DOCSLIB.ORG

Do Statins Have Adverse Cognitive Effects?

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Do Statins Have Adverse Cognitive Effects? CARDIOVASCULAR RISK AND DIABETES Diabetes Care Volume 39, Supplement 2, August 2016 S253 Remembering Statins: Do Statins Rafael Bitzur Have Adverse Cognitive Effects? Diabetes Care 2016;39(Suppl. 2):S253–S259 | DOI: 10.2337/dcS15-3022 The issue of statin-associated cognitive impairment has been a hot topic among both patients and health care providers, especially since the U.S. Food and Drug Administration (FDA) issued a statement regarding rare postmarketing reports of ill-defined cognitive impairment associated with statin use. This statement was based on case reports, and no objective measures of cognitive function were used. Nevertheless, many patients at high risk of cardiovascular disease have expressed concerns about possible cognitive decline and may have opted to forgo statin therapy. In this overview, the evidence leading to the statement by the FDA is reviewed. Potential mechanisms of the effect of LDL cholesterol reduction and statin therapy on cognition are discussed. Evidence from observational and prospective randomized trials is summarized, leading to the conclusion that as for now, there is no good evidence that statins cause cognitive impairment to a significant degree. Reported cases seem to be rare, and a causal relationship has not been established. Hydroxymethylglutaryl CoA reductase inhibitors (statins) are a major contributor to cardiovascular disease prevention in patients with diabetes. In a prospective meta- analysis of more than 18,000 people with diabetes (mean age 63 years, with 43% over the age of 65 years) in 14 randomized trials, statins were shown to reduce both cardiovascular morbidity and mortality (1). As a result, both European (2) and U.S. (3) guidelines recommend statin treatment for almost all patients with diabetes. It is estimated that for people over the age of 55 years, statins would be recommended for 96.4% of men and 65.8% of women by the American College of Cardiology/ American Heart Association guidelines and 66.1% of men and 39.1% of women by European Society of Cardiology guidelines (4). With so many people eligible for treatment, even rare adverse effects become important. In 2012, the U.S. Food and Drug Administration (FDA) issued a statement regarding rare postmarketing reports of ill-defined cognitive impairment associated The Bert W. Strassburger Lipid Center, Sheba with statin use that was reversible upon statin discontinuation (5). This has led many Medical Center, Tel Hashomer, Israel people, patients and health care providers alike, to erroneously associate statins Corresponding author: Rafael Bitzur, rafael.bitzur@ with dementia and may have contributed to low adherence rates. sheba.health.gov.il. This review will deal with the relationship between cholesterol and cognitive This publication is based on the presentations function and the possible effects of statins on short- and long-term cognitive at the 5th World Congress on Controversies to function. Consensus in Diabetes, Obesity and Hyperten- sion (CODHy). The Congress and the publication Cholesterol and Cognitive Function of this supplement were made possible in The human brain contains ;25% of the total cholesterol of the body. Cholesterol is a part by unrestricted educational grants from AstraZeneca. major lipid constituent of the myelin sheath and the membrane lipid rafts in neurons © 2016 by the American Diabetes Association. and astrocytes, participating in regulation of ion channel permeability, signal trans- Readers may use this article as long as the work is duction, and other cellular functions (6). Lipoproteins have very limited permeabil- properly cited, the use is educational and not for ity of the intact blood-brain barrier. Therefore, essentially all brain cholesterol is profit, and the work is not altered. S254 Statins and Cognition Diabetes Care Volume 39, Supplement 2, August 2016 locally synthesized in astrocytes, which for 21 years), cognitive impairment or Alternatively, statins may exert pleiotro- are the main source of cholesterol for dementia (diagnosed by the DSM-IV cri- pic effects unrelated to their effect on neurons. teria) developed in 9% of the subjects. cholesterol. Several preclinical studies One of the pathological hallmarks of High mid-life total cholesterol levels using cell cultures and animal models Alzheimer disease (AD) is the develop- were a risk factor for more severe cogni- of AD have demonstrated that statins ment of extracellular senile plaques, tive impairment later in life (9). On the increase a-secretase activity and de- composed mainly of a small peptide other hand, in a study looking at 382 crease Ab production (8). In humans, known as amyloid-b (Ab), thought to subjects aged 70 years and free from de- lovastatin decreased serum Ab levels be a major causative agent in the de- mentia at baseline who were followed in a dose-dependent manner when velopment of AD. Cholesterol is be- for 18 years, 24% developed dementia given to subjects without dementia (14). lieved to be an important factor in (diagnosed by the DSM-III-R criteria). In a study looking at brain autopsies the regulation of Ab production, with High cholesterol levels in late life were from 110 subjects, ages 65–79 years, high cholesterol levels being linked to associated with decreased dementia risk neuropathologic findings were com- increased Ab generation and deposi- (10). One way of avoiding the risk of re- pared between statin users and nonus- tion. Lower cholesterol levels shift verse causation is to look at genetic stud- ers. The risk for typical AD pathology amyloid precursor protein processing ies. In one small study, patients with (Braak stage IV and Consortium to to nonraft regions of the membrane familial hypercholesterolemia showed a Establish a Registry for Alzheimer’s Dis- where the benign a-secretase cleavage high incidence of mild cognitive impair- ease [CERAD] rating moderate) was re- pathway is favored (6). ment compared with subjects without duced in statin users (15). Unlike lipoproteins, oxysterols, like the disease. Importantly, this did not 27-hydroxycholesterol, efficiently pass seem to be due to vascular dementia, Case Reports Concerning Cognitive Effect the blood-brain barrier. Hypercholes- since patients with a history of stroke of Statins terolemia is associated with increased or transient ischemic attack were ex- In 2003, Wagstaff et al. (16), using the brain levels of 27-hydroxycholesterol, cluded and the finding was unrelated MedWatch drug surveillance system of which may affect Ab production. Alter- to findings on brain MRI (11). Another the FDA, found 60 reports of patients natively, high LDL cholesterol (LDL-C) study, using a Mendelian randomization who had memory loss associated with levels may damage the blood-brain approach, looked at the association be- statins. Since then, several other case re- barrier by inflammatory mechanisms, tween genotype risk scores for four ports and case series have suggested a thus enabling leakage of serum choles- blood lipid phenotypes (including total potential negative association between terol and other amyloidogenic factors to and LDL-C) and late-onset AD. No such statins and cognitive function. In most the brain. Thus, higher levels of LDL-C association was found, leading the au- reports, the main symptom related to were associated with greater brain thors to conclude that genetic predispo- statins was short-term memory loss amyloid measured by positron emis- sition to increased blood cholesterol is that occurred a few months after the sion tomography using the tracer carbon not associated with elevated AD risk start of statin therapy or after a dosage 11C-labeled Pittsburgh compound B, (12). increase. Cognitive impairment was which specifically binds to Ab plaques, usually reversible upon discontinuation independently of apolipoprotein E geno- Statins and Cognitive Function of statin therapy. The cases did not ap- type (7). Cholesterol is vitally important for brain pear to be associated with fixed or pro- Paradoxically, in some epidemiologi- function. While the brain represents ;2– gressive dementia, such as AD. No cal studies, a low serum cholesterol 3% of total body weight, 25% of the cho- association was found between cogni- level was associated with an increased lesterol in the body is found in the brain, tive impairment and a specificstatin risk of developing AD. However, this where it plays important roles in mem- (lipophilic or hydrophilic), age, statin finding may be due to reverse causa- brane function. Because cholesterol dose, or concomitant medications. tion, since some studies included el- synthesis is essential for the normal It should be noted that causality can- derly participants who might have functioning of the brain, it is theoreti- notbedeterminedbythistypeofstudy. already had AD at enrollment, making cally possible that excessive inhibition First, the patient population receiving it difficult to distinguish between effects of cholesterol synthetic pathways may statinsisalreadyatriskformemory of cholesterol on the development of AD result in neurocognitive adverse effects. loss because of cardiac risk factors and and alteration of cholesterol level Statins may reduce cholesterol synthe- advancing age, which could lead to de- because of the catabolic state and path- sis in the brain and interfere with myelin tection bias. Second, no objective mem- ophysiological changes that accompany formation and function. In a mouse ory tests were performed. In fact, a AD. Indeed, studies finding a negative model, simvastatin impaired
Load more

Recommended publications
  • 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.
    [Show full text]
  • The Role of Statins in Both Cognitive Impairment and Protection Against Dementia: a Tale of Two Mechanisms Bob G
    Schultz et al. Translational Neurodegeneration (2018) 7:5 https://doi.org/10.1186/s40035-018-0110-3 REVIEW Open Access The role of statins in both cognitive impairment and protection against dementia: a tale of two mechanisms Bob G. Schultz, Denise K. Patten and Daniel J. Berlau* Abstract Nearly 30% of adults 40 years and older in the United States are on a statin. Their widespread use heightens the importance of careful consideration of their varied effects on the body. Although randomized controlled trials have not confirmed cognitive impairing effects with statins, continuing evidence suggests statins have the ability to cause reversible cognitive impairment in some patients. Paradoxically, statins have also been shown to decrease the risk of dementia, Alzheimer’s disease, and improve cognitive impairment in some cases. However, randomized controlled trials have similarly failed to find the beneficial effect. Supporting evidence for both claims is compelling whereas known limitations of the clinical trials may explain the lack of findings. This narrative review aims to explain why there is still controversy and how both effects can, and may, be possible. The mechanisms that have been hypothesized for each effect are seemingly independent from one another and may explain the contradicting results. Being mindful of the complex effects of statins, health care providers need to be able to identify patients who are at risk for or already experiencing cognitive impairment from statin use while also identifying those who could potentially decrease their risk of dementia with statins. Keywords: Statin, Cognition, Dementia, Memory, Cholesterol, Alzheimer’s disease, Vascular dementia, Neuroprotection Background people in the United States (10% of Americans) are cur- Cardiovascular disease (CVD) is the leading cause of rently on a statin with an estimated 56 million people morbidity and mortality in the United States and ele- (24% of Americans) eligible to consider a statin.
    [Show full text]
  • Primary and Secondary Prevention Interventions for Cognitive Decline
    2016 Primary and secondary prevention interventions for cognitive decline and dementia Overview of reviews Published by The Norwegian Institute of Public Health Section for evidence summaries in the Knowledge Centre Title Primary and secondary prevention interventions for cognitive decline and dementia Norwegian title Primær‐ og sekundærforebyggende tiltak for kognitiv svikt og demens Responsible Camilla Stoltenberg, direktør Authors Gerd M Flodgren, project leader, researcher, the Knowledge Centre Rigmor C Berg, Head of Unit, for Social Welfare Research at the Knowledge Centre ISBN 978‐82‐8082‐745‐6 Projectnumber 798 Type of publication Overview of reviews No of pages 69 (110 inklusiv vedlegg) Client Nasjonalforeningen for folkehelsen MeSH terms Alzheimer’s disease, dementia, cognition, cognitive impairment, cognitive disorders, memory complaints, primary prevention, secondary prevention Citation Flodgren GM, Berg RC. Primary and secondary prevention interventions for cognitive decline and dementia. [Primær‐ og sekundærforebyggende tiltak for kognitiv svikt og demens] Rapport −2016. Oslo: Folkehelseinstituttet, 2016. 2 Table of contents Table of contents TABLE OF CONTENTS 3 KEY MESSAGES 5 EXECUTIVE SUMMARY 6 Background 6 Objectives 6 Methods 6 Results 6 Discussion 8 Conclusions 8 HOVEDFUNN (NORSK) 9 SAMMENDRAG (NORSK) 10 Bakgrunn 10 Problemstillinger 10 Metoder 10 Resultat 10 Diskusjon 12 Konklusjon 12 PREFACE 13 OBJECTIVES 15 BACKGROUND 16 Description of the condition 16 How the interventions may work 18 Why is it important to do this
    [Show full text]
  • Can the Treatment of Hypertension in the Middle-Aged Prevent Dementia in the Elderly?
    High Blood Press Cardiovasc Prev DOI 10.1007/s40292-016-0144-5 REVIEW ARTICLE Can the Treatment of Hypertension in the Middle-Aged Prevent Dementia in the Elderly? 1 1 1 1 Antonio Coca • Eila Monteagudo • Mo´nica Dome´nech • Miguel Camafort • Cristina Sierra1 Received: 16 February 2016 / Accepted: 28 March 2016 Ó Springer International Publishing Switzerland 2016 Abstract Hypertension, one of the main risk factors for 1 Introduction cardiovascular disease, is thought to play a crucial role in the pathophysiology of cognitive impairment. Studies have Cardiovascular disease (CVD) remains the leading cause of associated hypertension with subjective cognitive failures death worldwide. The Global Burden of Disease study and objective cognitive decline. Subjective cognitive fail- estimated that 29.6 % of all deaths were caused by CVD in ures may reflect the early phase of a long pathological 2010, more than all communicable, maternal, neonatal and process leading to cognitive decline and dementia that has nutritional disorders combined, and twice the number of been associated with hypertension and other cardiovascular deaths caused by cancer [1]. The burden of CVD in Europe risk factors. The underlying cerebral structural change remains heavy, although the prevalence varies dramatically associated with cognitive decline may be a consequence of among countries. More than four million Europeans die of the cerebral small-vessel disease induced by high blood CVD every year, and many more are hospitalized after pressure and may be detected on magnetic resonance acute episodes or are treated for chronic CVD [2]. The imaging as white matter hyperintensities, cerebral percentage of the population affected by hypertension, one microbleeds, lacunar infarcts or enlarged perivascular of the main risk factors for CVD, is remarkably high and, spaces.
    [Show full text]
  • Chapter 8 Neuropsychiatric Disorders, Including Dementia – Prevention Is Better Than Cure
    Chapter 8 Neuropsychiatric disorders, including dementia – prevention is better than cure I look up to the hills, but where will my help really come from? My help will come from the Lord, the Creator of heaven and earth. He will not let you fall. Your Protector will not fall asleep. Israel’s Protector does not get tired. He never sleeps. The Lord is your Protector. The Lord stands by your side, shading and protecting you. The sun cannot harm you during the day, and the moon cannot harm you at night. The Lord will protect you from every danger. He will protect your soul. The Lord will protect you as you come and go, both now and forever. Psalms 121: 1-8 ERV Chapter 8 Neuropsychiatric disorders, including dementia – prevention is better page 197 than cure Figure 8-1 Relationships between autoimmune diseases and dementia Autoimmune conditions and genetic factors can cause vascular dementia Chronic inflammation of brain cells due to Autoimmune conditions various autoimmune conditions leads to Lewy Vascular Multi- dementia Body Infarct Rheumatoid Arthritis dementia Consequences Underactive thyroid Look after yourself Systemic Lupus Immune system attacking central nervous system (CNS) Adrenal insufficiency Exercise, healthy diet and avoiding stress reduces inflammation of brain cells Brain cell death, plaque formation, leading to Type 1 and 2 diabetes SACD / MS-like presentation Less chance of developing dementia due to routine use of anti-inflammatories. Psoriasis CVD risks higher For example:aspirin and non steroidal anti- inflammatories Chapter 8 Neuropsychiatric disorders, including dementia – prevention is better page 198 than cure Vitamin B12 deficiency and neuropsychiatric symptoms – an overview Neuropsychiatric symptoms are among the most common presenting signs of vitamin B12 deficiency yet the diagnosis is often missed because of lack of awareness of this condition among clinicians (Lachner et al., 2012).
    [Show full text]
  • Risk Reduction of Cognitive Decline and Dementia: WHO Guidelines
    RISK REDUCTION OF COGNITIVE DECLINE AND DEMENTIA WHO GUIDELINES RISK REDUCTION OF COGNITIVE DECLINE AND DEMENTIA WHO GUIDELINES i Risk reduction of cognitive decline and dementia: WHO guidelines ISBN 978-92-4-155054-3 © World Health Organization 2019 Some rights reserved. This work is available under the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 IGO licence (CC BY-NC-SA 3.0 IGO; https://creativecommons.org/licenses/by-nc-sa/3.0/igo). Under the terms of this licence, you may copy, redistribute and adapt the work for non-commercial purposes, provided the work is appropriately cited, as indicated below. In any use of this work, there should be no suggestion that WHO endorses any specific organization, products or services. The use of the WHO logo is not permitted. If you adapt the work, then you must license your work under the same or equivalent Creative Commons licence. If you create a translation of this work, you should add the following disclaimer along with the suggested citation: “This translation was not created by the World Health Organization (WHO). WHO is not responsible for the content or accuracy of this translation. The original English edition shall be the binding and authentic edition”. Any mediation relating to disputes arising under the licence shall be conducted in accordance with the mediation rules of the World Intellectual Property Organization. Suggested citation. Risk reduction of cognitive decline and dementia: WHO guidelines. Geneva: World Health Organization; 2019. Licence: CC BY-NC-SA 3.0 IGO. Cataloguing-in-Publication (CIP) data. CIP data are available at http://apps.who.int/iris.
    [Show full text]
  • Causal Association of Circulating Cholesterol Levels with Dementia: a Mendelian Randomization Meta-Analysis
    Zhang et al. Translational Psychiatry (2020) 10:145 https://doi.org/10.1038/s41398-020-0822-x Translational Psychiatry ARTICLE Open Access Causal association of circulating cholesterol levels with dementia: a mendelian randomization meta-analysis Xiaoyu Zhang1, Qiuyue Tian1,DiLiu1,TaoGeng2,XizhuXu3,SiqiGe4, Deqiang Zheng1, Lijuan Wu1, Manshu Song1, Haifeng Hou3,WeiWang 5 and Youxin Wang 1 Abstract Prospective studies have shown that abnormally circulating cholesterol is associated with the risk of dementia. However, whether the association is causal or not remains unclear. We attempt to infer the causal association in a MR meta-analysis by using ApoE gene polymorphisms as instrument variables. Studies with dementia risk (27 studies) or circulating lipid levels (7 studies) were included, with totally 3136 dementia patients and 3103 healthy controls. The analyses showed that carriers of ε2 allele significantly were of decreased risk of AD (OR = 0.70; 95% CI: 0.58–0.84; P < 0.01), whereas carriers of ε4 allele were of increased risk of AD (OR = 3.62; 95% CI: 3.03–4.32; P < 0.05), compared to these of ε3 allele. Circulating TC was significantly reduced in carriers of ε2 allele (WMD = − 0.29 mmol/L; 95% CI: −0.54 to −0.03; P < 0.05) and increased in carriers of ε4 allele (WMD = 0.42 mmol/l; 95% CI: 0.001–0.84; P < 0.05). In addition, carriers of ε4 allele had reduction in circulating HDL-C (WMD = − 0.04 mmol/L; 95% CI: − 0.07 to −0.001; P < 0.05). In comparing allele ε2 with ε3, the predicted OR of having AD for 1 mg/dL increment in circulating TC was 0.97 (95% CI: 0.86–0.98; P < 0.05).
    [Show full text]
  • Association Between Physical Activity and Conversion from Mild Cognitive Impairment to Dementia
    Kim et al. Alzheimer's Research & Therapy (2020) 12:136 https://doi.org/10.1186/s13195-020-00707-1 RESEARCH Open Access Association between physical activity and conversion from mild cognitive impairment to dementia Yeo Jin Kim1, Kyung-Do Han2, Min Seok Baek3, Hanna Cho3* , Eun Joo Lee4 and Chul Hyoung Lyoo3 Abstract Background: Physical activity has been suggested to prevent the conversion of mild cognitive impairment (MCI) to dementia in patients. We investigated the association between the continuance and regularity of physical activity and the risk of developing dementia in patients with MCI. Methods: We analyzed 6-year followed up data for 247,149 individuals in the National Health Insurance Service (NHIS) cohort of Korea who were enrolled between January 1, 2009, and December 31, 2015. The patients were divided into four groups: those who did not engage in physical activity consistently (Never-PA group), those who initiated physical activity (Initiation-PA group), those who ceased physical activity (Withdrawal-PA group), and those who performed physical activity consistently (Maintenance-PA group). We also divided the patients into two groups: those who engaged in physical activity irregularly (Irregular-PA) and those who undertook physical activity regularly (Regular-PA). Results: When the risk for the Never-PA group was set as the benchmark (ref = 1), the Maintenance-PA group had the lowest incidence of dementia of the Alzheimer type (DAT) compared to the other groups (HR = 0.82, 95% CI 0.79–0.86). The DAT risk of the Initiation-PA group (HR = 0.89, 95% CI 0.85–0.93) was lower than the Never-PA group.
    [Show full text]
  • Evidence-To-Recommendation Table Problem
    29 Evidence profile: diabetes interventions and cognitive decline and/or dementia Evidence-to-recommendation table Problem Is the problem a priority? JUDGEMENT RESEARCH EVIDENCE ADDITIONAL CONSIDERATIONS ○ No The ageing population means that the absolute numbers of those living with cognitive decline Diabetes is a well established risk factor for cognitive decline and ○ Probably no or dementia continue to rise, with an estimated prevalence of 75 million by 2030 and a new dementia ○ Probably yes case of dementia diagnosed every three seconds(1). Anything that could reduce the incidence ● Yes of cognitive decline or dementia would have huge importance for individual health, society and ○ Varies health care providers. Diabetes mellitus is a chronic condition that occurs in approximately ○ Don't know 8.5% of the adult population and its prevalence increases with age. The presence of late-life diabetes has been found to be linked to an increased risk of dementia(2) Desirable Effects How substantial are the desirable anticipated effects? JUDGEMENT RESEARCH EVIDENCE ADDITIONAL CONSIDERATIONS ○ Trivial Treatment for diabetes in the form of medications for glycaemic control versus placebo or no Tuligenga(3) conducted a meta-analysis of RCTs comparing ○ Small intervention intensive versus standard glycaemic control and reported that ○ Moderate there was no statistically significant difference in cognitive ○ Large Desirable effects decline between the intensive glycaemic control group and the ○ Varies standard glycaemic control group (SDM = 0.02; 95% CI -0.03 to No data was available for MCI. For cognitive function the volume of evidence is low (2 RCTs) ● Don't know 0.08). They also noted that there was significant heterogeneity and the quality of evidence is moderate.
    [Show full text]
  • Nutrition and Dementia a Review of Available Research
    Nutrition and dementia A review of available research Supported by Nutrition and dementia Published by Alzheimer’s Disease International (ADI), London. February 2014 Reprinted October 2014 Copyright © Alzheimer’s Disease International. Authors Chapter 1: Dr Maëlenn Guerchet*, Dr Matthew Prina*, Professor Martin Prince* Chapter 2: Professor Emiliano Albanese*† Chapter 3: Dr Matthew Prina, Professor Emiliano Albanese Chapter 4: Professor Emiliano Albanese, Dr Matthew Prina Chapter 5: Professor Martin Prince, Dr Mario Siervo‡, Dr Daisy Acosta§, Dr Maëlenn Guerchet, Dr Matthew Prina * The Global Observatory for Ageing and Dementia Care, King’s College London † University of Geneva, Switzerland ‡ University of Newcastle § Universidad Nacional Pedro Henríquez Ureña, Dominican Republic This project was funded by a grant from Compass Group. ADI is fully responsible for the content Design by Julian Howell The Global Observatory for Ageing and Dementia Care The Global Observatory for Ageing and Dementia Care, hosted at the Health Service and Population Research Department, King’s College London, was founded in 2013. Supported by Alzheimer’s Disease International, and King’s College London, the Observatory has a tripartite mission: 1 To build upon ADI’s 10/66 Dementia Research Group programme of population-based and intervention research in low and middle income countries, maximising the impact that research findings from our data can have upon policy and practice. 2 To develop, evaluate, and promote primary care and community interventions for people with dementia. 3 To synthesise global evidence for policymakers and public, in particular, continuing and developing our role in the preparation of high impact evidence-based reports for Alzheimer’s Disease International (World Alzheimer Reports 2009, 2010, 2011 and 2013), the World Health Organization (Dementia: a public health priority, 2012) and other relevant intergovernmental organisations.
    [Show full text]
  • Association Between Previous Statin Use and Alzheimer's Disease
    brain sciences Article Association between Previous Statin Use and Alzheimer’s Disease: A Nested Case-Control Study Using a National Health Screening Cohort Ji Hee Kim 1 , Heui Seung Lee 1, Jee Hye Wee 2 , Yoo Hwan Kim 3, Chan Yang Min 4 , Dae Myoung Yoo 4 and Hyo Geun Choi 2,* 1 Department of Neurosurgery, College of Medicine, Hallym University, Anyang 14068, Korea; [email protected] (J.H.K.); [email protected] (H.S.L.) 2 Department of Otorhinolaryngology, College of Medicine, Hallym University, Anyang 14068, Korea; [email protected] 3 Department of Neurology, College of Medicine, Hallym University, Anyang 14068, Korea; [email protected] 4 Hallym Data Science Laboratory, College of Medicine, Hallym University, Anyang 14068, Korea; [email protected] (C.Y.M.); [email protected] (D.M.Y.) * Correspondence: [email protected]; Tel.: +82-031-380-3849 Abstract: A number of studies report the incidence of Alzheimer’s disease (AD) in patients taking statins, but the results are inconsistent. (1) Background: The present study investigated the cross- sectional association between previous statin use and the risk of AD development in Korean residents. (2) Methods: We used the Korean National Health Insurance Service-National Sample Cohort; 17,172 AD patients were matched by age, gender, income, and region of residence with 68,688 Citation: Kim, J.H.; Lee, H.S.; Wee, control participants at a ratio of 1:4. We used a multiple conditional logistic regression model J.H.; Kim, Y.H.; Min, C.Y.; Yoo, D.M.; to analyse the association between the number of days of statin use and AD occurrence.
    [Show full text]
  • What You Eat and Drink and Your Brain
    Dementia Q&A 7 What you eat and drink and your brain Diet is one factor researchers are investigating for its role in reducing the risk of dementia and for the assistance a healthy diet may provide to people who have dementia. This sheet outlines the part that diet can play in promoting a healthy brain. Can a healthy diet reduce the risk of developing dementia? Can a healthy diet help people with dementia? Some research has linked aspects of diet with the risk of developing Alzheimer’s disease and other dementias. Little research currently exists on whether diet can affect the progress of dementia. However, it is clear that a healthy balanced diet is important for everyone, to help prevent other health problems and ensure sufficient intake of essential nutrients. Which dietary factors might affect dementia risk A number of dietary factors have been associated with a reduced risk of developing dementia. These include: • Lower intake of saturated and transunsaturated fats • Higher intake of monounsaturated and polyunsaturated fats • Higher intake of omega-3 fats • Higher intake of some antioxidants and vitamins • Higher intake of vegetables and fruits • Moderate consumption of alcohol (with caution – too much alcohol poses a significant health risk) For language assistance National Dementia Helpline 1800 100 500 call 131 450 Dementia Q&A 7 Diet also affects the risk of developing heart disease and stroke, which are in turn risk factors for dementia. Too much saturated fat in the diet can contribute to high cholesterol levels, too much salt can result in high blood pressure (hypertension), and too much sugar raises the risk of type 2 diabetes.
    [Show full text]