***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Objectives To estimate survival after a diagnosis of dementia in primary care , compared with people without dementia , and to determine incidence of dementia . Design Cohort study using data from The Health Improvement Network ( THIN ) , a primary care data base . Setting 353 general practice s in the United Kingdom providing data to THIN . Participants All adults aged 60 years or over with a first ever code for dementia from 1990 to 2007 ( n=22 529 ) ; r and om sample of five participants without dementia for every participant with dementia matched on practice and time period ( n=112 645 ) . Main outcome measures Median survival by age and sex ; mortality rates ; incidence of dementia by age , sex , and deprivation . Results The median survival of people with dementia diagnosed at age 60 - 69 was 6.7 ( interquartile range 3.1 - 10.8 ) years , falling to 1.9 ( 0.7 - 3.6 ) years for those diagnosed at age 90 or over . Adjusted mortality rates were highest in the first year after diagnosis ( relative risk 3.68 , 95 % confidence interval 3.44 to 3.94 ) . This dropped to 2.49 ( 2.29 to 2.71 ) in the second year . The incidence of recorded dementia remained stable over time ( 3 - 4/1000 person years at risk ) . The incidence was higher in women and in younger age groups ( 60 - 79 years ) living in deprived areas . Conclusions Median survival was much lower than in screened population s. These clinical ly relevant estimates can assist patients and carers , clinicians , and policy makers when planning support for this population . The high risk of death in the first year after diagnosis may reflect diagnoses made at times of crisis or late in the disease trajectory . Late recording of diagnoses of dementia in primary care may result in missed opportunities for potential early interventions This pilot aims to better underst and the market for childcare in Saudi Arabia – both the supply and dem and sides – and to design a r and omized controlled experiment to test whether access to affordable day care ( in the form of subsidies , for example ) would incentivize Saudi mothers to search actively for employment and to remain employed once they are hired . In addition , the study seeks to underst and the degree to which employment early on in one ’s life impacts employment in later stages . The pilot will provide information on the groups of women the experiment should target , appropriate levels for the childcare subsidy , and the quality and current geographic locations of daycare sites . Expected Impact Determine the effects of facilitating childcare access on Saudi women ’s employment . PRINCIPAL INVESTIGATORS  Boston University Patricia Cortes  Harvard University Claudia Goldin  Swarthmore College Jennifer Background Globally , dengue infections constitute a significant public health burden . In recent decades , Malaysia has become a dengue hyper-endemic country with the co-circulation of the four dengue virus serotypes . The cyclical dominance of sub-types contributes to a pattern of major outbreaks . The consequences can be observed in the rising incidence of reported dengue cases and dengue related deaths . Underst and ing the complex interaction of the dengue virus , its human hosts and the mosquito vectors at the community level may help develop strategies for addressing the problem . Methods A prospect i ve cohort study will be conducted in Segamat district of Johor State in Peninsular Malaysia . Research ers received approval from the Malaysian Medical Research Ethics Committee and Monash University Human Research Ethics Committee . The study will be conducted at a Malaysian based health and demographic surveillance site over a 1 year period in three different setting s ( urban , semi-urban and rural ) . The study will recruit healthy adults ( male and female ) aged 18 years and over , from three ethnic groups ( Malay , Chinese and Indian ) . The sample size calculated using the Fleiss method with continuity correction is 333 . Sero-surveillance of participants will be undertaken to identify asymptomatic , otherwise healthy cases ; cases with dengue fever who are managed as out- patients ; and cases with dengue fever admitted to a hospital . A genetic analysis of the participants will be undertaken to determine whether there is a relationship between genetic predisposition and disease severity . A detailed medical history , past history of dengue infection , vaccination history against other flaviviruses such as Japanese encephalitis and Yellow fever , and the family history of dengue infection will also be collected . In addition , a mosquito surveillance will be carried out simultaneously in recruitment areas to determine the molecular taxonomy of circulating vectors . Discussion The research findings will estimate the burden of asymptomatic and symptomatic dengue at the community level . It will also examine the relationship between virus serotypes and host genotypes , and the association of the clinical manifestation of the early phase with the entire course of illness BACKGROUND Although statins reduce coronary and cerebrovascular morbidity and mortality in middle-aged individuals , their efficacy and safety in elderly people is not fully established . Our aim was to test the benefits of pravastatin treatment in an elderly cohort of men and women with , or at high risk of developing , cardiovascular disease and stroke . METHODS We did a r and omised controlled trial in which we assigned 5804 men ( n=2804 ) and women ( n=3000 ) aged 70 - 82 years with a history of , or risk factors for , vascular disease to pravastatin ( 40 mg per day ; n=2891 ) or placebo ( n=2913 ) . Baseline cholesterol concentrations ranged from 4.0 mmol/L to 9.0 mmol/L. Follow-up was 3.2 years on average and our primary endpoint was a composite of coronary death , non-fatal myocardial infa rct ion , and fatal or non-fatal stroke . Analysis was by intention-to-treat . FINDINGS Pravastatin lowered LDL cholesterol concentrations by 34 % and reduced the incidence of the primary endpoint to 408 events compared with 473 on placebo ( hazard ratio 0.85 , 95 % CI 0.74 - 0.97 , p=0.014 ) . Coronary heart disease death and non-fatal myocardial infa rct ion risk was also reduced ( 0.81 , 0.69 - 0.94 , p=0.006 ) . Stroke risk was unaffected ( 1.03 , 0.81 - 1.31 , p=0.8 ) , but the hazard ratio for transient ischaemic attack was 0.75 ( 0.55 - 1.00 , p=0.051 ) . New cancer diagnoses were more frequent on pravastatin than on placebo ( 1.25 , 1.04 - 1.51 , p=0.020 ) . However , incorporation of this finding in a meta- analysis of all pravastatin and all statin trials showed no overall increase in risk . Mortality from coronary disease fell by 24 % ( p=0.043 ) in the pravastatin group . Pravastatin had no significant effect on cognitive function or disability . INTERPRETATION Pravastatin given for 3 years reduced the risk of coronary disease in elderly individuals . PROSPER therefore extends to elderly individuals the treatment strategy currently used in middle aged people Sleep disturbances and decrements of daytime performance have been attributed to HMG-CoA reductase inhibitors . As a rule , lipophilic compounds more readily cross the blood-brain barrier and are more likely to affect central nervous system function . The authors compared the effects of lovastatin ( 40 mg ) , a lipophilic compound , to pravastatin ( 40 mg ) , a hydrophilic compound , in a 6-week , double-blind , r and omized , placebo-controlled , three-way Latin square design , cross-over study on 22 men with hypercholesterolemia . Patients had LDL cholesterol of more than 165 mg/dL and triglyceride of less than 350 mg/dL after 6 weeks of a low-fat ( < 30 % ) , low-cholesterol ( < 300 mg/day ) diet . Compared with placebo , there were no significant effects of lovastatin or pravastatin on the following subjective and polysomnographic sleep measures : changes in total sleep time , time in each sleep stage , sleep efficiency , sleep latency , REM density , REM activity , and number of arousals . Similarly , there were no effects of the two drugs on measures of cognitive performance . A significant increase in the duration of nocturnal tumescence ( NPT ) was observed after 2 weeks of treatment with both study drugs . This effect was not significant after 6 weeks of treatment . Both lovastatin and pravastatin caused significant ( P < .05 compared with placebo ) decreases in total cholesterol ( by 20.9 and 20.6 % , respectively ) , LDL cholesterol ( by 27.8 and 29.9 % ) , and triglycerides ( by 13.6 and 3.7 % ) . Subjects ' HDL increased by 2.3 % with lovastatin ( NS ) and by 3.1 % with pravastatin ( P < .05 ) . Lipoprotein(a ) increased by 20.5 % with lovastatin and by 1.1 % with pravastatin ; these changes were not significantly different from placebo . ( ABSTRACT TRUNCATED AT 250 WORDS The aim of this prospect i ve cohort study was to evaluate the effects of lipid lowering agent ( LLA ) intake on cognitive function in 6,830 community-dwelling elderly persons .  Cognitive performance ( global cognitive functioning , visual memory , verbal fluency , psychomotor speed , and executive function ) , clinical diagnosis of dementia , and fibrate and statin use , were evaluated at baseline , and 2 , 4 , and 7 year follow-up . Multivariate Cox models were stratified by gender and adjusted for sociodemographic characteristics , mental and physical health including vascular risk factors , and genetic vulnerability ( apolipoprotein E and cholesteryl ester transfer protein ) . For women but not men , fibrate use was specifically associated with an increased risk over 7 years of decline in visual memory only ( HR = 1.29 , 95 % CI = 1.09 - 1.54 , p = 0.004 ) , and did not increase risk for incident dementia . This association was independent of genetic vulnerability related to apolipoprotein E and cholesteryl exchange transfer protein polymorphisms and occurred only in women with higher low density lipoprotein (LDL)-cholesterol levels and treated with fibrate ( HR = 1.39 , 95 % CI = 1.08 - 1.79 , p = 0.01 ) and not in those with lower LDL-cholesterol levels irrespective of fibrate treatment . For both genders , no significant associations were found between statins ( irrespective of their lipophilicity ) and either cognitive decline or dementia incidence . This prospect i ve study , adjusting for multiple confounders , found no evidence that LLA given in late life reduced the risk of cognitive decline and dementia , but did raise the possibility that women with treatment-resistant high LDL-cholesterol may be at increased risk of decline in visual memory Because cerebrospinal fl(CSF ) abnormalities in presymptomatic subjects with PSEN1 ( presenilin 1 ) mutations may be observed 4 to 12 years prior to the estimated age at onset , it is possible to test putative therapies on the CSF analytes that correlate with neurodegeneration during this presymptomatic window of clinical opportunity . It is also possible to test the same therapy on a comparison group with increased risk status conferred by both hyperlipidemia and heterozygosity for apolipoprotein Ee4 . To our knowledge , the only putative therapy thus far tested in such a common design has been statin therapy . The results of these tests show increases in soluble amyloid precursor protein (sAPP)α correlating with statininduced decreases in serum cholesterol levels in the non-PSEN1 subjects . This result could be one functional correlate for part of the substantial risk reduction for late onset Alzheimer ’s disease recently reported in the Rotterdam study , a large , long-term prospect i ve statin trial . Statin therapy signifi cantly decreased both sAPPα and sAPPβ in presymptomatic PSEN1 subjects . Initially , elevated phospho-tau levels in PSEN1 subjects did not further increase during the 2 to 3 years of statin therapy , possibly indicative of a prophylactic eff ect . These results suggest that large and longer term trials of statin therapy correlating changes in CSF biomarker levels with clinical course may be warranted in both presymptomatic PSEN1 and non-PSEN1 subjects Background : Previously reported associations between statin use and incident dementia or cognitive decline  have been inconsistent . We report the results from a 3-year prospect i ve study on the association of statin use on cognitive decline  and incident dementia in elderly African Americans . Methods : A community-based cohort of 1,146 African Americans aged 70 and older living in Indianapolis , Indiana , was evaluated in 2001 and 2004 . The instrument used for cognitive assessment was the Community Screening Interview for Dementia ( CSI-D ) . Cognitive decline was defined as CSI-D scores measured at 2001 minus scores at 2004 . Measurements of low-density lipoprotein cholesterol ( LDL-C ) and C-reactive protein ( CRP ) were obtained from baseline blood sample s. Results : Adjusting for age at baseline , gender , education , and the possession of ApoE ε4 allele , baseline statin use was 
    Output:
    
Although observational studies that considered statin use at or near the time of dementia diagnosis suggest a protective effect of statins , these findings could be attributable to reverse causation .
RCTs and well-conducted observational studies of baseline statin use and subsequent cognition over several years of follow-up do not support a causal preventative effect of late-life statin use on cognitive decline or dementia .