Background: Both air pollution and dementia are current and growing global issues. There are plausible links between exposure to specific air pollutants and dementia. Objective: To systematically review the evidence base with respect to the relationship between air pollution and later cognitive decline and dementia. Methods: Medline, Embase, and PsychINFO ® were searched from their inception to September 2018, for publications reporting on longitudinal studies of exposure to air pollution and incident dementia or cognitive decline in adults. Studies reporting on exposure to tobacco smoke including passive smoking or on occupational exposure to pollutants were excluded. Using standard Cochrane methodology, two readers identified relevant abstracts, read full text publications, and extracted data into structured tables from relevant papers, as defined by inclusion and exclusion criteria. Papers were also assessed for validity. CRD42018094299 Results: From 3,720 records, 13 papers were found to be relevant, with studies from the USA, Canada, Taiwan, Sweden, and the UK. Study follow-up ranged from one to 15 years. Pollutants examined included particulate matter ≤2.5 μ (PM 2.5 ), nitrogen dioxide (NO 2 ), nitrous oxides (NO x ), carbon monoxide (CO), and ozone. Studies varied in their methodology, population selection, assessment of exposure to pollution, and method of cognitive testing. Greater exposure to PM 2.5 , NO 2 /NO x , and CO were all associated with increased risk of dementia. The evidence for air pollutant exposure and cognitive decline was more equivocal. Conclusion: Evidence is emerging that greater exposure to airborne pollutants is associated with increased risk of dementia.
Background: The translation of evidence on dementia risk factors into clinical advice requires careful evaluation of the methodology and scope of data from which risk estimates are obtained. Objective: To evaluate the quantity, quality, and representativeness of evidence, we conducted a review of reviews of risk factors for Alzheimer’s disease (AD), Vascular dementia (VaD), and Any Dementia. Methods: PubMed, Cochrane library, and the Global Index Medicus were searched to identify meta-analyses of observational studies of risk factors for AD, VaD, and Any Dementia. PROSPERO CRD42017053920. Results: Meta-analysis data were available for 34 risk factors for AD, 26 risk factors for Any Dementia and eight for VaD. Quality of evidence varied greatly in terms of the number of contributing studies, whether data on midlife exposure was available, and consistency of measures. The most evidence was available for cardiovascular risk factors. The most geographically representative evidence (five of six global regions) was available for alcohol, physical activity, diabetes, high midlife BMI, antihypertensives, and motor function. Evidence from Australia/Oceana or Africa was limited. With the exception of diabetes, meta-analysis data were unavailable from Latin America/Caribbean. Midlife specific data were only available for cholesterol and arthritis. Conclusion: There is a lack of midlife specific data, limited data on VaD, and a lack of geographical representation for many risk factors for dementia. The quality, quantity, and representativeness of evidence needs to be considered before recommendations are made about the relevance of risk factors in mid- or late-life or for dementia subtypes.
Noncommunicable disease now contributes to the World Health Organization top 10 causes of death in low-, middle- and high-income countries. Particular examples include stroke, coronary heart disease, dementia and certain cancers. Research linking clinical and lifestyle risk factors to increased risk of noncommunicable disease is now well established with examples of confirmed risk factors, including smoking, physical inactivity, obesity and hypertension. However, despite a need to target our resources to achieve risk reduction, relatively little work has examined the overlap between the risk factors for these main noncommunicable diseases. Our high-level review draws together the evidence in this area. Using a systematic overview of reviews, we demonstrate the likely commonality of established risk factors having an impact on multiple noncommunicable disease outcomes. For example, systematic reviews of the evidence on physical inactivity and poor diet found each to be associated with increased risk of cancers, coronary heart disease, stroke, diabetes mellitus and dementia. We highlight the potential for targeted risk reduction to simultaneously impact multiple noncommunicable disease areas. These relationships now need to be further quantified to allow the most effective development of public health interventions in this area.
The first WHO guidelines for risk reduction of cognitive decline and dementia marked an important milestone in the field of dementia prevention. In this paper, we discuss the evidence reviewed as part of the guidelines development and present the main themes emerged from its synthesis, to inform future research and policies on dementia risk reduction. The role of intervention effect-size; the mismatch between observational and intervention-based evidence; the heterogeneity of evidence among intervention trials; the importance of intervention duration; the role of timing of exposure to a certain risk factor and interventions; the relationship between intervention intensity and response; the link between individual risk factors and specific dementia pathologies; and the need for tailored interventions emerged as the main themes. The interaction and clustering of individual risk factors, including genetics, was identified as the overarching theme. The evidence collected indicates that multidomain approaches targeting simultaneously multiple risk factors and tailored at both individual and population level, are likely to be most effective and feasible in dementia risk reduction. The current status of multidomain intervention trials aimed to cognitive impairment/dementia prevention was also briefly reviewed. Primary results were presented focusing on methodological differences and the potential of design harmonization for improving evidence quality. Since multidomain intervention trials address a condition with slow clinical manifestation—like dementia—in a relatively short time frame, the need for surrogate outcomes was also discussed, with a specific focus on the potential utility of dementia risk scores. Finally, we considered how multidomain intervention could be most effectively implemented in a public health context and the implications world-wide for other non-communicable diseases targeting common risk factors, taking into account the limited evidence in low-middle income countries. In conclusion, the evidence from the first WHO guidelines for risk reduction of cognitive decline and dementia indicated that “one size does not fit all,” and multidomain approaches adaptable to different populations and individuals are likely to be the most effective. Harmonization in trial design, the use of appropriate outcome measures, and sustainability in large at-risk populations in the context of other chronic disorders also emerged as key elements.
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