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Alzheimer's Disease Prevention: from Risk Factors to Early Intervention

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Alzheimer's Disease Prevention: from Risk Factors to Early Intervention Crous-Bou et al. Alzheimer's Research & Therapy (2017) 9:71 DOI 10.1186/s13195-017-0297-z REVIEW Open Access Alzheimer’s disease prevention: from risk factors to early intervention Marta Crous-Bou1, Carolina Minguillón1, Nina Gramunt1,2 and José Luis Molinuevo1,2* Abstract Due to the progressive aging of the population, Alzheimer’s disease (AD) is becoming a healthcare burden of epidemic proportions for which there is currently no cure. Disappointing results from clinical trials performed in mild–moderate AD dementia combined with clear epidemiological evidence on AD risk factors are contributing to the development of primary prevention initiatives. In addition, the characterization of the long asymptomatic stage of AD is allowing the development of intervention studies and secondary prevention programmes on asymptomatic at-risk individuals, before substantial irreversible neuronal dysfunction and loss have occurred, an approach that emerges as highly relevant. In this manuscript, we review current strategies for AD prevention, from primary prevention strategies based on identifying risk factors and risk reduction, to secondary prevention initiatives based on the early detection of the pathophysiological hallmarks and intervention at the preclinical stage of the disease. Firstly, we summarize the evidence on several AD risk factors, which are the rationale for the establishment of primary prevention programmes as well as revising current primary prevention strategies. Secondly, we review the development of public–private partnerships for disease prevention that aim to characterize the AD continuum as well as serving as platforms for secondary prevention trials. Finally, we summarize currently ongoing clinical trials recruiting participants with preclinical AD or a higher risk for the onset of AD-related cognitive impairment. The growing body of research on the risk factors for AD and its preclinical stage is favouring the development of AD prevention programmes that, by delaying the onset of Alzheimer’s dementia for only a few years, would have a huge impact on public health. Keywords: Alzheimer’s disease, Amyloid beta, Prevention, Risk factors, Susceptibility, Early intervention, Clinical trials Background peptide, which is deposited extracellularly in diffuse and The prevalence of dementia worldwide is estimated to neuritic plaques, and hyperphosphorylated tau (p-tau), a be over 45 million people [1] and is predicted to triple microtubule assembly protein that accumulates intracel- by 2050 as a consequence of increased life expectancy, lularly as neurofibrillary tangles [3]. Initial diagnostic establishing dementia as one of the biggest global public efforts focused on patients at the dementia stage of the health challenges. Alzheimer’s disease (AD) is the most disease and, only recently, the importance of a long common form of dementia and accounts for 60–80% of pre-dementia stage, preceding the clinical onset of the cases [1]. AD is a progressive neurodegenerative disease, disease symptoms, has been recognized. As the disease pro- irreversible and disabling, causing a large socioeconomic gresses, the subject’s cognition changes from an initial burden [2]. phase where it is fully preserved to a final stage character- The criteria for AD diagnosis have been revised exten- ized by dementia [4]. The initial silent and asymptomatic sively, and experts agree that the hallmark pathological stage, referred to as preclinical AD, is characterized by a criteria include increased levels of amyloid-beta (Aβ) sequence of pathophysiological hallmarks that start to appear about 20 years before the onset of symptoms [5]. Unfortunately, none of the drugs tested to date in clinical * Correspondence: [email protected] 1Barcelonaβeta Brain Research Center—Pasqual Maragall Foundation, C/ trials in order to change the course of the disease have Wellington, 30, 08005 Barcelona, Spain shown effective results in AD dementia [6]. Therefore, 2CIBER Fragilidad y Envejecimiento Saludable (CIBERFES), Madrid, Spain © The Author(s). 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. Crous-Bou et al. Alzheimer's Research & Therapy (2017) 9:71 Page 2 of 9 many interventional studies are currently moving their the insulin-degrading enzyme [12, 13]. In contrast, other focus to cognitively healthy individuals at risk of devel- studies suggest that diabetes might increase the risk of oping AD (before substantial irreversible neuronal cerebrovascular but not AD pathology, and that at least network dysfunction and loss, associated with overt part of the relationship between diabetes and cognitive clinical symptoms, have occurred) as the best strategy impairment may be modified by neuropathology [14]. Even to reduce AD incidence and prevalence. though the association between high blood pressure and In this review, we will summarize current strategies AD risk is complex and age related, evidence suggest that for AD prevention, from primary prevention strategies mid-life, and not late-life, hypertension is associated with a based on identifying risk factors and risk reduction, to 50% increased risk of AD and dementia in later life. secondary prevention based on early detection of the Elevated blood pressure might increase the risk of AD by pathophysiological hallmarks and intervention at the decreasing the vascular integrity of the blood–brain barrier, preclinical stage. Furthermore, we will discuss a number resulting in protein extravasation into brain tissue, which of selected environmental risk factors for AD, and we can consequently lead to cell damage, apoptosis and an will describe currently ongoing interventional initiatives increase in Aβ accumulation [15]. However, the direction focused on primary prevention of AD, as well as some of a possible causal relationship between hypertension and of the public–private partnerships (PPPs) for disease subsequent cognitive decline is under debate since there is prevention that are setting up a framework to identify also increasing evidence that hypertension may be a and select individuals for clinical trials focused on protective response to cerebral hypoperfusion, which is preclinical stages. demonstrable 10 years prior to AD onset [16, 17]. Observa- tional studies have shown a U-shaped relationship between Primary prevention weight and cognitive performance: both low and high body Modifiable risk factors for AD weight have been associated with increased risk of AD and Since AD develops over a long preclinical stage that can cognitive impairment. This association might also have an last for several decades, the extent to which risk factors age-dependent component. Data also exist for reverse assessed in late life or shortly before the onset of clinical causation in the years preceding disease onset; that is, loss symptoms are a result of pathological changes rather of body weight might be caused by cognitive impairment than having a causal relationship has been discussed during the pre-dementia phase of AD. Consequently, the intensively. Longitudinal studies that include participants relationship between body weight and AD seems to be a in early mid-life have been crucial to assess the relation- consequence of mid-life obesity, which could increase the ship between early or mid-life exposures and cognitive risk of AD by 60%. Even though the underlying mecha- decline or AD later in life [7]. nisms of this association remain unknown, studies suggest Observational studies have identified several modifiable that insulin resistance and co-incidence with diabetes mel- risk factors for AD. Based on a comprehensive systematic litus may play a role [18]. review of the evidence related to risk factors for cognitive With regards to lifestyle-related factors, the association decline and AD, the US National Institutes of Health between smoking and AD risk has been controversial and highlighted diabetes mellitus, smoking, depression, mental remains unclear. Most observational studies show an inactivity, physical inactivity and poor diet as being associ- association between current smoking and increased risk of ated with increased risk of cognitive decline, AD, or both dementia, AD and cognitive decline. Even though relative [8]. Later on, this list was further extended to include risks for AD are relatively small (RR = 1.20–1.60), nearly hypertension, obesity and low educational attainment [9]. 14% of AD cases are estimated to be potentially attribut- Recently, an association was demonstrated between the able to smoking due to its high prevalence [9]. Smoking presence of vascular risk factors in mid-life and amyloid may increase AD risk through several mechanisms, mostly deposition later in life [10], even though some of these related to oxidative stress and inflammatory responses factors are still under debate. It has been estimated that [19]. Epidemiological studies have shown that physical up to a third of AD cases are potentially attributed to activity has a beneficial effect on
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