Silent Brain Infarcts and the Risk of Dementia and Cognitive Decline
Sarah E. Vermeer, M.D., Ph.D., Niels D. Prins, M.D., Tom den Heijer, M.D., Albert Hofman, M.D., Ph.D., Peter J. Koudstaal, M.D., Ph.D., and Monique M.B. Breteler, M.D., Ph.D.
Background Silent brain infarcts are frequently seen on magneticresonance imaging (MRI) in healthy elderly people and may beassociated with dementia and cognitive decline.
Methods We studied the association between silent brain infarctsand the risk of dementia and cognitive decline in 1015 participantsof the prospective, population-based Rotterdam Scan Study, whowere 60 to 90 years of age and free of dementia and stroke atbase line. Participants underwent neuropsychological testingand cerebral MRI at base line in 1995 to 1996 and again in 1999to 2000 and were monitored for dementia throughout the studyperiod. We performed Cox proportional-hazards and multiple linear-regressionanalyses, adjusted for age, sex, and level of education andfor the presence or absence of subcortical atrophy and white-matterlesions.
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 infarcts at base line more thandoubled the risk of dementia (hazard ratio, 2.26; 95 percentconfidence interval, 1.09 to 4.70). The presence of silent braininfarcts on the base-line MRI was associated with worse performanceon neuropsychological tests and a steeper decline in globalcognitive function. Silent thalamic infarcts were associatedwith a decline in memory performance, and nonthalamic infarctswith a decline in psychomotor speed. When participants withsilent brain infarcts at base line were subdivided into thosewith and those without additional infarcts at follow-up, thedecline in cognitive function was restricted to those with additionalsilent infarcts.
Conclusions Elderly people with silent brain infarcts have anincreased risk of dementia and a steeper decline in cognitivefunction than those without such lesions.
Dementia is a major health problem in Western countries. Dementiawill develop in one in four 55-year-olds,1 and the number ofpatients with dementia will rise as life expectancy increases.Evidence has accumulated that vascular abnormalities have arole in the development of dementia. Patients with stroke areat increased risk for both vascular dementia and Alzheimer'sdisease.2,3,4 People who were found at autopsy to have lacunarcerebral infarcts were more likely to have had dementia thanthose without infarcts, and fewer pathological findings of Alzheimer'sdisease were needed in persons with such infarcts for clinicalsymptoms of dementia to be present.5,6 Patients with Alzheimer'sdisease more frequently have asymptomatic (i.e., silent) braininfarcts on magnetic resonance imaging (MRI) than do controlsubjects without dementia.7,8 The prevalence of silent braininfarcts is also high in elderly populations without dementia,9,10,11but little is known about their prognostic relevance. We thereforeexamined the relation between silent brain infarcts and therisk of dementia and cognitive decline in the general population.
Methods
Participants
The Rotterdam Scan Study is a prospective, population-basedcohort study designed to study the causes and consequences ofbrain changes in the elderly.12 In 1995 to 1996, we randomlyselected 1717 participants 60 to 90 years of age, with stratificationaccording to age (in five-year groups) and sex, from two ongoingpopulation-based studies.13,14 A total of 1077 elderly peoplewithout dementia participated (63 percent). Participants weresignificantly younger and more highly educated and performedbetter on the Mini–Mental State Examination than nonparticipants.15The medical ethics committee of the Erasmus Medical Center approvedthe study, and each participant gave written informed consent.
The base-line examination in 1995 to 1996 comprised a structuredinterview, physical examination, blood sampling, and neuropsychologicaltests at the research center, as well as a cerebral MRI scan.For the present study we excluded 62 participants with a historyof stroke before the base-line evaluation (Figure 1).16 We monitoredall 1015 participants throughout the study by reviewing medicalrecords from their general practitioners after base line fordeath and major complications, including cognitive problems,dementia, stroke, and transient ischemic attack. In 1999 to2000, we reinvited 914 of the 1015 participants for a secondexamination, of whom 739 participated (81 percent) (Figure 1).The remaining 101 participants were not reinvited, for the followingreasons: 75 had died, 15 had been institutionalized for dementia,7 had already been examined in 1999 as part of the regular examinationfor the Rotterdam Study,14 3 had moved abroad, and 1 could notbe reached.
The various study samples are indicated by double-lined boxes. MRI denotes magnetic resonance imaging.
People who were ineligible or who declined to undergo the secondexamination were significantly older, were less highly educated,and performed worse on the neuropsychological tests at baseline than participants in the second examination. People whodeclined to undergo the second examination did not differ significantlyfrom those who participated with respect to the presence orabsence of silent brain infarcts at base line, whereas ineligibleparticipants had a nonsignificantly higher prevalence of silentbrain infarcts than participants (absolute age- and sex-adjusteddifference, 5 percent; 95 percent confidence interval, –3to 14 percent). Thirteen of the 739 participants were ineligibleto undergo a second MRI of the brain because of a contraindicationto MRI, and 97 declined to undergo the procedure. In total,629 of the 901 eligible participants (70 percent) underwenta second MRI in 1999 to 2000.
Cerebral Infarcts and Other MRI Measures
All 1015 participants underwent MRI of the brain at base linein 1995 to 1996. We made axial T1-weighted, T2-weighted, andproton-density–weighted scans on 1.5-Tesla MRI scanners(MR Gyroscan, Philips, or MR VISION, Siemens).11 In 1999 to2000, 629 participants underwent a second MRI with use of theMR VISION scanner and the same sequences.
The presence of brain infarcts was rated similarly at base lineand follow-up. We defined brain infarcts as areas of focal hyperintensityon T2-weighted images that were at least 3 mm in diameter. Proton-densityscans were used to distinguish infarcts from dilated perivascularspaces. Areas of hyperintensity in the white matter also hadto have corresponding prominent hypointensity on T1-weightedimages, in order to distinguish them from cerebral white-matterlesions. A single trained physician who was unaware of the patients'history of stroke and transient ischemic attack scored infarctson both the base-line and second MRI with respect to their locationand size. An intrarater study for detecting infarcts (110 imagesrandomly selected from both scanners) showed good agreement(=0.80).
We obtained information on any history of stroke and transientischemic attack from the participants themselves and by checkingmedical records of all participants, independently of theirMRI results. An experienced neurologist subsequently reviewedthe participants' medical history and scans and categorizedinfarcts as silent or symptomatic. We defined silent brain infarctsas evidence on MRI of one or more infarcts, without a historyof a (corresponding) stroke or transient ischemic attack. Ifa prior stroke or transient ischemic attack did correspond witha lesion, the latter was defined as a symptomatic infarct. Theintrarater reliability for the classification of infarcts assilent or symptomatic was excellent (=1.0). If participantshad both symptomatic and silent infarcts, they were includedin the group with symptomatic infarcts.
White-matter lesions and subcortical atrophy of the brain wererated on the base-line MRI scans.12 White-matter lesions wereconsidered present if they were hyperintense on proton-densityand T2-weighted images, without prominent hypointensity on T1-weightedscans. The severity of periventricular white-matter lesionswas determined by adding three region-specific scores (gradesranged from 0 to 9, with higher grades indicating greater severity).The volume of subcortical white-matter lesions was approximatedon the basis of the number and size of lesions (volume range,0 to 29.5 ml). The severity of subcortical atrophy of the brainwas estimated by calculating the ratio of ventricle to brain(the average of assessments at the frontal and occipital hornsand the caudate nucleus) on T1-weighted images.17 Both intrareaderand interreader studies (100 of each) showed good-to-excellentagreement.12
Dementia
All participants were free of dementia at base line. We screenedall participants for dementia at follow-up using the Mini–MentalState Examination and the Geriatric Mental State Schedule.1Participants who were positive at screening underwent additionalcognitive testing with the Cambridge Mental Disorders of theElderly Examination. People who were then thought to have dementiawere examined by a neurologist and underwent extensive neuropsychologicaltesting. In addition, we continually monitored the medical recordsof all participants at their general practitioners' officesand the Regional Institute for Ambulatory Mental Health Careto obtain information on newly diagnosed dementia until March1, 2000. Dementia and its subtypes were diagnosed by a panelthat reviewed all available information according to standardizedcriteria.18,19,20 The onset of dementia was defined as the dateon which the clinical symptoms allowed the diagnosis of dementiato be made. We had complete follow-up data for dementia on allparticipants through our system of monitoring general practitioners.
Cognitive Decline
Participants underwent the following neuropsychological testsat the base-line examination: the Mini–Mental State Examination,the 15-word verbal-learning test, the Stroop test, the Paper-and-PencilMemory Scanning Task, and the Letter–Digit SubstitutionTask.15 We used alternative versions of the same neuropsychologicaltests at the second examination. For each participant, we calculatedz scores (individual test score minus mean test score dividedby the standard deviation) for the neuropsychological testsat base line and at follow-up using the mean and standard deviationof the base-line tests. We constructed compound scores for memoryperformance by averaging the z scores of the total of threeimmediate recall trials and the delayed-recall trial of the15-word verbal-learning test. The compound score for psychomotorspeed was the average of the z scores for the reading subtaskof the Stroop test, the one-letter subtask of the Paper-and-PencilMemory Scanning Task, and the Letter–Digit SubstitutionTask. The compound score for global cognitive function was constructedby calculating the average of the z scores for all the abovetests.15 Cognitive decline was calculated by subtracting thez scores for memory performance, psychomotor speed, and globalcognitive function at follow-up from the z scores at base line.
Statistical Analysis
First, we used Cox proportional-hazards regression analysisto examine the relation between the presence of silent braininfarcts at base line and the risk of subsequent dementia inthe 1015 participants who were free of dementia and stroke atbase line. The duration of follow-up was calculated from thedate of the MRI at base line until death, the diagnosis of dementia,or the end of follow-up, whichever came first. We also investigatedthe association of white-matter lesions and subcortical atrophyof the brain with dementia and whether these structural changesin the brain affected the relation between silent brain infarctsand dementia. Second, we estimated the association between thepresence of silent brain infarcts at base line and subsequentcognitive decline by multiple linear-regression analysis inthe subsample of 739 participants who underwent neuropsychologicaltests at follow-up. We also investigated whether this relationwith cognitive decline differed between silent infarcts in thethalamus and infarcts elsewhere, because thalamic nuclei areinvolved in storage and short-term memory.21,22 Third, we examinedthe contribution of newly detected silent infarcts to the rateof cognitive decline. This analysis was based on 619 participantswithout symptomatic infarcts on the second MRI (Figure 1).
We adjusted all analyses for age, sex, and level of education.In the analyses of cognitive decline, we also adjusted for theinterval between the two sets of neuropsychological tests.
Results
During 3697 person-years of follow-up (mean per person, 3.6years), dementia developed in 30 participants (3 percent), 26of whom had Alzheimer's disease (1 with cerebrovascular disease),2 vascular dementia, and 1 multisystem atrophy; in 1, the subtypewas unknown. Four patients with dementia died, but no autopsywas performed.
Table 1 shows the base-line characteristics of the participants.Eleven of the 217 participants with silent brain infarcts atbase line had cortical infarcts, 202 had lacunar infarcts —171 in the basal ganglia and 31 in the subcortex — and4 had infarcts in the cerebellum or brainstem. Fourteen of the30 participants in whom dementia developed had one or more silentbrain infarcts present on the base-line MRI, 7 of whom had multipleinfarcts.
Table 1. Base-Line Characteristics of All Participants Who Were Free of Dementia and Stroke in 1995 to 1996, Those Who Underwent the Second Neuropsychological Examination, and Those Who Underwent the Second MRI Scan in 1999 to 2000.
The presence of silent brain infarcts at base line more thandoubled the risk of dementia, and this result remained largelyunchanged after adjustment for the severity of white-matterlesions and subcortical atrophy (Table 2). A greater severityof periventricular white-matter lesions was also associatedwith an increased risk of dementia (Table 2), as was a greaterseverity of subcortical atrophy of the brain (hazard ratio perincrease of 1 SD in severity, 1.78; 95 percent confidence interval,1.26 to 2.51).
Table 2. Relation between the Presence of Silent Brain Infarcts at Base Line, the Severity of Periventricular and Subcortical White-Matter Lesions, and the Risk of Dementia.
There was no significant difference in risk between participantswith Mini–Mental State Examination scores below 26 andthose with a score of 26 or above at base line or between carriersof the apolipoprotein E 4 allele and noncarriers. The exclusionof participants who used aspirin or oral anticoagulants at baseline did not materially change the results. Nineteen of the30 participants in whom dementia developed underwent a secondcerebral MRI or computed tomographic scan; a symptomatic infarctwas found in 3 (16 percent) and a new silent brain infarct wasfound in 4 (21 percent). This rate was higher than that amongthe 618 participants without dementia at follow-up, of whom8 (1 percent) had a symptomatic brain infarct and 71 (11 percent)a silent brain infarct on the second MRI scan.
Global cognitive function was significantly worse in participantswith silent brain infarcts on the base-line MRI than in thosewithout such infarcts (adjusted mean difference in z score,–0.11; 95 percent confidence interval, –0.20 to–0.01). The presence of silent brain infarcts at baseline was associated with a steeper decline in cognitive function(Table 3). The presence of multiple silent infarcts showed astronger relation with cognitive decline than the presence ofsingle silent infarcts (adjusted mean difference in z scorefor multiple infarcts, –0.34; 95 percent confidence interval,–0.51 to –0.17; and for single infarcts, –0.07;95 percent confidence interval, –0.20 to 0.06). Silentinfarcts in the thalamus were associated with a greater declinein memory performance, whereas infarcts located elsewhere resultedin a greater decline in psychomotor speed (Table 3). There wasno association between the presence of silent brain infarctsat base line and a decline in the Mini–Mental State Examinationscore (adjusted mean difference in the score, –0.01; 95percent confidence interval, –0.44 to 0.33).
Table 3. Association between the Presence of Silent Brain Infarcts on Magnetic Resonance Imaging in 1995–1996 and Subsequent Cognitive Decline.
When participants were subdivided into four groups accordingto the presence or absence of silent brain infarcts on the base-lineand follow-up MRI, the decline in cognitive function was restrictedto those with new silent brain infarcts on the follow-up scan,regardless of whether they had silent infarcts at base line(Figure 2). Memory performance improved for all participants,as expected owing to the learning effect. There were no significantchanges in scores on the Mini–Mental State Examinationamong the various groups.
Figure 2. Mean Change in Memory Performance, Psychomotor Speed, and Global Cognitive Function among Participants with and Those without Silent Brain Infarcts on Magnetic Resonance Imaging at Base Line (1995 to 1996) and at Follow-up (1999 to 2000), after Adjustment for Age, Sex, Level of Education, and Interval between Neuropsychological Tests.
Bars are 95 percent confidence intervals. P values are for the comparison with participants who did not have infarcts at base line or follow-up.
Discussion
We found that the presence of silent brain infarcts on MRI atbase line in the general population doubled the risk of dementia.People with silent infarcts had a steeper decline in cognitivefunction than those without silent infarcts, but this declinewas confined to people who had additional silent brain infarctsafter base line.
The strengths of this study are the large number of elderlyparticipants and its population-based design. Furthermore, wehad no losses to follow-up for the analyses of dementia. Notwithstandinggood-to-excellent intrareader agreement, we still may have incorrectlyidentified brain infarcts or misclassified infarcts as silentor symptomatic. However, because silent brain infarcts wereidentified and classified in a blinded fashion from data ondementia and neuropsychological tests, any misclassificationwould have resulted in an underestimation of the associations.
The dementia diagnoses in our study were clinical diagnoses.We intentionally refrained from analyzing subtypes of dementia,because a distinction based on clinical information is hardto make, especially in elderly people, in whom dementia oftenis a heterogeneous disorder. There is increasing evidence thatvascular factors may contribute to the development of Alzheimer'sdisease.23,24 After a stroke, dementia, including Alzheimer'sdisease, develops in approximately 30 percent of patients withsymptomatic infarcts.2,3,4 We found that silent brain infarctsincrease the risk of dementia, the majority of cases of whichin our study were of the Alzheimer's subtype. Furthermore, weshowed that a greater severity of periventricular white-matterlesions, also thought to result from small-vessel disease, wasassociated with an increased risk of dementia.
Our findings of a large number of new infarcts in the participantsin whom dementia developed and a steeper decline in cognitionin those with a new infarct support the notion that people withsilent brain infarcts are at high risk for additional infarcts,both silent and symptomatic,25 which may contribute to dementia.Perhaps an infarct in a brain already affected by Alzheimer'sdisease–related abnormalities further impairs cognition,leading to clinically evident dementia. This notion is supportedby autopsy findings showing that fewer plaques and tangles ledto clinical Alzheimer's disease in the presence of lacunar infarcts.5Alternatively, silent brain infarcts may trigger the developmentof senile plaques and neurofibrillary tangles or reflect cerebralvulnerability or a certain vascular risk profile that enhancesthe abnormalities associated with Alzheimer's disease. However,several clinicopathological studies found that patients withAlzheimer's disease who had infarcts had a similar amount ofplaques and tangles or even fewer than those without infarcts.26,27,28,29
We found that silent brain infarcts — those without relevantstroke symptoms — are associated with worse cognition,confirming the results of a cross-sectional study.9 Recently,we reported that the presence of periventricular white-matterlesions is associated with a steeper cognitive decline,30 andwe have now found that this is also true for silent brain infarcts.That the relation between infarcts and cognitive decline wasstronger for multiple infarcts than for single infarcts strengthensthese findings. Furthermore, we found that this decline in cognitivefunction was confined to persons with incident silent infarcts,which may suggest a stepwise decline after an infarct occurs.
The reason that we found no relation between a decline in thescore on the Mini–Mental State Examination and the presenceof silent brain infarcts is probably that this test, althoughuseful as a screening tool for dementia, is not a very sensitivemeans of detecting subtle changes in cognitive function. TheCardiovascular Health Study did find an association betweenevidence of infarcts on MRI and a decline in a modified Mini–MentalState Examination score, which comprised 100 rather than 30questions and examined a broader range of cognitive function.31Furthermore, we found that the decline in different cognitivedomains varied with the location of silent brain infarcts onMRI. Strategic infarcts in the thalamus, which is involved instorage and short-term memory,21,22 were associated with a worseperformance in memory tasks.
Our finding that in both participants with and those withoutsilent brain infarcts memory performance improved at the secondexamination may be explained by a learning effect.32 This learningeffect does not seem to have a major role in tests specificfor psychomotor speed. The presence of silent infarcts thatwere not in the thalamus resulted in a decline in psychomotorspeed. These infarcts probably interrupt various connectingfibers in the white matter that are involved in these psychomotortasks.
In conclusion, the presence of silent brain infarcts on MRIidentifies persons at increased risk for dementia, probablybecause these people continue to have additional brain infarcts,both silent and symptomatic, that decrease their cognitive function.
Supported by a grant from the Netherlands Heart Foundation (97.152)and the Netherlands Organization for Scientific Research (904.61.096).Dr. Breteler is a fellow of the Royal Netherlands Academy ofArts and Sciences.
We are indebted to the Regional Institute for Ambulatory MentalHealth Care and to the general practitioners of Rotterdam andZoetermeer for their collaboration.
Source Information
From the Departments of Epidemiology and Biostatistics (S.E.V., N.D.P., T.H., A.H., M.M.B.B.), and Neurology (S.E.V., N.D.P., T.H., P.J.K.), Erasmus Medical Center, Rotterdam, the Netherlands.
Address reprint requests to Dr. Breteler at the Department of Epidemiology and Biostatistics, Erasmus Medical Center, P.O. Box 1738, 3000 DR Rotterdam, the Netherlands, or at m.breteler{at}erasmusmc.nl.
References
Ott A, Breteler MMB, van Harskamp F, Stijnen T, Hofman A. Incidence and risk of dementia: the Rotterdam Study. Am J Epidemiol 1998;147:574-580. [Free Full Text]
Pohjasvaara T, Erkinjuntti T, Ylikoski R, Hietanen M, Vataja R, Kaste M. Clinical determinants of poststroke dementia. Stroke 1998;29:75-81. [Free Full Text]
Desmond DW, Moroney JT, Paik MC, et al. Frequency and clinical determinants of dementia after ischemic stroke. Neurology 2000;54:1124-1131. [Free Full Text]
Hénon H, Durieu I, Guerouaou D, Lebert F, Pasquier F, Leys D. Poststroke dementia: incidence and relationship to prestroke cognitive decline. Neurology 2001;57:1216-1222. [Free Full Text]
Snowdon DA, Greiner LH, Mortimer JA, Riley KP, Greiner PA, Markesbery WR. Brain infarction and the clinical expression of Alzheimer's disease: the Nun Study. JAMA 1997;277:813-817. [Free Full Text]
Neuropathology Group of the Medical Research Council Cognitive Function and Ageing Study (MRC CFAS). Pathological correlates of late-onset dementia in a multicentre, community-based population in England and Wales. Lancet 2001;357:169-175. [CrossRef][Web of Science][Medline]
Skoog I, Nilsson L, Palmertz B, Andreasson L-A, Svanborg A. A population-based study of dementia in 85-year-olds. N Engl J Med 1993;328:153-158. [Free Full Text]
Barber R, Scheltens P, Gholkar A, et al. White matter lesions on magnetic resonance imaging in dementia with Lewy bodies, Alzheimer's disease, vascular dementia, and normal aging. J Neurol Neurosurg Psychiatry 1999;67:66-72. [Free Full Text]
Longstreth WT Jr, Bernick C, Manolio TA, Bryan N, Jungreis CA, Price TR. Lacunar infarcts defined by magnetic resonance imaging of 3660 elderly people: the Cardiovascular Health Study. Arch Neurol 1998;55:1217-1225. [Free Full Text]
Howard G, Wagenknecht LE, Cai J, Cooper L, Kraut MA, Toole JF. Cigarette smoking and other risk factors for silent cerebral infarction in the general population. Stroke 1998;29:913-917. [Free Full Text]
Vermeer SE, Koudstaal PJ, Oudkerk M, Hofman A, Breteler MMB. Prevalence and risk factors of silent brain infarcts in the population-based Rotterdam Scan Study. Stroke 2002;33:21-25. [Free Full Text]
de Leeuw FE, de Groot JC, Achten E, et al. Prevalence of cerebral white matter lesions in elderly people: a population based magnetic resonance imaging study: the Rotterdam Scan Study. J Neurol Neurosurg Psychiatry 2001;70:9-14. [Free Full Text]
Hofman A, van Laar A, Klein F, Valkenburg HA. Coffee and cholesterol. N Engl J Med 1983;309:1248-1249. [Medline]
Hofman A, Ott A, Breteler MM, et al. Atherosclerosis, apolipoprotein E, and prevalence of dementia and Alzheimer's disease in the Rotterdam Study. Lancet 1997;349:151-154. [CrossRef][Web of Science][Medline]
de Groot JC, de Leeuw FE, Oudkerk M, et al. Cerebral white matter lesions and cognitive function: the Rotterdam Scan Study. Ann Neurol 2000;47:145-151. [CrossRef][Web of Science][Medline]
Vermeer SE, van Dijk EJ, Koudstaal PJ, et al. Homocysteine, silent brain infarcts, and white matter lesions: the Rotterdam Scan Study. Ann Neurol 2002;51:285-289. [CrossRef][Web of Science][Medline]
den Heijer T, Oudkerk M, Launer LJ, van Duijn CM, Hofman A, Breteler MMB. Hippocampal, amygdalar, and global brain atrophy in different apolipoprotein E genotypes. Neurology 2002;59:746-748. [Free Full Text]
Diagnostic and statistical manual of mental disorders, 3rd ed. rev.: DSM-III-R. Washington, D.C.: American Psychiatric Association, 1987.
McKahnn G, Drachman D, Folstein M, Katzman R, Price D, Stadlan EM. Clinical diagnosis of Alzheimer's disease: report of the NINCDS-ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer's Disease. Neurology 1984;34:939-944. [Free Full Text]
Roman GC, Tatemichi TK, Erkinjuntti T, et al. Vascular dementia: diagnostic criteria for research studies: report of the NINDS-AIREN International Workshop. Neurology 1993;43:250-260. [Free Full Text]
Bogousslavsky J, Regli F, Uske A. Thalamic infarcts: clinical syndromes, etiology, and prognosis. Neurology 1988;38:837-848. [Erratum, Neurology 1988;38:1335.] [Free Full Text]
Tatemichi TK, Steinke W, Duncan C, et al. Paramedian thalamopeduncular infarction: clinical syndromes and magnetic resonance imaging. Ann Neurol 1992;32:162-171. [CrossRef][Web of Science][Medline]
Sparks DL, Scheff SW, Liu H, Landers TM, Coyne CM, Hunsaker JC III. Increased incidence of neurofibrillary tangles (NFT) in non-demented individuals with hypertension. J Neurol Sci 1995;131:162-169. [CrossRef][Web of Science][Medline]
Breteler MMB. Vascular risk factors for Alzheimer's disease: an epidemiologic perspective. Neurobiol Aging 2000;21:153-160. [Web of Science][Medline]
Bernick C, Kuller L, Dulberg C, et al. Silent MRI infarcts and the risk of future stroke: the Cardiovascular Health Study. Neurology 2001;57:1222-1229. [Free Full Text]
Heyman A, Fillenbaum GG, Welsh-Bohmer KA, et al. Cerebral infarcts in patients with autopsy-proven Alzheimer's disease: CERAD, part XVIII. Neurology 1998;51:159-162. [Erratum, Neurology 1998;51:1809.] [Free Full Text]
Berg L, McKeel DW Jr, Miller JP, et al. Clinicopathologic studies in cognitively healthy aging and Alzheimer's disease: relation of histologic markers to dementia severity, age, sex, and apolipoprotein E genotype. Arch Neurol 1998;55:326-335. [Free Full Text]
Petrovitch H, White LR, Izmirilian G, et al. Midlife blood pressure and neuritic plaques, neurofibrillary tangles, and brain weight at death: the HAAS: Honolulu-Asia aging Study. Neurobiol Aging 2000;21:57-62. [Web of Science][Medline]
de la Monte SM, Lu BX, Sohn YK, et al. Aberrant expression of nitric oxide synthase III in Alzheimer's disease: relevance to cerebral vasculopathy and neurodegeneration. Neurobiol Aging 2000;21:309-319. [CrossRef][Web of Science][Medline]
de Groot JC, de Leeuw FE, Oudkerk M, et al. Periventricular cerebral white matter lesions predict rate of cognitive decline. Ann Neurol 2002;52:335-341. [CrossRef][Web of Science][Medline]
Kuller LH, Shemanski L, Manolio T, et al. Relationship between ApoE, MRI findings, and cognitive function in the Cardiovascular Health Study. Stroke 1998;29:388-398. [Free Full Text]
Small SA, Stern Y, Tang M, Mayeux R. Selective decline in memory function among healthy elderly. Neurology 1999;52:1392-1396. [Free Full Text]
Reitz, C., Brickman, A. M., Brown, T. R., Manly, J., DeCarli, C., Small, S. A., Mayeux, R.
(2009). Linking Hippocampal Structure and Function to Memory Performance in an Aging Population. Arch Neurol
66: 1385-1392
[Abstract][Full Text]
Khatri, M., Nickolas, T., Moon, Y. P., Paik, M. C., Rundek, T., Elkind, M. S. V., Sacco, R. L., Wright, C. B.
(2009). CKD Associates with Cognitive Decline. J. Am. Soc. Nephrol.
20: 2427-2432
[Abstract][Full Text]
Santos, M., Gold, G., Kovari, E., Herrmann, F. R., Bozikas, V. P., Bouras, C., Giannakopoulos, P.
(2009). Differential Impact of Lacunes and Microvascular Lesions on Poststroke Depression. Stroke
40: 3557-3562
[Abstract][Full Text]
Wright, C. B., Moon, Y., Paik, M. C., Brown, T. R., Rabbani, L., Yoshita, M., DeCarli, C., Sacco, R., Elkind, M. S.V.
(2009). Inflammatory Biomarkers of Vascular Risk as Correlates of Leukoariosis. Stroke
40: 3466-3471
[Abstract][Full Text]
Homma, S., Sloop, G. D., Zieske, A. W.
(2009). The Effect of Age and Other Atherosclerotic Risk Factors on Carotid Artery Blood Velocity in Individuals Ranging From Young Adults to Centenarians. ANGIOLOGY
60: 637-643
[Abstract]
Okereke, O. I., Xia, W., Selkoe, D. J., Grodstein, F.
(2009). Ten-Year Change in Plasma Amyloid {beta} Levels and Late-Life Cognitive Decline. Arch Neurol
66: 1247-1253
[Abstract][Full Text]
Lesage, S. R., Mosley, T. H., Wong, T. Y., Szklo, M., Knopman, D., Catellier, D. J., Cole, S. R., Klein, R., Coresh, J., Coker, L. H., Sharrett, A. R.
(2009). Retinal microvascular abnormalities and cognitive decline: The ARIC 14-year follow-up study. Neurology
73: 862-868
[Abstract][Full Text]
Pikula, A., Boger, R. H., Beiser, A. S., Maas, R., DeCarli, C., Schwedhelm, E., Himali, J. J., Schulze, F., Au, R., Kelly-Hayes, M., Kase, C. S., Vasan, R. S., Wolf, P. A., Seshadri, S.
(2009). Association of Plasma ADMA Levels With MRI Markers of Vascular Brain Injury: Framingham Offspring Study. Stroke
40: 2959-2964
[Abstract][Full Text]
Segura, B., Jurado, M. A., Freixenet, N., Falcon, C., Junque, C., Arboix, A.
(2009). Microstructural white matter changes in metabolic syndrome: A diffusion tensor imaging study. Neurology
73: 438-444
[Abstract][Full Text]
Luchsinger, J. A., Brickman, A. M., Reitz, C., Cho, S. J., Schupf, N., Manly, J. J., Tang, M. X., Small, S. A., Mayeux, R., DeCarli, C., Brown, T. R.
(2009). Subclinical cerebrovascular disease in mild cognitive impairment. Neurology
73: 450-456
[Abstract][Full Text]
Chen, X., Wen, W., Anstey, K. J., Sachdev, P. S.
(2009). Prevalence, incidence, and risk factors of lacunar infarcts in a community sample. Neurology
73: 266-272
[Abstract][Full Text]
Kirchhof, P., Bax, J., Blomstrom-Lundquist, C., Calkins, H., Camm, A. J., Cappato, R., Cosio, F., Crijns, H., Diener, H.-C., Goette, A., Israel, C. W., Kuck, K.-H., Lip, G. Y.H., Nattel, S., Page, R. L., Ravens, U., Schotten, U., Steinbeck, G., Vardas, P., Waldo, A., Wegscheider, K., Willems, S., Breithardt, G.
(2009). Early and comprehensive management of atrial fibrillation: Proceedings from the 2nd AFNET/EHRA consensus conference on atrial fibrillation entitled 'research perspectives in atrial fibrillation'. Europace
11: 860-885
[Full Text]
Buyck, J.-F., Dufouil, C., Mazoyer, B., Maillard, P., Ducimetiere, P., Alperovitch, A., Bousser, M.-G., Kurth, T., Tzourio, C.
(2009). Cerebral White Matter Lesions Are Associated With the Risk of Stroke But Not With Other Vascular Events: The 3-City Dijon Study. Stroke
40: 2327-2331
[Abstract][Full Text]
Wilcock, D. M., Gharkholonarehe, N., Van Nostrand, W. E., Davis, J., Vitek, M. P., Colton, C. A.
(2009). Amyloid Reduction by Amyloid-{beta} Vaccination Also Reduces Mouse Tau Pathology and Protects from Neuron Loss in Two Mouse Models of Alzheimer's Disease. J. Neurosci.
29: 7957-7965
[Abstract][Full Text]
Putaala, J., Kurkinen, M., Tarvos, V., Salonen, O., Kaste, M., Tatlisumak, T.
(2009). Silent brain infarcts and leukoaraiosis in young adults with first-ever ischemic stroke. Neurology
72: 1823-1829
[Abstract][Full Text]
Benisty, S, Gouw, A A, Porcher, R, Madureira, S, Hernandez, K, Poggesi, A, van der Flier, W M, Van Straaten, E C W, Verdelho, A, Ferro, J, Pantoni, L, Inzitari, D, Barkhof, F, Fazekas, F, Chabriat, H, on behalf of the LADIS Study group,
(2009). Location of lacunar infarcts correlates with cognition in a sample of non-disabled subjects with age-related white-matter changes: the LADIS study. J. Neurol. Neurosurg. Psychiatry
80: 478-483
[Abstract][Full Text]
Thompson, C. S., Hakim, A. M.
(2009). Living Beyond Our Physiological Means: Small Vessel Disease of the Brain Is an Expression of a Systemic Failure in Arteriolar Function: A Unifying Hypothesis. Stroke
40: e322-e330
[Abstract][Full Text]
Romero, J. R., Beiser, A., Seshadri, S., Benjamin, E. J., Polak, J. F., Vasan, R. S., Au, R., DeCarli, C., Wolf, P. A.
(2009). Carotid Artery Atherosclerosis, MRI Indices of Brain Ischemia, Aging, and Cognitive Impairment: The Framingham Study. Stroke
40: 1590-1596
[Abstract][Full Text]
Kantarci, K., Weigand, S. D., Przybelski, S. A., Shiung, M. M., Whitwell, J. L., Negash, S., Knopman, D. S., Boeve, B. F., O'Brien, P. C., Petersen, R. C., Jack, C. R. Jr
(2009). Risk of dementia in MCI: Combined effect of cerebrovascular disease, volumetric MRI, and 1H MRS. Neurology
72: 1519-1525
[Abstract][Full Text]
Minati, L., Edginton, T., Grazia Bruzzone, M., Giaccone, G.
(2009). Reviews: Current Concepts in Alzheimer's Disease: A Multidisciplinary Review. AM J ALZHEIMERS DIS OTHER DEMEN
24: 95-121
[Abstract]
Vitaliano, P. P., Zhang, J., Young, H. M., Caswell, L. W., Scanlan, J. M., Echeverria, D.
(2009). Depressed Mood Mediates Decline in Cognitive Processing Speed in Caregivers. The Gerontologist
0: gnp004v4-gnp004
[Abstract][Full Text]
Staekenborg, S. S., Koedam, E. L.G.E., Henneman, W. J.P., Stokman, P., Barkhof, F., Scheltens, P., van der Flier, W. M.
(2009). Progression of Mild Cognitive Impairment to Dementia: Contribution of Cerebrovascular Disease Compared With Medial Temporal Lobe Atrophy. Stroke
40: 1269-1274
[Abstract][Full Text]
Saczynski, J. S., Sigurdsson, S., Jonsdottir, M. K., Eiriksdottir, G., Jonsson, P. V., Garcia, M. E., Kjartansson, O., Lopez, O., van Buchem, M. A., Gudnason, V., Launer, L. J.
(2009). Cerebral Infarcts and Cognitive Performance: Importance of Location and Number of Infarcts. Stroke
40: 677-682
[Abstract][Full Text]
Baune, B. T.
(2009). The Puzzle of Predicting the Impact of Brain Infarcts on Cognitive Impairment in the Aging Brain. Stroke
40: 667-669
[Full Text]
Rosenberg, G. A.
(2009). Inflammation and White Matter Damage in Vascular Cognitive Impairment. Stroke
40: S20-S23
[Abstract][Full Text]
Black, S., Gao, F., Bilbao, J.
(2009). Understanding White Matter Disease: Imaging-Pathological Correlations in Vascular Cognitive Impairment. Stroke
40: S48-S52
[Abstract][Full Text]
Rafnsson, S. B, Deary, I. J, Fowkes, F.
(2009). Peripheral arterial disease and cognitive function. Vasc Med
14: 51-61
[Abstract]
Friedlander, A. H., Yoshikawa, T. T., Chang, D. S., Feliciano, Z., Scully, C.
(2009). Atrial Fibrillation: Pathogenesis, Medical-Surgical Management and Dental Implications. Journal of the American Dental Association
140: 167-177
[Abstract][Full Text]
Henneman, W. J.P., Sluimer, J. D., Cordonnier, C., Baak, M. M.E., Scheltens, P., Barkhof, F., van der Flier, W. M.
(2009). MRI Biomarkers of Vascular Damage and Atrophy Predicting Mortality in a Memory Clinic Population. Stroke
40: 492-498
[Abstract][Full Text]
Kissela, B., Lindsell, C. J., Kleindorfer, D., Alwell, K., Moomaw, C. J., Woo, D., Flaherty, M. L., Air, E., Broderick, J., Tsevat, J.
(2009). Clinical Prediction of Functional Outcome After Ischemic Stroke: The Surprising Importance of Periventricular White Matter Disease and Race. Stroke
40: 530-536
[Abstract][Full Text]
Viswanathan, A., Rocca, W. A., Tzourio, C.
(2009). Vascular risk factors and dementia: How to move forward?. Neurology
72: 368-374
[Abstract][Full Text]
Baune, B. T., Roesler, A., Knecht, S., Berger, K.
(2009). Single and Combined Effects of Cerebral White Matter Lesions and Lacunar Infarctions on Cognitive Function in an Elderly Population. J Gerontol A Biol Sci Med Sci
0: gln004v2-gln004
[Abstract][Full Text]
Kobayashi, M., Hirawa, N., Yatsu, K., Kobayashi, Y., Yamamoto, Y., Saka, S., Andoh, D., Toya, Y., Yasuda, G., Umemura, S.
(2009). Relationship between silent brain infarction and chronic kidney disease. Nephrol Dial Transplant
24: 201-207
[Abstract][Full Text]
Han, B. H., Zhou, M.-l., Abousaleh, F., Brendza, R. P., Dietrich, H. H., Koenigsknecht-Talboo, J., Cirrito, J. R., Milner, E., Holtzman, D. M., Zipfel, G. J.
(2008). Cerebrovascular Dysfunction in Amyloid Precursor Protein Transgenic Mice: Contribution of Soluble and Insoluble Amyloid-{beta} Peptide, Partial Restoration via {gamma}-Secretase Inhibition. J. Neurosci.
28: 13542-13550
[Abstract][Full Text]
Kantarci, K., Petersen, R. C., Przybelski, S. A., Weigand, S. D., Shiung, M. M., Whitwell, J. L., Negash, S., Ivnik, R. J., Boeve, B. F., Knopman, D. S., Smith, G. E., Jack, C. R. Jr
(2008). Hippocampal Volumes, Proton Magnetic Resonance Spectroscopy Metabolites, and Cerebrovascular Disease in Mild Cognitive Impairment Subtypes. Arch Neurol
65: 1621-1628
[Abstract][Full Text]
T. Cuenco, K., Lunetta, K. L., Baldwin, C. T., McKee, A. C., Guo, J., Cupples, L. A., Green, R. C., St. George-Hyslop, P. H., Chui, H., DeCarli, C., Farrer, L. A., for the MIRAGE Study Group,
(2008). Association of Distinct Variants in SORL1 With Cerebrovascular and Neurodegenerative Changes Related to Alzheimer Disease. Arch Neurol
65: 1640-1648
[Abstract][Full Text]
Mitchell, G. F.
(2008). Effects of central arterial aging on the structure and function of the peripheral vasculature: implications for end-organ damage. J. Appl. Physiol.
105: 1652-1660
[Abstract][Full Text]
Das, R. R., Seshadri, S., Beiser, A. S., Kelly-Hayes, M., Au, R., Himali, J. J., Kase, C. S., Benjamin, E. J., Polak, J. F., O'Donnell, C. J., Yoshita, M., D'Agostino, R. B. Sr, DeCarli, C., Wolf, P. A.
(2008). Prevalence and Correlates of Silent Cerebral Infarcts in the Framingham Offspring Study. Stroke
39: 2929-2935
[Abstract][Full Text]
De Rango, P., Caso, V., Leys, D., Paciaroni, M., Lenti, M., Cao, P.
(2008). The Role of Carotid Artery Stenting and Carotid Endarterectomy in Cognitive Performance: A Systematic Review. Stroke
39: 3116-3127
[Abstract][Full Text]
Schofer, J., Arendt, M., Tubler, T., Sandstede, J., Schluter, M.
(2008). Late Cerebral Embolization After Emboli-Protected Carotid Artery Stenting Assessed by Sequential Diffusion-Weighted Magnetic Resonance Imaging. J Am Coll Cardiol Intv
1: 571-577
[Abstract][Full Text]
van Dijk, E. J., Prins, N. D., Vrooman, H. A., Hofman, A., Koudstaal, P. J., Breteler, M. M.B.
(2008). Progression of Cerebral Small Vessel Disease in Relation to Risk Factors and Cognitive Consequences: Rotterdam Scan Study. Stroke
39: 2712-2719
[Abstract][Full Text]
Goette, A., Braun-Dullaeus, R. C.
(2008). Atrial fibrillation is associated with impaired cognitive function and hippocampal atrophy: silent cerebral ischaemia vs. Alzheimer's disease?. Eur Heart J
29: 2067-2069
[Full Text]
van Oijen, M, Cheung, E Y L, Geluk, C E M, Hofman, A, Koudstaal, P J, Breteler, M M B, de Maat, M P
(2008). Haplotypes of the fibrinogen gene and cerebral small vessel disease: the Rotterdam scan study. J. Neurol. Neurosurg. Psychiatry
79: 799-803
[Abstract][Full Text]
Bombois, S., Debette, S., Bruandet, A., Delbeuck, X., Delmaire, C., Leys, D., Pasquier, F.
(2008). Vascular Subcortical Hyperintensities Predict Conversion to Vascular and Mixed Dementia in MCI Patients. Stroke
39: 2046-2051
[Abstract][Full Text]
Park, K, Yasuda, N, Toyonaga, S, Tsubosaki, E, Nakabayashi, H, Shimizu, K
(2008). Significant associations of metabolic syndrome and its components with silent lacunar infarction in middle aged subjects. J. Neurol. Neurosurg. Psychiatry
79: 719-721
[Abstract][Full Text]
Guo, S., Kim, W. J., Lok, J., Lee, S.-R., Besancon, E., Luo, B.-H., Stins, M. F., Wang, X., Dedhar, S., Lo, E. H.
(2008). Neuroprotection via matrix-trophic coupling between cerebral endothelial cells and neurons. Proc. Natl. Acad. Sci. USA
105: 7582-7587
[Abstract][Full Text]
Cheung, W. D., Hart, G. W.
(2008). AMP-activated Protein Kinase and p38 MAPK Activate O-GlcNAcylation of Neuronal Proteins during Glucose Deprivation. J. Biol. Chem.
283: 13009-13020
[Abstract][Full Text]
Sun, X., Steffens, D. C., Au, R., Folstein, M., Summergrad, P., Yee, J., Rosenberg, I., Mwamburi, D. M., Qiu, W. Q.
(2008). Amyloid-Associated Depression: A Prodromal Depression of Alzheimer Disease?. Arch Gen Psychiatry
65: 542-550
[Abstract][Full Text]
Geerlings, M. I., den Heijer, T., Koudstaal, P. J., Hofman, A., Breteler, M.M.B.
(2008). History of depression, depressive symptoms, and medial temporal lobe atrophy and the risk of Alzheimer disease. Neurology
70: 1258-1264
[Abstract][Full Text]
Wright, C. B., Festa, J. R., Paik, M. C., Schmiedigen, A., Brown, T. R., Yoshita, M., DeCarli, C., Sacco, R., Stern, Y.
(2008). White Matter Hyperintensities and Subclinical Infarction: Associations With Psychomotor Speed and Cognitive Flexibility. Stroke
39: 800-805
[Abstract][Full Text]
Benisty, S., Hernandez, K., Viswanathan, A., Reyes, S., Kurtz, A., O'Sullivan, M., Bousser, M.-G., Dichgans, M., Chabriat, H.
(2008). Diagnostic Criteria of Vascular Dementia in CADASIL. Stroke
39: 838-844
[Abstract][Full Text]
Longstreth, W. T. Jr, Vermeer, S. E.
(2008). The growing specter of MRI-defined brain infarcts. Neurology
70: 416-417
[Full Text]
Prabhakaran, S., Wright, C. B., Yoshita, M., Delapaz, R., Brown, T., DeCarli, C., Sacco, R. L.
(2008). Prevalence and determinants of subclinical brain infarction: The Northern Manhattan Study. Neurology
70: 425-430
[Abstract][Full Text]
Smith, E. E., Egorova, S., Blacker, D., Killiany, R. J., Muzikansky, A., Dickerson, B. C., Tanzi, R. E., Albert, M. S., Greenberg, S. M., Guttmann, C. R. G.
(2008). Magnetic Resonance Imaging White Matter Hyperintensities and Brain Volume in the Prediction of Mild Cognitive Impairment and Dementia. Arch Neurol
65: 94-100
[Abstract][Full Text]
O'Sullivan, M.
(2008). Prestroke Cognitive Function and Cerebrovascular Disease: If They Interact, It May Not Be Through Symptomatic Stroke. Stroke
39: 3-4
[Full Text]
Purandare, N, Oude Voshaar, R C, McCollum, C, Jackson, A, Burns, A
(2008). Paradoxical embolisation and cerebral white matter lesions in dementia. Br. J. Radiol.
81: 30-34
[Abstract][Full Text]
Reitz, C., Bos, M. J., Hofman, A., Koudstaal, P. J., Breteler, M. M.B.
(2008). Prestroke Cognitive Performance, Incident Stroke, and Risk of Dementia: The Rotterdam Study. Stroke
39: 36-41
[Abstract][Full Text]
Reitz, C., Tang, M.-X., Manly, J., Mayeux, R., Luchsinger, J. A.
(2007). Hypertension and the Risk of Mild Cognitive Impairment. Arch Neurol
64: 1734-1740
[Abstract][Full Text]
Hakim, A. M.
(2007). Vascular Disease: The Tsunami of Health Care. Stroke
38: 3296-3301
[Abstract][Full Text]
Khatri, M., Wright, C. B., Nickolas, T. L., Yoshita, M., Paik, M. C., Kranwinkel, G., Sacco, R. L., DeCarli, C.
(2007). Chronic Kidney Disease Is Associated With White Matter Hyperintensity Volume: The Northern Manhattan Study (NOMAS). Stroke
38: 3121-3126
[Abstract][Full Text]
KNOPMAN, D S
(2007). Cerebrovascular disease and dementia. Br. J. Radiol.
80: S121-S127
[Abstract][Full Text]
Newman, G. C., Bang, H., Hussain, S. I., Toole, J. F.
(2007). Association of diabetes, homocysteine, and HDL with cognition and disability after stroke. Neurology
69: 2054-2062
[Abstract][Full Text]
Kirchhof, P., Auricchio, A., Bax, J., Crijns, H., Camm, J., Diener, H.-C., Goette, A., Hindricks, G., Hohnloser, S., Kappenberger, L., Kuck, K.-H., Lip, G. Y.H., Olsson, B., Meinertz, T., Priori, S., Ravens, U., Steinbeck, G., Svernhage, E., Tijssen, J., Vincent, A., Breithardt, G.
(2007). Outcome parameters for trials in atrial fibrillation: executive summary: Recommendations from a consensus conference organized by the German Atrial Fibrillation Competence NETwork (AFNET) and the European Heart Rhythm Association (EHRA). Eur Heart J
28: 2803-2817
[Abstract][Full Text]
O'Rourke, M. F.
(2007). Arterial aging: pathophysiological principles. Vasc Med
12: 329-341
[Abstract]
Vernooij, M. W., Ikram, M. A., Tanghe, H. L., Vincent, A. J.P.E., Hofman, A., Krestin, G. P., Niessen, W. J., Breteler, M. M.B., van der Lugt, A.
(2007). Incidental Findings on Brain MRI in the General Population. NEJM
357: 1821-1828
[Abstract][Full Text]
Gold, G., Giannakopoulos, P., Herrmann, F. R, Bouras, C., Kovari, E.
(2007). Identification of Alzheimer and vascular lesion thresholds for mixed dementia. Brain
130: 2830-2836
[Abstract][Full Text]
Kirchhof, P., Auricchio, A., Bax, J., Crijns, H., Camm, J., Diener, H.-C., Goette, A., Hindricks, G., Hohnloser, S., Kappenberger, L., Kuck, K.-H., Lip, G. Y.H., Olsson, B., Meinertz, T., Priori, S., Ravens, U., Steinbeck, G., Svernhage, E., Tijssen, J., Vincent, A., Breithardt, G.
(2007). Outcome parameters for trials in atrial fibrillation: Recommendations from a consensus conference organized by the German Atrial Fibrillation Competence NETwork and the European Heart Rhythm Association. Europace
9: 1006-1023
[Abstract][Full Text]
Debette, S., Bombois, S., Bruandet, A., Delbeuck, X., Lepoittevin, S., Delmaire, C., Leys, D., Pasquier, F.
(2007). Subcortical Hyperintensities Are Associated With Cognitive Decline in Patients With Mild Cognitive Impairment. Stroke
38: 2924-2930
[Abstract][Full Text]
Howard, G., Safford, M. M., Meschia, J. F., Moy, C. S., Howard, V. J., Pulley, L., Gomez, C. R., Crowther, M.
(2007). Stroke Symptoms in Individuals Reporting No Prior Stroke or Transient Ischemic Attack Are Associated With a Decrease in Indices of Mental and Physical Functioning. Stroke
38: 2446-2452
[Abstract][Full Text]
Miyasaka, Y., Barnes, M. E., Petersen, R. C., Cha, S. S., Bailey, K. R., Gersh, B. J., Casaclang-Verzosa, G., Abhayaratna, W. P., Seward, J. B., Iwasaka, T., Tsang, T. S.M.
(2007). Risk of dementia in stroke-free patients diagnosed with atrial fibrillation: data from a community-based cohort. Eur Heart J
28: 1962-1967
[Abstract][Full Text]
Viswanathan, A., Gschwendtner, A., Guichard, J. -P., Buffon, F., Cumurciuc, R., O'Sullivan, M., Holtmannspotter, M., Pachai, C., Bousser, M. -G., Dichgans, M., Chabriat, H.
(2007). Lacunar lesions are independently associated with disability and cognitive impairment in CADASIL. Neurology
69: 172-179
[Abstract][Full Text]
O'Rourke, M. F., Hashimoto, J.
(2007). Mechanical Factors in Arterial Aging: A Clinical Perspective. J Am Coll Cardiol
50: 1-13
[Abstract][Full Text]
Baker, M. L., Marino Larsen, E. K., Kuller, L. H., Klein, R., Klein, B. E.K., Siscovick, D. S., Bernick, C., Manolio, T. A., Wong, T. Y.
(2007). Retinal Microvascular Signs, Cognitive Function, and Dementia in Older Persons: The Cardiovascular Health Study. Stroke
38: 2041-2047
[Abstract][Full Text]
Authors/Task Force Members:, , Mancia, G., De Backer, G., Dominiczak, A., Cifkova, R., Fagard, R., Germano, G., Grassi, G., Heagerty, A. M., Kjeldsen, S. E., Laurent, S., Narkiewicz, K., Ruilope, L., Rynkiewicz, A., Schmieder, R. E., Struijker Boudier, H. A.J., Zanchetti, A., ESC Committee for Practice Guidelines (CPG):, , Vahanian, A., Camm, J., De Caterina, R., Dean, V., Dickstein, K., Filippatos, G., Funck-Brentano, C., Hellemans, I., Kristensen, S. D., McGregor, K., Sechtem, U., Silber, S., Tendera, M., Widimsky, P., Zamorano, J. L., ESH Scientific Council:, , Kjeldsen, S. E., Erdine, S., Narkiewicz, K., Kiowski, W., Agabiti-Rosei, E., Ambrosioni, E., Cifkova, R., Dominiczak, A., Fagard, R., Heagerty, A. M., Laurent, S., Lindholm, L. H., Mancia, G., Manolis, A., Nilsson, P. M., Redon, J., Schmieder, R. E., Struijker-Boudier, H. A.J., Viigimaa, M., Document Reviewers:, , Filippatos, G., Adamopoulos, S., Agabiti-Rosei, E., Ambrosioni, E., Bertomeu, V., Clement, D., Erdine, S., Farsang, C., Gaita, D., Kiowski, W., Lip, G., Mallion, J.-M., Manolis, A. J., Nilsson, P. M., O'Brien, E., Ponikowski, P., Redon, J., Ruschitzka, F., Tamargo, J., van Zwieten, P., Viigimaa, M., Waeber, B., Williams, B., Zamorano, J. L.
(2007). 2007 Guidelines for the Management of Arterial Hypertension: The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). Eur Heart J
0: ehm236v1-75
[Full Text]
Jouvent, E., Viswanathan, A., Mangin, J.-F., O'Sullivan, M., Guichard, J.-P., Gschwendtner, A., Cumurciuc, R., Buffon, F., Peters, N., Pachai, C., Bousser, M.-G., Dichgans, M., Chabriat, H.
(2007). Brain Atrophy Is Related to Lacunar Lesions and Tissue Microstructural Changes in CADASIL. Stroke
38: 1786-1790
[Abstract][Full Text]
Sacco, R. L.
(2007). The 2006 William Feinberg Lecture: Shifting the Paradigm From Stroke to Global Vascular Risk Estimation. Stroke
38: 1980-1987
[Abstract][Full Text]
Schneider, J. A.
(2007). Brain Microbleeds and Cognitive Function. Stroke
38: 1730-1731
[Full Text]
Panza, F., Capurso, C., D'Introno, A., Colacicco, A. M., Chirico, M., Capurso, A., Solfrizzi, V., O'Brien, R.
(2007). EFFECT OF A CLINICAL STROKE ON THE RISK OF DEMENTIA IN A PROSPECTIVE COHORT. Neurology
68: 1748-1749
[Full Text]
Cook, D. J., Huston, J. III, Trenerry, M. R., Brown, R. D. Jr, Zehr, K. J., Sundt, T. M. III
(2007). Postcardiac Surgical Cognitive Impairment in the Aged Using Diffusion-Weighted Magnetic Resonance Imaging. Ann. Thorac. Surg.
83: 1389-1395
[Abstract][Full Text]
Luchsinger, J. A., Reitz, C., Patel, B., Tang, M.-X., Manly, J. J., Mayeux, R.
(2007). Relation of Diabetes to Mild Cognitive Impairment. Arch Neurol
64: 570-575
[Abstract][Full Text]
Aono, Y., Ohkubo, T., Kikuya, M., Hara, A., Kondo, T., Obara, T., Metoki, H., Inoue, R., Asayama, K., Shintani, Y., Hashimoto, J., Totsune, K., Hoshi, H., Satoh, H., Izumi, S.-I., Imai, Y.
(2007). Plasma Fibrinogen, Ambulatory Blood Pressure, and Silent Cerebrovascular Lesions: The Ohasama Study. Arterioscler. Thromb. Vasc. Bio.
27: 963-968
[Abstract][Full Text]
=0.80). 
4 allele and noncarriers. The exclusion of participants who used aspirin or oral anticoagulants at base line did not materially change the results. Nineteen of the 30 participants in whom dementia developed underwent a second cerebral MRI or computed tomographic scan; a symptomatic infarct was found in 3 (16 percent) and a new silent brain infarct was found in 4 (21 percent). This rate was higher than that among the 618 participants without dementia at follow-up, of whom 8 (1 percent) had a symptomatic brain infarct and 71 (11 percent) a silent brain infarct on the second MRI scan. 
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