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  • Ovid Technologies (Wolters Kluwer Health)  (32)
  • Vernooij, Meike W.  (32)
  • van der Lugt, Aad  (32)
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  • Ovid Technologies (Wolters Kluwer Health)  (32)
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  • 1
    Online Resource
    Online Resource
    Genetic and lifestyle risk factors for MRI-defined brain infarcts in a population-based setting
    Ovid Technologies (Wolters Kluwer Health) ; 2019
    In:  Neurology Vol. 92, No. 5 ( 2019-01-29)
    Details
    In: Neurology, Ovid Technologies (Wolters Kluwer Health), Vol. 92, No. 5 ( 2019-01-29)
    Type of Medium: Online Resource
    ISSN: 0028-3878 , 1526-632X
    URL: Article
    DOI: 10.1212/WNL.0000000000006851
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2019
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  • 2
    Online Resource
    Online Resource
    Multiethnic Genome-Wide Association Study of Cerebral White Matter Hyperintensities on MRI
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Circulation: Cardiovascular Genetics Vol. 8, No. 2 ( 2015-04), p. 398-409
    Details
    In: Circulation: Cardiovascular Genetics, Ovid Technologies (Wolters Kluwer Health), Vol. 8, No. 2 ( 2015-04), p. 398-409
    Abstract: The burden of cerebral white matter hyperintensities (WMH) is associated with an increased risk of stroke, dementia, and death. WMH are highly heritable, but their genetic underpinnings are incompletely characterized. To identify novel genetic variants influencing WMH burden, we conducted a meta-analysis of multiethnic genome-wide association studies. Methods and Results— We included 21 079 middle-aged to elderly individuals from 29 population-based cohorts, who were free of dementia and stroke and were of European (n=17 936), African (n=1943), Hispanic (n=795), and Asian (n=405) descent. WMH burden was quantified on MRI either by a validated automated segmentation method or a validated visual grading scale. Genotype data in each study were imputed to the 1000 Genomes reference. Within each ethnic group, we investigated the relationship between each single-nucleotide polymorphism and WMH burden using a linear regression model adjusted for age, sex, intracranial volume, and principal components of ancestry. A meta-analysis was conducted for each ethnicity separately and for the combined sample. In the European descent samples, we confirmed a previously known locus on chr17q25 ( P =2.7×10 −19 ) and identified novel loci on chr10q24 ( P =1.6×10 −9 ) and chr2p21 ( P =4.4×10 −8 ). In the multiethnic meta-analysis, we identified 2 additional loci, on chr1q22 ( P =2.0×10 −8 ) and chr2p16 ( P =1.5×10 −8 ). The novel loci contained genes that have been implicated in Alzheimer disease (chr2p21 and chr10q24), intracerebral hemorrhage (chr1q22), neuroinflammatory diseases (chr2p21), and glioma (chr10q24 and chr2p16). Conclusions— We identified 4 novel genetic loci that implicate inflammatory and glial proliferative pathways in the development of WMH in addition to previously proposed ischemic mechanisms.
    Type of Medium: Online Resource
    ISSN: 1942-325X , 1942-3268
    URL: Article
    DOI: 10.1161/CIRCGENETICS.114.000858
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 2927603-2
    detail.hit.zdb_id: 2457085-0
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  • 3
    Online Resource
    Online Resource
    Structural disconnectivity and the risk of dementia in the general population
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Neurology Vol. 95, No. 11 ( 2020-09-15), p. e1528-e1537
    Details
    In: Neurology, Ovid Technologies (Wolters Kluwer Health), Vol. 95, No. 11 ( 2020-09-15), p. e1528-e1537
    Abstract: The disconnectivity hypothesis postulates that partial loss of connecting white matter fibers between brain regions contributes to the development of dementia. Using diffusion MRI to quantify global and tract-specific white matter microstructural integrity, we tested this hypothesis in a longitudinal population-based study. Methods Global and tract-specific fractional anisotropy (FA) and mean diffusivity (MD) were obtained in 4,415 people without dementia (mean age 63.9 years, 55.0% women) from the prospective population-based Rotterdam Study with brain MRI between 2005 and 2011. We modeled the association of these diffusion measures with risk of dementia (follow-up until 2016) and with changes on repeated cognitive assessment after on average 5.4 years, adjusting for age, sex, education, macrostructural MRI markers, depressive symptoms, cardiovascular risk factors, and APOE genotype. Results During a median follow-up of 6.8 years, 101 participants had incident dementia, of whom 83 had clinical Alzheimer disease (AD). Lower global values of FA and higher values of MD were associated with an increased risk of dementia (adjusted hazard ratio [95% confidence interval (CI)] per SD increase for MD 1.79 [1.44–2.23] and FA 0.65 [0.52–0.80]). Similarly, lower global values of FA and higher values of MD related to more cognitive decline in people without dementia (difference in global cognition per SD increase in MD [95% CI] was −0.04 [−0.07 to −0.01]). Associations were most profound in the projection, association, and limbic system tracts. Conclusions Structural disconnectivity is associated with an increased risk of dementia and more pronounced cognitive decline in the general population.
    Type of Medium: Online Resource
    ISSN: 0028-3878 , 1526-632X
    URL: Article
    DOI: 10.1212/WNL.0000000000010231
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
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  • 4
    Online Resource
    Online Resource
    Retinal microvasculature and white matter microstructure : The Rotterdam Study
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Neurology Vol. 87, No. 10 ( 2016-09-06), p. 1003-1010
    Details
    In: Neurology, Ovid Technologies (Wolters Kluwer Health), Vol. 87, No. 10 ( 2016-09-06), p. 1003-1010
    Type of Medium: Online Resource
    ISSN: 0028-3878 , 1526-632X
    URL: Article
    DOI: 10.1212/WNL.0000000000003080
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
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  • 5
    Online Resource
    Online Resource
    Carotid Plaque Composition and Prediction of Incident Atherosclerotic Cardiovascular Disease
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Circulation: Cardiovascular Imaging Vol. 15, No. 3 ( 2022-03)
    Details
    In: Circulation: Cardiovascular Imaging, Ovid Technologies (Wolters Kluwer Health), Vol. 15, No. 3 ( 2022-03)
    Abstract: Whether information on carotid plaque composition contributes to prediction of incident atherosclerotic cardiovascular disease (ASCVD) remains to be investigated. We determined the sex-specific added value of carotid plaque components for predicting incident ASCVD events, beyond traditional cardiovascular risk factors. Methods: Between 2007 and 2012, participants from the population-based Rotterdam Study with asymptomatic carotid wall thickening 〉 2.5 mm on ultrasonography were invited for carotid magnetic resonance imaging. Among 1349 participants (mean age: 72 years [SD±9.3], 49.5% women) without cardiovascular disease, we assessed plaque thickness, luminal stenosis ( 〉 30%), presence of intraplaque hemorrhage, lipid-rich necrotic core, and calcification. Follow-up for ASCVD was complete until January 1, 2015. Using Cox proportional hazards models, we fitted sex-specific prediction models including traditional cardiovascular risk factors (base model). We extended the base model by single and simultaneous additions of plaque characteristics and calculated improvement of model performance by the C statistics. Results: During a median follow-up of 4.8 years, 60 men and 48 women developed ASCVD. In women, presence of intraplaque hemorrhage was associated with incident ASCVD (adjusted hazard ratio, 3.37 [95% CI, 1.81–6.25]). The C statistic (95% CI) improved from 0.73 (0.66–0.79) to 0.76 (0.70–0.83) after single addition of intraplaque hemorrhage to the base model. Simultaneous addition of plaque components, plaque thickness, and stenosis did not change the results. In men, only carotid stenosis was statistically significantly associated with incident ASCVD (adjusted hazard ratio, 1.75 [95% CI, 1.00–3.08]); yet, the association diminished after the addition of other plaque characteristics, and no improvements were observed in C statistics. Conclusions: Presence of intraplaque hemorrhage contributes to the prediction of incident ASCVD in women, beyond traditional cardiovascular risk factors, other plaque components, plaque size, and stenosis.
    Type of Medium: Online Resource
    ISSN: 1941-9651 , 1942-0080
    URL: Article
    DOI: 10.1161/CIRCIMAGING.121.013602
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 2440475-5
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  • 6
    Online Resource
    Online Resource
    Association of common genetic variants with brain microbleeds : A genome-wide association study
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Neurology Vol. 95, No. 24 ( 2020-12-15), p. e3331-e3343
    Details
    In: Neurology, Ovid Technologies (Wolters Kluwer Health), Vol. 95, No. 24 ( 2020-12-15), p. e3331-e3343
    Abstract: To identify common genetic variants associated with the presence of brain microbleeds (BMBs). Methods We performed genome-wide association studies in 11 population-based cohort studies and 3 case–control or case-only stroke cohorts. Genotypes were imputed to the Haplotype Reference Consortium or 1000 Genomes reference panel. BMBs were rated on susceptibility-weighted or T2*-weighted gradient echo MRI sequences, and further classified as lobar or mixed (including strictly deep and infratentorial, possibly with lobar BMB). In a subset, we assessed the effects of APOE ε2 and ε4 alleles on BMB counts. We also related previously identified cerebral small vessel disease variants to BMBs. Results BMBs were detected in 3,556 of the 25,862 participants, of which 2,179 were strictly lobar and 1,293 mixed. One locus in the APOE region reached genome-wide significance for its association with BMB (lead single nucleotide polymorphism rs769449; odds ratio [OR] any BMB [95% confidence interval (CI)] 1.33 [1.21–1.45] ; p = 2.5 × 10 −10 ). APOE ε4 alleles were associated with strictly lobar (OR [95% CI] 1.34 [1.19–1.50] ; p = 1.0 × 10 −6 ) but not with mixed BMB counts (OR [95% CI] 1.04 [0.86–1.25] ; p = 0.68). APOE ε2 alleles did not show associations with BMB counts. Variants previously related to deep intracerebral hemorrhage and lacunar stroke, and a risk score of cerebral white matter hyperintensity variants, were associated with BMB. Conclusions Genetic variants in the APOE region are associated with the presence of BMB, most likely due to the APOE ε4 allele count related to a higher number of strictly lobar BMBs. Genetic predisposition to small vessel disease confers risk of BMB, indicating genetic overlap with other cerebral small vessel disease markers.
    Type of Medium: Online Resource
    ISSN: 0028-3878 , 1526-632X
    URL: Article
    DOI: 10.1212/WNL.0000000000010852
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
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  • 7
    Online Resource
    Online Resource
    Genetic Determinants of Unruptured Intracranial Aneurysms in the General Population
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Stroke Vol. 46, No. 10 ( 2015-10), p. 2961-2964
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 46, No. 10 ( 2015-10), p. 2961-2964
    Abstract: Genome-wide association studies have identified single-nucleotide polymorphisms (SNPs) for intracranial aneurysms in clinical samples. In addition, SNPs have been discovered for blood pressure, one of the strongest risk factors for intracranial aneurysms. We studied the role of these genetic variants on occurrence and size of unruptured intracranial aneurysms, discovered incidentally in a general community-dwelling population. Methods— In 4890 asymptomatic participants from the Rotterdam Study, 120 intracranial aneurysms were identified on brain imaging and segmented for maximum diameter and volume. Genetic risk scores (GRS) were calculated for intracranial aneurysms (10 SNPs), systolic blood pressure (33 SNPs), and diastolic blood pressure (41 SNPs). Results— The GRS for intracranial aneurysms was not statistically significantly associated with presence of aneurysms in this population (OR, 1.16; 95% CI, 0.96–1.40; P =0.119), but showed a significant association with both maximum diameter (difference in log-transformed mm per SD increase of GRS, 0.10; 95% CI, 0.02–0.19; P =0.018) and volume (difference in log-transformed µL per SD increase of GRS, 0.21; 95% CI, 0.01–0.41; P =0.040) of aneurysms. GRSs for blood pressures were associated with neither presence nor size of aneurysms. Conclusions— Genetic variants previously identified for intracranial aneurysms in clinical studies relate to the size rather than the presence of incidentally discovered, unruptured intracranial aneurysms in the general population.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/STROKEAHA.115.010414
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 1467823-8
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  • 8
    Online Resource
    Online Resource
    Heritability and Genome-Wide Association Analyses of Intracranial Carotid Artery Calcification : The Rotterdam Study
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Stroke Vol. 47, No. 4 ( 2016-04), p. 912-917
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 47, No. 4 ( 2016-04), p. 912-917
    Abstract: Intracranial carotid artery calcification (ICAC) is one of the most important risk factors for stroke. Although several environmental risk factors for ICAC have been identified, its genetic background remains unclear. Methods— Between 2003 and 2006, 2034 participants from the prospective population-based Rotterdam study (mean age: 69.6±6.8 years; 51.7% female) underwent computed tomography to quantify vascular calcification in the intracranial internal carotid artery. Blood samples were drawn for genotyping. Genotypes of the participants were imputed to the 1000 Genomes reference panel to generate genetic relationship matrices for the estimation of the heritability of ICAC volume. Adjustments were made for age and sex. Subsequently, genome-wide association analyses were performed to identify specific variants. Results— The age- and sex-adjusted heritability ( h 2 ) of ICAC was 47% [standard error (SE): 19%; P =0.009]. Genome-wide association analyses identified a variant on chromosome 9p21.3 (rs1537372; N=2034; P =4.75×10 −9 ) and 1 variant on chromosome 11p11.2 (rs11038042, N=2034; P =3.27×10 −8 ) that were significantly associated with ICAC volume. Rs1537372 replicated in an independent sample of 716 stroke patients ( P combined =1.38×10 −10 ). Conclusions— ICAC volume is a heritable trait, which is partly explained by common genetic variation. We identified specific genetic variants associated with ICAC, which given the importance of ICAC in stroke risk, needs replication in larger-scale studies to further elucidate its genetic basis.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/STROKEAHA.115.012248
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 1467823-8
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  • 9
    Online Resource
    Online Resource
    Vascular Brain Disease and Depression in the Elderly
    Ovid Technologies (Wolters Kluwer Health) ; 2010
    In:  Epidemiology Vol. 21, No. 1 ( 2010-01), p. 78-81
    Details
    In: Epidemiology, Ovid Technologies (Wolters Kluwer Health), Vol. 21, No. 1 ( 2010-01), p. 78-81
    Type of Medium: Online Resource
    ISSN: 1044-3983
    URL: Article
    DOI: 10.1097/EDE.0b013e3181c1fa0d
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2010
    detail.hit.zdb_id: 2042095-X
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  • 10
    Online Resource
    Online Resource
    Genetic Loci for Coronary Calcification and Serum Lipids Relate to Aortic and Carotid Calcification
    Ovid Technologies (Wolters Kluwer Health) ; 2013
    In:  Circulation: Cardiovascular Genetics Vol. 6, No. 1 ( 2013-02), p. 47-53
    Details
    In: Circulation: Cardiovascular Genetics, Ovid Technologies (Wolters Kluwer Health), Vol. 6, No. 1 ( 2013-02), p. 47-53
    Abstract: Atherosclerosis in different vessel beds shares lifestyle and environmental risk factors. It is unclear whether this holds for genetic risk factors. Hence, for the current study genetic loci for coronary artery calcification and serum lipid levels, one of the strongest risk factors for atherosclerosis, were used to assess their relation with atherosclerosis in different vessel beds. Methods and Results— From 1987 persons of the population-based Rotterdam Study, 3 single-nucleotide polymorphisms (SNPs) for coronary artery calcification and 132 SNPs for total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol or triglycerides were used. To quantify atherosclerotic calcification as a marker of atherosclerosis, all participants underwent nonenhanced computed tomography of the aortic arch and carotid arteries. Associations between genetic risk scores of the joint effect of the SNPs and of all calcification were investigated. The joint effect of coronary artery calcification–SNPs was associated with larger calcification volumes in all vessel beds (difference in calcification volume per SD increase in genetic risk score: 0.15 [95% confidence interval, 0.11–0.20] in aorta, 0.14 [95% confidence interval, 0.10–0.18] in extracranial carotids, and 0.11 [95% confidence interval, 0.07–0.16] in intracranial carotids). The joint effect of total cholesterol SNPs, low-density lipoprotein SNPs, and of all lipid SNPs together was associated with larger calcification volumes in both the aortic arch and the carotid arteries but attenuated after adjusting for the lipid fraction and lipid-lowering medication. Conclusions— The genetic basis for aortic arch and carotid artery calcification overlaps with the most important loci of coronary artery calcification. Furthermore, serum lipids share a genetic predisposition with both calcification in the aortic arch and the carotid arteries, providing novel insights into the cause of atherosclerosis.
    Type of Medium: Online Resource
    ISSN: 1942-325X , 1942-3268
    URL: Article
    DOI: 10.1161/CIRCGENETICS.112.963934
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2013
    detail.hit.zdb_id: 2927603-2
    detail.hit.zdb_id: 2457085-0
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