***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: Background and Purpose — Exposure to vascular risk factors has a gradual deleterious effect on brain MRI and cognitive measures . We explored whether a pattern of these measures exists that predicts stroke and Alzheimer disease ( AD ) risk . Methods — A cognitive battery was administered to 1679 dementia and stroke-free Framingham offspring ( age , > 55 years ; mean , 65.7±7.0 ) between 1999 and 2004 ; participants were also free of other neurological conditions that could affect cognition and > 90 % also had brain MRI examination . We related cognitive and MRI measures to risks of incident stroke and AD ⩽10 years of follow-up . As a secondary analysis , we explored these associations in The Framingham Heart Study original cohort ( mean age , 67.5±7.3 and 84.8±3.3 years at the cognitive assessment and MRI examination , respectively ) . Results — A total of 55 Offspring participants sustained strokes and 31 developed AD . Offspring who scored < 1.5 SD below predicted mean scores , for age and education , on an executive function test , had a higher risk of future stroke ( hazard ratio [ HR ] , 2.27 ; 95 % confidence interval [ CI ] , 1.06–4.85 ) and AD ( HR , 3.60 ; 95 % CI , 1.52–8.52 ) ; additional cognitive tests also predicted AD . Participants with low ( < 20 percentile ) total brain volume and high ( > 20 percentile ) white matter hyperintensity volume had a higher risk of stroke ( HR , 1.97 ; 95 % CI , 1.03–3.77 and HR , 2.74 ; 95 % CI , 1.51–5.00 , respectively ) but not AD . Hippocampal volume at the bottom quintile predicted AD in the offspring and original cohorts ( HR , 4.41 ; 95 % CI , 2.00–9.72 and HR , 2.37 ; 95 % CI , 1.12–5.00 , respectively ) . A stepwise increase in stroke risk was apparent with increasing numbers of these cognitive and imaging markers . Conclusions — Specific patterns of cognitive and brain structural measures observed even in early aging predict stroke risk and may serve as biomarkers for risk prediction BACKGROUND Analyses of some r and omised trials show that calcium-channel blockers reduce the risk of stroke more than expected on the basis of mean blood pressure alone and that beta blockers are less effective than expected . We aim ed to investigate whether the effects of these drugs on variability in blood pressure might explain these disparities in effect on stroke risk . METHODS The Anglo-Sc and inavian Cardiac Outcomes Trial Blood Pressure Lowering Arm ( ASCOT-BPLA ) compared amlodipine-based regimens with atenolol-based regimens in 19 257 patients with hypertension and other vascular risk factors and the Medical Research Council ( MRC ) trial compared atenolol-based and diuretic-based regimens versus placebo in 4396 hypertensive patients aged 65 - 74 years . We expressed visit-to-visit variability of blood pressure during follow-up in the two trials as st and ard deviation ( SD ) and as transformations uncorrelated with mean blood pressure . For ASCOT-BPLA , we also studied within-visit variability and variability on 24 h ambulatory blood-pressure monitoring ( ABPM ) . RESULTS In ASCOT-BPLA , group systolic blood pressure ( SBP ) SD was lower in the amlodipine group than in the atenolol group at all follow-up visits ( p<0.0001 ) , mainly because of lower within-individual visit-to-visit variability . Within-visit and ABPM variability in SBP were also lower in the amlodipine group than in the atenolol group ( all p<0.0001 ) . Analysis of changes from baseline showed that variability decreased over time in the amlodipine group and increased in the atenolol group . The lower risk of stroke in the amlodipine group ( hazard ratio 0.78 , 95 % CI 0.67 - 0.90 ) was partly attenuated by adjusting for mean SBP during follow-up ( 0.84 , 0.72 - 0.98 ) , but was abolished by also adjusting for within-individual SD of clinic SBP ( 0.99 , 0.85 - 1.16 ) . Findings were similar for coronary events . In the ABPM sub study , reduced variability in daytime SBP in the amlodipine group ( p<0.0001 ) partly accounted for the reduced risk of vascular events , but reduced visit-to-visit variability in clinic SBP had a greater effect . In the MRC trial , group SD SBP and all measures of within-individual visit-to-visit variability in SBP were increased in the atenolol group compared with both the placebo group and the diuretic group during initial follow-up ( all p<0.0001 ) . Subsequent temporal trends in variability in blood pressure during follow-up in the atenolol group correlated with trends in stroke risk . INTERPRETATION The opposite effects of calcium-channel blockers and beta blockers on variability of blood pressure account for the disparity in observed effects on risk of stroke and expected effects based on mean blood pressure . To prevent stroke most effectively , blood-pressure-lowering drugs should reduce mean blood pressure without increasing variability ; ideally they should reduce both Background and Purpose — The association between stroke and subsequent dementia or Alzheimer disease is well established . What is less understood is the extent to which this association is dependent on prestroke cognitive functioning . The study estimated the occurrence in poststroke dementia as a function of prestroke cognitive status and incident stroke . Methods — Study data were derived from the English Longitudinal Study of Ageing , a 10-year long prospect i ve cohort study of older adults living in Engl and . Baseline data ( 2002/2003 ) were used to group participants into tertiles of cognitive , memory , and executive functioning before an incident stroke . Data from 4 follow-up surveys were used to identify new stroke and poststroke dementia events . Results — The analyses were based on 10 809 participants aged ≥50 years at baseline . High prestroke executive functioning was associated with lower relative risk ( RR ) of dementia ( RR , 0.24 ; 95 % confidence interval , 0.13–0.45 ; P<0.001 ) . Stroke was associated with increased RR of poststroke dementia ( RR , 2.63 ; 95 % confidence interval , 1.80–3.84 ; P<0.001 ) . The association of stroke with poststroke dementia was greater for participants with higher prestroke executive functioning ( interaction term RR , 4.4 ; 95 % confidence interval , 1.35–14.63 ; P=0.014 ) . For participants with higher executive functioning , the probability of dementia was 0.3 % without stroke and 3.1 % after stroke , compared with 1.9 % and 5.2 % for lower executive functioning . Conclusions — Stroke and prestroke cognition were independently associated with increased probability of poststroke dementia . Stroke results in disproportionate increase in the risk of dementia when premorbid cognitive functioning is high BACKGROUND Silent brain infa rcts are frequently seen on magnetic resonance imaging ( MRI ) in healthy elderly people and may be associated with dementia and cognitive decline . METHODS We studied the association between silent brain infa rcts and the risk of dementia and cognitive decline in 1015 participants of the prospect i ve , population -based Rotterdam Scan Study , who were 60 to 90 years of age and free of dementia and stroke at base line . Participants underwent neuropsychological testing and cerebral MRI at base line in 1995 to 1996 and again in 1999 to 2000 and were monitored for dementia throughout the study period . We performed Cox proportional-hazards and multiple linear-regression analyses , adjusted for age , sex , and level of education and for the presence or absence of subcortical atrophy and white-matter lesions . RESULTS During 3697 person-years of follow-up ( mean per person , 3.6 years ) , dementia developed in 30 of the 1015 participants . The presence of silent brain infa rcts at base line more than doubled the risk of dementia ( hazard ratio , 2.26 ; 95 percent confidence interval , 1.09 to 4.70 ) . The presence of silent brain infa rcts on the base-line MRI was associated with worse performance on neuropsychological tests and a steeper decline in global cognitive function . Silent thalamic infa rcts were associated with a decline in memory performance , and nonthalamic infa rcts with a decline in psychomotor speed . When participants with silent brain infa rcts at base line were subdivided into those with and those without additional infa rcts at follow-up , the decline in cognitive function was restricted to those with additional silent infa rcts . CONCLUSIONS Elderly people with silent brain infa rcts have an increased risk of dementia and a steeper decline in cognitive function than those without such lesions OBJECTIVES To investigate the effect of cognitive impairment on fatal and nonfatal incident stroke  in older adults . DESIGN A large , national , prospect i ve , population -based study of a representative cohort of older Canadians followed over a 10-year period . SETTING Secondary analyses were conducted using data from the Canadian Study of Health and Aging , a population -based study of older adults followed prospect ively from 1991 to 2001 . PARTICIPANTS Nine thous and four hundred fifty-one adults aged 65 and older who had not previously been diagnosed with stroke at baseline ( in 1991 ) . MEASUREMENTS In addition to known risk factors , the independent contribution of  cognitive function  ( diagnosed in a clinical examination ) was examined as a risk for stroke in older adults . RESULTS Multinomial logistic regression analyses showed that cognitive impairment was associated with twice the odds of fatal incident stroke , controlling for well-established risk factors . CONCLUSION This study provides further evidence for the need to consider cognitive function in relation to stroke risk in older population OBJECTIVE Recent studies have suggested that vascular dementia in older persons is more common than previously hypothesized . A substantial proportion of dementia in old age may be an early manifestation of cerebrovascular disease ( CVD ) , that eventually becomes clinical ly evident as an acute cerebrovascular accident . This study was aim ed at assessing whether cognitive impairment and cognitive decline in older persons free of stroke are associated with higher risk of future stroke , independently of other risk factors . DESIGN Population -based prospect i ve study . PARTICIPANTS A total of 5024 subjects from the Established Population s for Epidemiologic Studies of the Elderly , who were alive and had no history of previous stroke at the sixth follow-up visit . Subjects who had reported a stroke in a previous interview or with a diagnosis of cerebrovascular disease in a hospitalization record during the previous 3 years were excluded . MEASUREMENTS Cognitive function was assessed by the Short Portable Mental Status Question naire ( SPMSQ ) . Occurrence of a stroke was prospect ively assessed by examining hospital discharge diagnoses and death certificates . RESULTS During 19,533 person-years of follow-up , 259 strokes were recorded ( 13.3/1000 person-years ) . Stroke incidence was lowest in those with normal SPMSQ score ( 12.1/1000 person-years ) , intermediate in those with moderate impairment ( 16.3/1000 person-years ) , and highest in those with severe impairment ( 30.9/1000 person-years ) . Adjusting for age , education , smoking , history of hypertension , blood pressure , heart attack , diabetes , and disability , the relative risks of stroke for moderate and severe cognitive impairment were 1.2 ( 0.9 - 1.6 ) and 2.2 ( 1.2 - 3.8 ) , respectively . The association between cognitive impairment and incident stroke was not mediated by hypertension or diabetes . Compared with subjects with stable or improved SPMSQ score in the previous 3 years , those who declined had higher risk of stroke . CONCLUSIONS The elevated risk of subsequent strokes in older persons with cognitive impairment suggests that CVD may play larger role in causing cognitive impairment then previously suspected . It remains to be demonstrated whether reducing modifiable risk factors for CVD decreases the burden of cognitive impairment in older persons without stroke Background and Purpose — Several studies indicate that stroke increases the risk of dementia . Most of these studies lacked the ability to take accurately assessed prestroke cognitive function into account . Whether the effects of stroke merely unravel an ongoing underlying dementing process or in fact cause the dementia has implication s for the prevention of dementia in persons with cerebrovascular disease . We explored in a prospect i ve cohort study whether stroke occurrence was related to a higher risk of subsequent dementia and whether this association was dependent on prestroke slope of cognitive function . Methods — Cox proportional hazard models were used to relate incident stroke as a time-varying exposure with the risk of dementia in 6724 participants of the Rotterdam Study without dementia or stroke at baseline ( 49 361 person years of follow-up ) . Subsequently Cox proportional hazard models were performed to assess whether this association was dependent on slope of prestroke cognitive performance and other risk factors for cognitive decline . Results — Independent 
    Output:
    
INTERPRETATION Baseline cognitive impairment was associated with a significantly higher risk of future stroke , especially ischemic and fatal stroke