National Institutes of Health State-of-the-Science Conference Statement: Preventing Alzheimer Disease and Cognitive Decline

Daviglus, Martha L.; Bell, Carl C.; Berrettini, Wade H.; Bowen, Phyllis E.; Connolly, E. Sander; Cox, Nancy J.; Dunbar‐Jacob, Jacqueline; Granieri, Evelyn; Hunt, Gail; McGarry, Kathleen; Patel, Dinesh Kumar; Potosky, Arnold L.; Sanders‐Bush, Elaine; Silberberg, Donald H.; Trevisan, Maurizio

doi:10.7326/0003-4819-153-3-201008030-00260

Cited by 390 publications

(330 citation statements)

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“…Evidence for past smoking is less consistent (Daviglus et al 2010). In the LBC1936, those still smoking at the age of 70 performed more poorly than ex-and never-smokers on most of the concurrently performed cognitive tasks .…”

Section: Smokingmentioning

confidence: 88%

“…Statin users in both LBC cohorts had lower childhood IQs, but the cross-sectional associations with cognitive function at age 70 in the LBC1936 were not robust in the final models, which adjusted for total cholesterol levels . In other literature, there is no consistent epidemiological evidence that exists for an association of cognitive decline with statins, anti-hypertensive medications or anti-inflammatory drugs (Daviglus et al 2010). …”

Section: Medicationsmentioning

confidence: 98%

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Healthy cognitive ageing in the Lothian Birth Cohort studies: marginal gains not magic bullet

2017

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In the face of shifting demographics and an increase in human longevity, it is important to examine carefully what is known about cognitive ageing, and to identify and promote possibly malleable lifestyle and health-related factors that might mitigate age-associated cognitive decline. The Lothian Birth Cohorts of 1921 (LBC1921, n = 550) and 1936 (LBC1936, n = 1091) are longitudinal studies of cognitive and brain ageing based in Scotland. Childhood IQ data are available for these participants, who were recruited in later life and then followed up regularly. This overview summarises some of the main LBC findings to date, illustrating the possible genetic and environmental contributions to cognitive function (level and change) and brain imaging biomarkers in later life. Key associations include genetic variation, health and fitness, psychosocial and lifestyle factors, and aspects of the brain's structure. It addresses some key methodological issues such as confounding by early-life intelligence and social factors and emphasises areas requiring further investigation. Overall, the findings that have emerged from the LBC studies highlight that there are multiple correlates of cognitive ability level in later life, many of which have small effects, that there are as yet few reliable predictors of cognitive change, and that not all of the correlates have independent additive associations. The concept of marginal gains, whereby there might be a cumulative effect of small incremental improvements across a wide range of lifestyle and health-related factors, may offer a useful way to think about and promote a multivariate recipe for healthy cognitive and brain ageing.

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Section: Smokingmentioning

confidence: 88%

Section: Medicationsmentioning

confidence: 98%

Healthy cognitive ageing in the Lothian Birth Cohort studies: marginal gains not magic bullet

2017

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“…1 Observational studies have identified a wide range of potentially modifiable risk factors for AD and dementia, including cardiovascular risk factors (e.g., hypertension, diabetes, obesity), psychosocial factors (e.g., depression) and health behaviors (e.g., low level of physical or mental activity, smoking). 6 However, few randomized, controlled trials (RCTs) have examined the impact of risk factor modification on AD incidence and even fewer have investigated several factors at once.…”

mentioning

confidence: 99%

O3‐06‐06: The Projected impact of risk factor reduction on Alzheimer's disease prevalence

Barnes

Yaffe

2011

Alzheimer's & Dementia

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There are currently approximately 33.9 million individuals with Alzheimer's disease (AD) worldwide, and prevalence is expected to triple over the next 40 years. The goal of this review was to summarize the evidence regarding seven potentially modifiable AD risk factors: diabetes, midlife hypertension, mid-life obesity, smoking, depression, low educational attainment and physical inactivity. In addition, we projected the impact of risk factor reduction on AD prevalence by calculating population attributable risks (PARs, the percent of cases attributable to a given factor) and the number of AD cases that could potentially be prevented by 10% and 25% risk factor reductions worldwide and in the US. Together, these factors contributed to up to half of AD cases globally (17.2 million) and in the US (2.9 million). A 10%-25% reduction in all seven risk factors could potentially prevent as many as 1.1-3.0 million cases worldwide and 184,000-492,000 cases in the US.

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“…Because of this long asymptomatic phase, AD may be particularly amenable to prevention. Furthermore, epidemiological studies have identified numerous modifiable factors, such as diet, physical exercise, cognitive reserve and cardiovascular risk factors, which are associated with AD risk [24]. It has been estimated that a preventive intervention able to delay disease (dementia) onset by just 1 year could result in 9 million fewer cases by 2050 [25].…”

Section: Introductionmentioning

confidence: 99%

Prevention Studies in Alzheimer’s Disease: Progress Towards the Development of New Therapeutics

2015

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Alzheimer's disease (AD) is the most common form of dementia and is a major cause of disability and dependency amongst older people. AD drugs approved so far are symptomatic treatments and are not thought to affect the underlying disease process. Trials conducted with agents aiming to slow or stop disease progression in patients with AD have all failed, perhaps because they were tested too late in the disease process. Therefore, there has been a move towards prevention of AD. This paper presents an overview of trials testing pharmacological interventions for sporadic AD prevention. Those tested to date were initially developed for the treatment of AD or for the treatment of other conditions, rather than being specifically developed for AD prevention. Associated issues, such as evidence of 'proof-of-concept,' doses and safety, are discussed. A major shift has taken place in the methodology of AD prevention trials since the results of the first trials were published in the 1990s. New directions that are currently being considered in ongoing or future prevention trials are discussed, in terms of endpoints, target populations, and study design. The use of AD-specific drugs to prevent AD in high-risk individuals is currently limited by a lack of validated predictive and surrogate markers. Population approaches, such as lifestyle changes, are an alternative strategy that could be of public health interest, but may provide only limited benefits for individuals. The best chance of preventing AD may come from a combination of individual and population prevention approaches. Key PointsFollowing the failure of treatment trials in symptomatic Alzheimer's disease (AD), there has been a move towards prevention of AD.To date, no specific pharmacological intervention has been developed for sporadic AD prevention and trial results have been disappointing.A major shift has taken place in the methodology of AD prevention trials and new directions are being considered in terms of endpoints, target populations, and study design.

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National Institutes of Health State-of-the-Science Conference Statement: Preventing Alzheimer Disease and Cognitive Decline

Cited by 390 publications

References 0 publications

Healthy cognitive ageing in the Lothian Birth Cohort studies: marginal gains not magic bullet

Healthy cognitive ageing in the Lothian Birth Cohort studies: marginal gains not magic bullet

O3‐06‐06: The Projected impact of risk factor reduction on Alzheimer's disease prevalence

Prevention Studies in Alzheimer’s Disease: Progress Towards the Development of New Therapeutics

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