading Enzyme ◽  
Significant Difference

Background: β-amyloid (Aβ) accumulates abnormally to senile plaque which is the initiator of Alzheimer's disease (AD). As one of the Aβ-degrading enzymes, Insulin-degrading enzyme (IDE) remains controversial for its protein level and activity in Alzheimer's brain. Methods: The electronic databases PubMed, EMBASE, The Cochrane Library, OVID and Sinomed were systemically searched up to Sep. 20th, 2017. And the published case-control or cohort studies were retrieved to perform the meta-analysis. Results: Seven studies for IDE protein level (AD cases = 293; controls = 126), three for mRNA level (AD cases = 138; controls = 81), and three for enzyme activity (AD cases = 123; controls = 75) were pooling together. The IDE protein level was significantly lower in AD cases than in controls (SMD = - 0.47, 95% CI [-0.69, -0.24], p < 0.001), but IDE mRNA and enzyme activity had no significant difference (SMD = 0.02, 95% CI [-0.40, 0.43] and SMD = 0.06, 95% CI [-0.41, 0.53] respectively). Subgroup analyses found that IDE protein level was decreased in both cortex and hippocampus of AD cases (SMD = -0.43, 95% CI [-0.71, -0.16], p = 0.002 and SMD = -0.53, 95% CI [-0.91, -0.15], p = 0.006 respectively). However, IDE mRNA was higher in cortex of AD cases (SMD = 0.71, 95% CI [0.14, 1.29], p = 0.01), not in hippocampus (SMD = -0.26, 95% CI [-0.58, 0.06]). Conclusions: Our results indicate that AD patients may have lower IDE protease level. Further relevant studies are still needed to verify whether IDE is one of the factors affecting Aβ abnormal accumulation and throw new insights for AD detection or therapy.

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