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2. Cerebral small vessel disease genomics and its implications across the lifespan.

Author

Sargurupremraj, Muralidharan, Suzuki, Hideaki, Jian, Xueqiu, Sarnowski, Chloé, Evans, Tavia E, Bis, Joshua C, Eiriksdottir, Gudny, Sakaue, Saori, Terzikhan, Natalie, Habes, Mohamad, Zhao, Wei, Armstrong, Nicola J, Hofer, Edith, Yanek, Lisa R, Hagenaars, Saskia P, Kumar, Rajan B, van den Akker, Erik B, McWhirter, Rebekah E, Trompet, Stella, Mishra, Aniket, Saba, Yasaman, Satizabal, Claudia L, Beaudet, Gregory, Petit, Laurent, Tsuchida, Ami, Zago, Laure, Schilling, Sabrina, Sigurdsson, Sigurdur, Gottesman, Rebecca F, Lewis, Cora E, Aggarwal, Neelum T, Lopez, Oscar L, Smith, Jennifer A, Valdés Hernández, Maria C, van der Grond, Jeroen, Wright, Margaret J, Knol, Maria J, Dörr, Marcus, Thomson, Russell J, Bordes, Constance, Le Grand, Quentin, Duperron, Marie-Gabrielle, Smith, Albert V, Knopman, David S, Schreiner, Pamela J, Evans, Denis A, Rotter, Jerome I, Beiser, Alexa S, Maniega, Susana Muñoz, Beekman, Marian, Trollor, Julian, Stott, David J, Vernooij, Meike W, Wittfeld, Katharina, Niessen, Wiro J, Soumaré, Aicha, Boerwinkle, Eric, Sidney, Stephen, Turner, Stephen T, Davies, Gail, Thalamuthu, Anbupalam, Völker, Uwe, van Buchem, Mark A, Bryan, R Nick, Dupuis, Josée, Bastin, Mark E, Ames, David, Teumer, Alexander, Amouyel, Philippe, Kwok, John B, Bülow, Robin, Deary, Ian J, Schofield, Peter R, Brodaty, Henry, Jiang, Jiyang, Tabara, Yasuharu, Setoh, Kazuya, Miyamoto, Susumu, Yoshida, Kazumichi, Nagata, Manabu, Kamatani, Yoichiro, Matsuda, Fumihiko, Psaty, Bruce M, Bennett, David A, De Jager, Philip L, Mosley, Thomas H, Sachdev, Perminder S, Schmidt, Reinhold, Warren, Helen R, Evangelou, Evangelos, Trégouët, David-Alexandre, International Network against Thrombosis (INVENT) Consortium, International Headache Genomics Consortium (IHGC), Ikram, Mohammad A, Wen, Wei, DeCarli, Charles, Srikanth, Velandai K, Jukema, J Wouter, Slagboom, Eline P, and Kardia, Sharon LR

Subjects
International Network against Thrombosis (INVENT) Consortium, International Headache Genomics Consortium, Humans, Alzheimer Disease, Hypertension, Medical History Taking, Risk Assessment, Risk Factors, Adult, Aged, Aged, 80 and over, Middle Aged, Female, Male, Stroke, Genome-Wide Association Study, Young Adult, Diffusion Tensor Imaging, Genetic Loci, Mendelian Randomization Analysis, Cerebral Small Vessel Diseases, White Matter, and over
Abstract

White matter hyperintensities (WMH) are the most common brain-imaging feature of cerebral small vessel disease (SVD), hypertension being the main known risk factor. Here, we identify 27 genome-wide loci for WMH-volume in a cohort of 50,970 older individuals, accounting for modification/confounding by hypertension. Aggregated WMH risk variants were associated with altered white matter integrity (p = 2.5×10-7) in brain images from 1,738 young healthy adults, providing insight into the lifetime impact of SVD genetic risk. Mendelian randomization suggested causal association of increasing WMH-volume with stroke, Alzheimer-type dementia, and of increasing blood pressure (BP) with larger WMH-volume, notably also in persons without clinical hypertension. Transcriptome-wide colocalization analyses showed association of WMH-volume with expression of 39 genes, of which four encode known drug targets. Finally, we provide insight into BP-independent biological pathways underlying SVD and suggest potential for genetic stratification of high-risk individuals and for genetically-informed prioritization of drug targets for prevention trials.

Published
2020

3. Distribution of cerebral microbleeds in the East and West: Individual participant meta-analysis.

Author

Yakushiji, Yusuke, Wilson, Duncan, Ambler, Gareth, Charidimou, Andreas, Beiser, Alexa, van Buchem, Mark A, DeCarli, Charles, Ding, Ding, Gudnason, Villi, Hara, Hideo, Imaizumi, Toshio, Kohara, Katsuhiko, Kwon, Hyung-Min, Launer, Lenore J, Mok, Vincent, Phan, Thanh, Preis, Sarah R, Romero, José Rafael, Seshadri, Sudha, Srikanth, Velandai, Takashima, Yuki, Tsushima, Yoshito, Wang, Zhaolu, Wolf, Philip A, Xiong, Yunyun, Yamaguchi, Shuhei, and Werring, David J

Subjects
Biomedical and Clinical Sciences, Neurosciences, Clinical Sciences, Clinical Research, Stroke, Brain Disorders, Aged, Cerebral Hemorrhage, Female, Humans, Male, Middle Aged, Cognitive Sciences, Neurology & Neurosurgery, Clinical sciences
Abstract

ObjectiveWe investigated differences in the anatomical distribution of cerebral microbleeds (CMBs) on MRI, hypothesized to indicate the type of underlying cerebral small vessel disease (SVD), between Eastern and Western general populations.MethodsWe analyzed data from 11 studies identified by a PubMed search between 1996 and April 2014 according to the Preferred Reporting Items for a Systematic Review and Meta-analysis of Individual Participant Data. Study quality measures indicated low or medium risk of bias. We included stroke-free participants from populations aged between 55 and 75 years, categorized by geographic location (Eastern or Western). We categorized CMB distribution (strictly lobar, deep and/or infratentorial [D/I], or mixed [i.e., CMBs located in both lobar and D/I regions]). We tested the hypothesis that Eastern and Western populations have different anatomical distributions of CMBs using multivariable mixed effects logistic regression analyses adjusted for age, sex, and hypertension and clustering by institution.ResultsAmong 8,595 stroke-free individuals (mean age [SD] 66.7 [5.6] years; 48% male; 42% from a Western population), 624 (7.3%) had CMBs (strictly lobar in 3.1%; D/I or mixed in 4.2%). In multivariable mixed effects models, Eastern populations had higher odds of D/I or mixed CMBs (adjusted odds ratio 2.78, 95% confidence interval [CI] 1.77-4.35) compared to Western populations. Eastern populations had a higher number of D/I or mixed CMBs (adjusted prevalence ratio 2.83, 95% CI 1.27-6.31).ConclusionsEastern and Western general populations have different anatomical distributions of CMBs, suggesting differences in the spectrum of predominant underlying SVDs, with potential implications for SVD diagnosis and treatment.

Published
2019

4. Vascular dysfunction-The disregarded partner of Alzheimer's disease.

Author

Sweeney, Melanie D, Montagne, Axel, Sagare, Abhay P, Nation, Daniel A, Schneider, Lon S, Chui, Helena C, Harrington, Michael G, Pa, Judy, Law, Meng, Wang, Danny JJ, Jacobs, Russell E, Doubal, Fergus N, Ramirez, Joel, Black, Sandra E, Nedergaard, Maiken, Benveniste, Helene, Dichgans, Martin, Iadecola, Costantino, Love, Seth, Bath, Philip M, Markus, Hugh S, Salman, Rustam A, Allan, Stuart M, Quinn, Terence J, Kalaria, Rajesh N, Werring, David J, Carare, Roxana O, Touyz, Rhian M, Williams, Steve CR, Moskowitz, Michael A, Katusic, Zvonimir S, Lutz, Sarah E, Lazarov, Orly, Minshall, Richard D, Rehman, Jalees, Davis, Thomas P, Wellington, Cheryl L, González, Hector M, Yuan, Chun, Lockhart, Samuel N, Hughes, Timothy M, Chen, Christopher LH, Sachdev, Perminder, O'Brien, John T, Skoog, Ingmar, Pantoni, Leonardo, Gustafson, Deborah R, Biessels, Geert Jan, Wallin, Anders, Smith, Eric E, Mok, Vincent, Wong, Adrian, Passmore, Peter, Barkof, Frederick, Muller, Majon, Breteler, Monique MB, Román, Gustavo C, Hamel, Edith, Seshadri, Sudha, Gottesman, Rebecca F, van Buchem, Mark A, Arvanitakis, Zoe, Schneider, Julie A, Drewes, Lester R, Hachinski, Vladimir, Finch, Caleb E, Toga, Arthur W, Wardlaw, Joanna M, and Zlokovic, Berislav V

Subjects
Blood-Brain Barrier, Brain, Humans, Alzheimer Disease, Vascular Diseases, Cerebrovascular Circulation, United States, National Institute on Aging (U.S.), Amyloid beta-Peptides, White Matter, Biomarkers, Alzheimer's disease, Blood-brain barrier, Cerebral blood flow, MRI, Vascular, National Institute on Aging, Neurosciences, Clinical Sciences, Geriatrics
Abstract

Increasing evidence recognizes Alzheimer's disease (AD) as a multifactorial and heterogeneous disease with multiple contributors to its pathophysiology, including vascular dysfunction. The recently updated AD Research Framework put forth by the National Institute on Aging-Alzheimer's Association describes a biomarker-based pathologic definition of AD focused on amyloid, tau, and neuronal injury. In response to this article, here we first discussed evidence that vascular dysfunction is an important early event in AD pathophysiology. Next, we examined various imaging sequences that could be easily implemented to evaluate different types of vascular dysfunction associated with, and/or contributing to, AD pathophysiology, including changes in blood-brain barrier integrity and cerebral blood flow. Vascular imaging biomarkers of small vessel disease of the brain, which is responsible for >50% of dementia worldwide, including AD, are already established, well characterized, and easy to recognize. We suggest that these vascular biomarkers should be incorporated into the AD Research Framework to gain a better understanding of AD pathophysiology and aid in treatment efforts.

Published
2019

5. The Boston criteria version 2.0 for cerebral amyloid angiopathy: a multicentre, retrospective, MRI–neuropathology diagnostic accuracy study

Author

Charidimou, Andreas, Boulouis, Gregoire, Frosch, Matthew P, Baron, Jean-Claude, Pasi, Marco, Albucher, Jean Francois, Banerjee, Gargi, Barbato, Carmen, Bonneville, Fabrice, Brandner, Sebastian, Calviere, Lionel, Caparros, François, Casolla, Barbara, Cordonnier, Charlotte, Delisle, Marie-Bernadette, Deramecourt, Vincent, Dichgans, Martin, Gokcal, Elif, Herms, Jochen, Hernandez-Guillamon, Mar, Jäger, Hans Rolf, Jaunmuktane, Zane, Linn, Jennifer, Martinez-Ramirez, Sergi, Martínez-Sáez, Elena, Mawrin, Christian, Montaner, Joan, Moulin, Solene, Olivot, Jean-Marc, Piazza, Fabrizio, Puy, Laurent, Raposo, Nicolas, Rodrigues, Mark A, Roeber, Sigrun, Romero, Jose Rafael, Samarasekera, Neshika, Schneider, Julie A, Schreiber, Stefanie, Schreiber, Frank, Schwall, Corentin, Smith, Colin, Szalardy, Levente, Varlet, Pascale, Viguier, Alain, Wardlaw, Joanna M, Warren, Andrew, Wollenweber, Frank A, Zedde, Marialuisa, van Buchem, Mark A, Gurol, M Edip, Viswanathan, Anand, Al-Shahi Salman, Rustam, Smith, Eric E, Werring, David J, and Greenberg, Steven M

Published
2022
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6. Microstructural white matter damage on MRI is associated with disease severity in Dutch-type cerebral amyloid angiopathy.

Author

Rasing, Ingeborg, Vlegels, Naomi, Schipper, Manon R, Voigt, Sabine, Koemans, Emma A, Kaushik, Kanishk, van Dort, Rosemarie, van Harten, Thijs W, De Luca, Alberto, van Etten, Ellis S, van Zwet, Erik W, van Buchem, Mark A, Middelkoop, Huub AM, Biessels, Geert Jan, Terwindt, Gisela M, van Osch, Matthias JP, van Walderveen, Marianne AA, and Wermer, Marieke JH

Abstract

Peak width of skeletonized mean diffusivity (PSMD) is an emerging diffusion-MRI based marker to study subtle early alterations to white matter microstructure. We assessed PSMD over the clinical continuum in Dutch-type hereditary CAA (D-CAA) and its association with other CAA-related MRI-markers and cognitive symptoms. We included (pre)symptomatic D-CAA mutation-carriers and calculated PSMD from diffusion-MRI data. Associations between PSMD-levels, cognitive performance and CAA-related MRI-markers were assessed with linear regression models. We included 59 participants (25/34 presymptomatic/symptomatic; mean age 39/58 y). PSMD-levels increased with disease severity and were higher in symptomatic D-CAA mutation-carriers (median [range] 4.90 [2.77–9.50]mm2/s × 10−4) compared with presymptomatic mutation-carriers (2.62 [1.96–3.43]mm2/s × 10−4) p = <0.001. PSMD was positively correlated with age, CAA-SVD burden on MRI (adj.B [confidence interval] = 0.42 [0.16–0.67], p = 0.002), with number of cerebral microbleeds (adj.B = 0.30 [0.08–0.53], p = 0.009), and with both deep (adj.B = 0.46 [0.22–0.69], p = <0.001) and periventricular (adj.B = 0.38 [0.13–0.62], p = 0.004) white matter hyperintensities. Increasing PSMD was associated with decreasing Trail Making Test (TMT)-A performance (B = −0.42 [−0.69–0.14], p = 0.04. In D-CAA mutation-carriers microstructural white matter damage is associated with disease phase, CAA burden on MRI and cognitive impairment as reflected by a decrease in information processing speed. PSMD, as a global measure of alterations to the white matter microstructure, may be a useful tool to monitor disease progression in CAA. [ABSTRACT FROM AUTHOR]

Published
2024
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8. Exome Chip Analysis Identifies Low-Frequency and Rare Variants in MRPL38 for White Matter Hyperintensities on Brain Magnetic Resonance Imaging

Author

Jian, Xueqiu, Satizabal, Claudia L, Smith, Albert V, Wittfeld, Katharina, Bis, Joshua C, Smith, Jennifer A, Hsu, Fang-Chi, Nho, Kwangsik, Hofer, Edith, Hagenaars, Saskia P, Nyquist, Paul A, Mishra, Aniket, Adams, Hieab HH, Li, Shuo, Teumer, Alexander, Zhao, Wei, Freedman, Barry I, Saba, Yasaman, Yanek, Lisa R, Chauhan, Ganesh, van Buchem, Mark A, Cushman, Mary, Royle, Natalie A, Bryan, R Nick, Niessen, Wiro J, Windham, Beverly G, DeStefano, Anita L, Habes, Mohamad, Heckbert, Susan R, Palmer, Nicholette D, Lewis, Cora E, Eiriksdottir, Gudny, Maillard, Pauline, Mathias, Rasika A, Homuth, Georg, Valdés-Hernández, Maria del C, Divers, Jasmin, Beiser, Alexa S, Langner, Sönke, Rice, Kenneth M, Bastin, Mark E, Yang, Qiong, Maldjian, Joseph A, Starr, John M, Sidney, Stephen, Risacher, Shannon L, Uitterlinden, André G, Gudnason, Vilmundur G, Nauck, Matthias, Rotter, Jerome I, Schreiner, Pamela J, Boerwinkle, Eric, van Duijn, Cornelia M, Mazoyer, Bernard, von Sarnowski, Bettina, Gottesman, Rebecca F, Levy, Daniel, Sigurdsson, Sigurdur, Vernooij, Meike W, Turner, Stephen T, Schmidt, Reinhold, Wardlaw, Joanna M, Psaty, Bruce M, Mosley, Thomas H, DeCarli, Charles S, Saykin, Andrew J, Bowden, Donald W, Becker, Diane M, Deary, Ian J, Schmidt, Helena, Kardia, Sharon LR, Ikram, M Arfan, Debette, Stéphanie, Grabe, Hans J, Longstreth, WT, Seshadri, Sudha, Launer, Lenore J, and Fornage, Myriam

Subjects
Epidemiology, Health Sciences, Alzheimer's Disease Related Dementias (ADRD), Dementia, Human Genome, Cerebrovascular, Clinical Research, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Stroke, Brain Disorders, Acquired Cognitive Impairment, Neurodegenerative, Aging, Minority Health, Genetics, Neurosciences, Biotechnology, 2.1 Biological and endogenous factors, Neurological, Brain, Cohort Studies, Exome, Genetic Variation, Humans, Magnetic Resonance Imaging, Mitochondrial Proteins, White Matter, cerebral small vessel disease, exome, magnetic resonance imaging, meta-analysis, white matter, neuroCHARGE Working Group, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Neurology & Neurosurgery, Clinical sciences, Allied health and rehabilitation science
Abstract

Background and Purpose- White matter hyperintensities (WMH) on brain magnetic resonance imaging are typical signs of cerebral small vessel disease and may indicate various preclinical, age-related neurological disorders, such as stroke. Though WMH are highly heritable, known common variants explain a small proportion of the WMH variance. The contribution of low-frequency/rare coding variants to WMH burden has not been explored. Methods- In the discovery sample we recruited 20 719 stroke/dementia-free adults from 13 population-based cohort studies within the Cohorts for Heart and Aging Research in Genomic Epidemiology consortium, among which 17 790 were of European ancestry and 2929 of African ancestry. We genotyped these participants at ≈250 000 mostly exonic variants with Illumina HumanExome BeadChip arrays. We performed ethnicity-specific linear regression on rank-normalized WMH in each study separately, which were then combined in meta-analyses to test for association with single variants and genes aggregating the effects of putatively functional low-frequency/rare variants. We then sought replication of the top findings in 1192 adults (European ancestry) with whole exome/genome sequencing data from 2 independent studies. Results- At 17q25, we confirmed the association of multiple common variants in TRIM65, FBF1, and ACOX1 ( P

Published
2018

9. Association of Cerebral Amyloid-β Aggregation With Cognitive Functioning in Persons Without Dementia

Author

Jansen, Willemijn J, Ossenkoppele, Rik, Tijms, Betty M, Fagan, Anne M, Hansson, Oskar, Klunk, William E, van der Flier, Wiesje M, Villemagne, Victor L, Frisoni, Giovanni B, Fleisher, Adam S, Lleó, Alberto, Mintun, Mark A, Wallin, Anders, Engelborghs, Sebastiaan, Na, Duk L, Chételat, Gäel, Molinuevo, José Luis, Landau, Susan M, Mattsson, Niklas, Kornhuber, Johannes, Sabri, Osama, Rowe, Christopher C, Parnetti, Lucilla, Popp, Julius, Fladby, Tormod, Jagust, William J, Aalten, Pauline, Lee, Dong Young, Vandenberghe, Rik, de Oliveira, Catarina Resende, Kapaki, Elisabeth, Froelich, Lutz, Ivanoiu, Adrian, Gabryelewicz, Tomasz, Verbeek, Marcel M, Sanchez-Juan, Páscual, Hildebrandt, Helmut, Camus, Vincent, Zboch, Marzena, Brooks, David J, Drzezga, Alexander, Rinne, Juha O, Newberg, Andrew, de Mendonça, Alexandre, Sarazin, Marie, Rabinovici, Gil D, Madsen, Karine, Kramberger, Milica G, Nordberg, Agneta, Mok, Vincent, Mroczko, Barbara, Wolk, David A, Meyer, Philipp T, Tsolaki, Magda, Scheltens, Philip, Verhey, Frans RJ, Visser, Pieter Jelle, Aarsland, Dag, Alcolea, Daniel, Alexander, Myriam, Almdahl, Ina S, Arnold, Steven E, Baldeiras, Inês, Barthel, Henryk, van Berckel, Bart NM, Blennow, Kaj, van Buchem, Mark A, Cavedo, Enrica, Chen, Kewei, Chipi, Elena, Cohen, Ann D, Förster, Stefan, Fortea, Juan, Frederiksen, Kristian S, Freund-Levi, Yvonne, Gkatzima, Olymbia, Gordon, Mark Forrest, Grimmer, Timo, Hampel, Harald, Hausner, Lucrezia, Hellwig, Sabine, Herukka, Sanna-Kaisa, Johannsen, Peter, Klimkowicz-Mrowiec, Aleksandra, Köhler, Sebastian, Koglin, Norman, van Laere, Koen, de Leon, Mony, Lisetti, Viviana, Maier, Wolfgang, Marcusson, Jan, Meulenbroek, Olga, Møllergård, Hanne M, Morris, John C, Nordlund, Arto, Novak, Gerald P, Paraskevas, George P, Perera, Gayan, Peters, Oliver, and Ramakers, Inez HGB

Subjects
Health Services and Systems, Health Sciences, Acquired Cognitive Impairment, Alzheimer's Disease Related Dementias (ADRD), Neurosciences, Aging, Dementia, Brain Disorders, Behavioral and Social Science, Neurodegenerative, Alzheimer's Disease, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Clinical Research, Aetiology, 2.1 Biological and endogenous factors, Neurological, Mental health, Aged, Alzheimer Disease, Amyloid beta-Peptides, Brain, Cognition Disorders, Cognitive Dysfunction, Cross-Sectional Studies, Female, Humans, Male, Memory, Episodic, Mental Status and Dementia Tests, Middle Aged, Positron-Emission Tomography, Reference Values, Amyloid Biomarker Study Group, Other Medical and Health Sciences, Psychology, Cognitive Sciences, Clinical sciences, Clinical and health psychology
Abstract

ImportanceCerebral amyloid-β aggregation is an early event in Alzheimer disease (AD). Understanding the association between amyloid aggregation and cognitive manifestation in persons without dementia is important for a better understanding of the course of AD and for the design of prevention trials.ObjectiveTo investigate whether amyloid-β aggregation is associated with cognitive functioning in persons without dementia.Design, setting, and participantsThis cross-sectional study included 2908 participants with normal cognition and 4133 with mild cognitive impairment (MCI) from 53 studies in the multicenter Amyloid Biomarker Study. Normal cognition was defined as having no cognitive concerns for which medical help was sought and scores within the normal range on cognitive tests. Mild cognitive impairment was diagnosed according to published criteria. Study inclusion began in 2013 and is ongoing. Data analysis was performed in January 2017.Main outcomes and measuresGlobal cognitive performance as assessed by the Mini-Mental State Examination (MMSE) and episodic memory performance as assessed by a verbal word learning test. Amyloid aggregation was measured with positron emission tomography or cerebrospinal fluid biomarkers and dichotomized as negative (normal) or positive (abnormal) according to study-specific cutoffs. Generalized estimating equations were used to examine the association between amyloid aggregation and low cognitive scores (MMSE score ≤27 or memory z score≤-1.28) and to assess whether this association was moderated by age, sex, educational level, or apolipoprotein E genotype.ResultsAmong 2908 persons with normal cognition (mean [SD] age, 67.4 [12.8] years), amyloid positivity was associated with low memory scores after age 70 years (mean difference in amyloid positive vs negative, 4% [95% CI, 0%-7%] at 72 years and 21% [95% CI, 10%-33%] at 90 years) but was not associated with low MMSE scores (mean difference, 3% [95% CI, -1% to 6%], P = .16). Among 4133 patients with MCI (mean [SD] age, 70.2 [8.5] years), amyloid positivity was associated with low memory (mean difference, 16% [95% CI, 12%-20%], P

Published
2018

12. Neuroimaging in Dementia

Author

Vernooij, Meike W., van Buchem, Mark A., Hodler, Juerg, Series Editor, Kubik-Huch, Rahel A., Series Editor, and von Schulthess, Gustav K., Series Editor

Published
2020
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15. Identification of Distinct Brain MRI Phenotypes and Their Association With Long-Term Dementia Risk in Community-Dwelling Older Adults

Author

Onderzoek Brain at Risk, Keller, Jasmin Annica, Sigurdsson, Sigurdur, Schmitz Abecassis, Bárbara, Kant, Ilse M.J., Van Buchem, Mark A., Launer, Lenore J., van Osch, Matthias J.P., Gudnason, Vilmundur, de Bresser, Jeroen, Onderzoek Brain at Risk, Keller, Jasmin Annica, Sigurdsson, Sigurdur, Schmitz Abecassis, Bárbara, Kant, Ilse M.J., Van Buchem, Mark A., Launer, Lenore J., van Osch, Matthias J.P., Gudnason, Vilmundur, and de Bresser, Jeroen

Published
2024

16. Fluid biomarkers in cerebral amyloid angiopathy

Author

Savar, Seyed Mehrdad, primary, Ma, Bin, additional, Hone, Eugene, additional, Jahan, Farzana, additional, Markovic, Shaun, additional, Pedrini, Steve, additional, Shemehsavar, Soudabeh, additional, Easwaran, Vandhana, additional, Taddei, Kevin, additional, Gardener, Samantha, additional, Chhatwal, Jasmeer P., additional, van Etten, Ellis S., additional, van Osch, Matthias J. P., additional, Clarke, Daniel, additional, Gnjec, Anastazija, additional, van Buchem, Mark A., additional, Wermer, Marieke J. H., additional, Hankey, Graeme J., additional, Greenberg, Steven M., additional, Martins, Ralph N., additional, and Sohrabi, Hamid R., additional

Published
2024
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19. White Matter Lesion Progression

Author

Hofer, Edith, Cavalieri, Margherita, Bis, Joshua C, DeCarli, Charles, Fornage, Myriam, Sigurdsson, Sigurdur, Srikanth, Velandai, Trompet, Stella, Verhaaren, Benjamin FJ, Wolf, Christiane, Yang, Qiong, Adams, Hieab HH, Amouyel, Philippe, Beiser, Alexa, Buckley, Brendan M, Callisaya, Michele, Chauhan, Ganesh, de Craen, Anton JM, Dufouil, Carole, van Duijn, Cornelia M, Ford, Ian, Freudenberger, Paul, Gottesman, Rebecca F, Gudnason, Vilmundur, Heiss, Gerardo, Hofman, Albert, Lumley, Thomas, Martinez, Oliver, Mazoyer, Bernard, Moran, Chris, Niessen, Wiro J, Phan, Thanh, Psaty, Bruce M, Satizabal, Claudia L, Sattar, Naveed, Schilling, Sabrina, Shibata, Dean K, Slagboom, P Eline, Smith, Albert, Stott, David J, Taylor, Kent D, Thomson, Russell, Töglhofer, Anna M, Tzourio, Christophe, van Buchem, Mark, Wang, Jing, Westendorp, Rudi GJ, Windham, B Gwen, Vernooij, Meike W, Zijdenbos, Alex, Beare, Richard, Debette, Stéphanie, Ikram, M Arfan, Jukema, J Wouter, Launer, Lenore J, Longstreth, WT, Mosley, Thomas H, Seshadri, Sudha, Schmidt, Helena, and Schmidt, Reinhold

Subjects
Aging, Clinical Research, Genetics, Human Genome, Prevention, Cardiovascular, Aetiology, 2.1 Biological and endogenous factors, Adult, Aged, Cohort Studies, Disease Progression, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Leukoencephalopathies, Male, Middle Aged, Prospective Studies, White Matter, Cohorts for Heart and Aging Research in Genomic Epidemiology Consortium, aging, biological factors, cerebral small vessel diseases, magnetic resonance imaging, white matter lesions, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Neurosciences, Neurology & Neurosurgery
Abstract

Background and purposeWhite matter lesion (WML) progression on magnetic resonance imaging is related to cognitive decline and stroke, but its determinants besides baseline WML burden are largely unknown. Here, we estimated heritability of WML progression, and sought common genetic variants associated with WML progression in elderly participants from the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium.MethodsHeritability of WML progression was calculated in the Framingham Heart Study. The genome-wide association study included 7773 elderly participants from 10 cohorts. To assess the relative contribution of genetic factors to progression of WML, we compared in 7 cohorts risk models including demographics, vascular risk factors plus single-nucleotide polymorphisms that have been shown to be associated cross-sectionally with WML in the current and previous association studies.ResultsA total of 1085 subjects showed WML progression. The heritability estimate for WML progression was low at 6.5%, and no single-nucleotide polymorphisms achieved genome-wide significance (P

Published
2015

20. Prevalence of Cerebral Amyloid Pathology in Persons Without Dementia: A Meta-analysis

Author

Jansen, Willemijn J, Ossenkoppele, Rik, Knol, Dirk L, Tijms, Betty M, Scheltens, Philip, Verhey, Frans RJ, Visser, Pieter Jelle, Aalten, Pauline, Aarsland, Dag, Alcolea, Daniel, Alexander, Myriam, Almdahl, Ina S, Arnold, Steven E, Baldeiras, Inês, Barthel, Henryk, van Berckel, Bart NM, Bibeau, Kristen, Blennow, Kaj, Brooks, David J, van Buchem, Mark A, Camus, Vincent, Cavedo, Enrica, Chen, Kewei, Chetelat, Gael, Cohen, Ann D, Drzezga, Alexander, Engelborghs, Sebastiaan, Fagan, Anne M, Fladby, Tormod, Fleisher, Adam S, van der Flier, Wiesje M, Ford, Lisa, Förster, Stefan, Fortea, Juan, Foskett, Nadia, Frederiksen, Kristian S, Freund-Levi, Yvonne, Frisoni, Giovanni B, Froelich, Lutz, Gabryelewicz, Tomasz, Gill, Kiran Dip, Gkatzima, Olymbia, Gómez-Tortosa, Estrella, Gordon, Mark Forrest, Grimmer, Timo, Hampel, Harald, Hausner, Lucrezia, Hellwig, Sabine, Herukka, Sanna-Kaisa, Hildebrandt, Helmut, Ishihara, Lianna, Ivanoiu, Adrian, Jagust, William J, Johannsen, Peter, Kandimalla, Ramesh, Kapaki, Elisabeth, Klimkowicz-Mrowiec, Aleksandra, Klunk, William E, Köhler, Sebastian, Koglin, Norman, Kornhuber, Johannes, Kramberger, Milica G, Van Laere, Koen, Landau, Susan M, Lee, Dong Young, de Leon, Mony, Lisetti, Viviana, Lleó, Alberto, Madsen, Karine, Maier, Wolfgang, Marcusson, Jan, Mattsson, Niklas, de Mendonça, Alexandre, Meulenbroek, Olga, Meyer, Philipp T, Mintun, Mark A, Mok, Vincent, Molinuevo, José Luis, Møllergård, Hanne M, Morris, John C, Mroczko, Barbara, Van der Mussele, Stefan, Na, Duk L, Newberg, Andrew, Nordberg, Agneta, Nordlund, Arto, Novak, Gerald P, Paraskevas, George P, Parnetti, Lucilla, Perera, Gayan, Peters, Oliver, Popp, Julius, Prabhakar, Sudesh, Rabinovici, Gil D, Ramakers, Inez HGB, Rami, Lorena, de Oliveira, Catarina Resende, Rinne, Juha O, Rodrigue, Karen M, and Rodríguez-Rodríguez, Eloy

Subjects
Health Services and Systems, Health Sciences, Clinical Research, Alzheimer's Disease, Vascular Cognitive Impairment/Dementia, Acquired Cognitive Impairment, Neurosciences, Alzheimer's Disease Related Dementias (ADRD), Brain Disorders, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Cerebrovascular, Neurodegenerative, Prevention, Dementia, Aging, 4.2 Evaluation of markers and technologies, Detection, screening and diagnosis, Aetiology, 2.1 Biological and endogenous factors, Neurological, Adult, Age Factors, Aged, Aged, 80 and over, Amyloid beta-Peptides, Apolipoprotein E4, Biomarkers, Brain, Cerebrospinal Fluid, Cognitive Dysfunction, Female, Genotype, Humans, Male, Middle Aged, Positron-Emission Tomography, Prevalence, Risk Factors, Amyloid Biomarker Study Group, Medical and Health Sciences, General & Internal Medicine, Biomedical and clinical sciences, Health sciences
Abstract

ImportanceCerebral amyloid-β aggregation is an early pathological event in Alzheimer disease (AD), starting decades before dementia onset. Estimates of the prevalence of amyloid pathology in persons without dementia are needed to understand the development of AD and to design prevention studies.ObjectiveTo use individual participant data meta-analysis to estimate the prevalence of amyloid pathology as measured with biomarkers in participants with normal cognition, subjective cognitive impairment (SCI), or mild cognitive impairment (MCI).Data sourcesRelevant biomarker studies identified by searching studies published before April 2015 using the MEDLINE and Web of Science databases and through personal communication with investigators.Study selectionStudies were included if they provided individual participant data for participants without dementia and used an a priori defined cutoff for amyloid positivity.Data extraction and synthesisIndividual records were provided for 2914 participants with normal cognition, 697 with SCI, and 3972 with MCI aged 18 to 100 years from 55 studies.Main outcomes and measuresPrevalence of amyloid pathology on positron emission tomography or in cerebrospinal fluid according to AD risk factors (age, apolipoprotein E [APOE] genotype, sex, and education) estimated by generalized estimating equations.ResultsThe prevalence of amyloid pathology increased from age 50 to 90 years from 10% (95% CI, 8%-13%) to 44% (95% CI, 37%-51%) among participants with normal cognition; from 12% (95% CI, 8%-18%) to 43% (95% CI, 32%-55%) among patients with SCI; and from 27% (95% CI, 23%-32%) to 71% (95% CI, 66%-76%) among patients with MCI. APOE-ε4 carriers had 2 to 3 times higher prevalence estimates than noncarriers. The age at which 15% of the participants with normal cognition were amyloid positive was approximately 40 years for APOE ε4ε4 carriers, 50 years for ε2ε4 carriers, 55 years for ε3ε4 carriers, 65 years for ε3ε3 carriers, and 95 years for ε2ε3 carriers. Amyloid positivity was more common in highly educated participants but not associated with sex or biomarker modality.Conclusions and relevanceAmong persons without dementia, the prevalence of cerebral amyloid pathology as determined by positron emission tomography or cerebrospinal fluid findings was associated with age, APOE genotype, and presence of cognitive impairment. These findings suggest a 20- to 30-year interval between first development of amyloid positivity and onset of dementia.

Published
2015

21. Multiethnic Genome-Wide Association Study of Cerebral White Matter Hyperintensities on MRI

Author

Verhaaren, Benjamin FJ, Debette, Stéphanie, Bis, Joshua C, Smith, Jennifer A, Ikram, M Kamran, Adams, Hieab H, Beecham, Ashley H, Rajan, Kumar B, Lopez, Lorna M, Barral, Sandra, van Buchem, Mark A, van der Grond, Jeroen, Smith, Albert V, Hegenscheid, Katrin, Aggarwal, Neelum T, de Andrade, Mariza, Atkinson, Elizabeth J, Beekman, Marian, Beiser, Alexa S, Blanton, Susan H, Boerwinkle, Eric, Brickman, Adam M, Bryan, R Nick, Chauhan, Ganesh, Chen, Christopher PLH, Chouraki, Vincent, de Craen, Anton JM, Crivello, Fabrice, Deary, Ian J, Deelen, Joris, De Jager, Philip L, Dufouil, Carole, Elkind, Mitchell SV, Evans, Denis A, Freudenberger, Paul, Gottesman, Rebecca F, Guðnason, Vilmundur, Habes, Mohamad, Heckbert, Susan R, Heiss, Gerardo, Hilal, Saima, Hofer, Edith, Hofman, Albert, Ibrahim-Verbaas, Carla A, Knopman, David S, Lewis, Cora E, Liao, Jiemin, Liewald, David CM, Luciano, Michelle, van der Lugt, Aad, Martinez, Oliver O, Mayeux, Richard, Mazoyer, Bernard, Nalls, Mike, Nauck, Matthias, Niessen, Wiro J, Oostra, Ben A, Psaty, Bruce M, Rice, Kenneth M, Rotter, Jerome I, von Sarnowski, Bettina, Schmidt, Helena, Schreiner, Pamela J, Schuur, Maaike, Sidney, Stephen S, Sigurdsson, Sigurdur, Slagboom, P Eline, Stott, David JM, van Swieten, John C, Teumer, Alexander, Töglhofer, Anna Maria, Traylor, Matthew, Trompet, Stella, Turner, Stephen T, Tzourio, Christophe, Uh, Hae-Won, Uitterlinden, André G, Vernooij, Meike W, Wang, Jing J, Wong, Tien Y, Wardlaw, Joanna M, Windham, B Gwen, Wittfeld, Katharina, Wolf, Christiane, Wright, Clinton B, Yang, Qiong, Zhao, Wei, Zijdenbos, Alex, Jukema, J Wouter, Sacco, Ralph L, Kardia, Sharon LR, Amouyel, Philippe, Mosley, Thomas H, Longstreth, WT, DeCarli, Charles C, van Duijn, Cornelia M, Schmidt, Reinhold, Launer, Lenore J, Grabe, Hans J, and Seshadri, Sudha S

Subjects
Aging, Brain Disorders, Neurodegenerative, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Biotechnology, Human Genome, Genetics, Acquired Cognitive Impairment, Clinical Research, Dementia, Alzheimer's Disease, Prevention, Stroke, Neurosciences, Aetiology, 2.1 Biological and endogenous factors, Aged, Aged, 80 and over, Chromosomes, Human, Female, Genetic Loci, Genome-Wide Association Study, Humans, Male, Meta-Analysis as Topic, Middle Aged, Models, Genetic, Racial Groups, White Matter, cerebral small vessel diseases, cerebrovascular disorders, genome-wide association study, hypertension, leukoencephalopathies, polymorphisms, single nucleotide, Medical Biotechnology, Cardiorespiratory Medicine and Haematology, Cardiovascular System & Hematology
Abstract

BackgroundThe 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 resultsWe 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).ConclusionsWe identified 4 novel genetic loci that implicate inflammatory and glial proliferative pathways in the development of WMH in addition to previously proposed ischemic mechanisms.

Published
2015

24. Incidence and Clinical Significance of Cerebral Embolism During Atrial Fibrillation Ablation With Duty-Cycled Phased-Radiofrequency Versus Cooled-Radiofrequency: A Randomized Controlled Trial

Author

Keçe, Fehmi, Bruggemans, Eline F., de Riva, Marta, Alizadeh Dehnavi, Reza, Wijnmaalen, Adrianus P., Meulman, Tamara J., Brugman, Julia A., Rooijmans, Anouk M., van Buchem, Mark A., Middelkoop, Huub A., Eikenboom, Jeroen, Schalij, Martin J., Zeppenfeld, Katja, and Trines, Serge A.

Published
2019
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25. Vascular dysfunction—The disregarded partner of Alzheimer's disease

Author

Sweeney, Melanie D., Montagne, Axel, Sagare, Abhay P., Nation, Daniel A., Schneider, Lon S., Chui, Helena C., Harrington, Michael G., Pa, Judy, Law, Meng, Wang, Danny J.J., Jacobs, Russell E., Doubal, Fergus N., Ramirez, Joel, Black, Sandra E., Nedergaard, Maiken, Benveniste, Helene, Dichgans, Martin, Iadecola, Costantino, Love, Seth, Bath, Philip M., Markus, Hugh S., Salman, Rustam A., Allan, Stuart M., Quinn, Terence J., Kalaria, Rajesh N., Werring, David J., Carare, Roxana O., Touyz, Rhian M., Williams, Steve C.R., Moskowitz, Michael A., Katusic, Zvonimir S., Lutz, Sarah E., Lazarov, Orly, Minshall, Richard D., Rehman, Jalees, Davis, Thomas P., Wellington, Cheryl L., González, Hector M., Yuan, Chun, Lockhart, Samuel N., Hughes, Timothy M., Chen, Christopher L.H., Sachdev, Perminder, O'Brien, John T., Skoog, Ingmar, Pantoni, Leonardo, Gustafson, Deborah R., Biessels, Geert Jan, Wallin, Anders, Smith, Eric E., Mok, Vincent, Wong, Adrian, Passmore, Peter, Barkof, Frederick, Muller, Majon, Breteler, Monique M.B., Román, Gustavo C., Hamel, Edith, Seshadri, Sudha, Gottesman, Rebecca F., van Buchem, Mark A., Arvanitakis, Zoe, Schneider, Julie A., Drewes, Lester R., Hachinski, Vladimir, Finch, Caleb E., Toga, Arthur W., Wardlaw, Joanna M., and Zlokovic, Berislav V.

Published
2019
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28. Prevalence of the apolipoprotein E ε4 allele in amyloid β positive subjects across the spectrum of Alzheimer's disease

Author

Mattsson, Niklas, Groot, Colin, Jansen, Willemijn J., Landau, Susan M., Villemagne, Victor L., Engelborghs, Sebastiaan, Mintun, Mark M., Lleo, Alberto, Molinuevo, José Luis, Jagust, William J., Frisoni, Giovanni B., Ivanoiu, Adrian, Chételat, Gaël, Resende de Oliveira, Catarina, Rodrigue, Karen M., Kornhuber, Johannes, Wallin, Anders, Klimkowicz-Mrowiec, Aleksandra, Kandimalla, Ramesh, Popp, Julius, Aalten, Pauline P., Aarsland, Dag, Alcolea, Daniel, Almdahl, Ina S., Baldeiras, Inês, van Buchem, Mark A., Cavedo, Enrica, Chen, Kewei, Cohen, Ann D., Förster, Stefan, Fortea, Juan, Frederiksen, Kristian S., Freund-Levi, Yvonne, Gill, Kiran Dip, Gkatzima, Olymbia, Grimmer, Timo, Hampel, Harald, Herukka, Sanna-Kaisa, Johannsen, Peter, van Laere, Koen, de Leon, Mony J., Maier, Wolfgang, Marcusson, Jan, Meulenbroek, Olga, Møllergård, Hanne M., Morris, John C., Mroczko, Barbara, Nordlund, Arto, Prabhakar, Sudesh, Peters, Oliver, Rami, Lorena, Rodríguez-Rodríguez, Eloy, Roe, Catherine M., Rüther, Eckart, Santana, Isabel, Schröder, Johannes, Seo, Sang W., Soininen, Hilkka, Spiru, Luiza, Stomrud, Erik, Struyfs, Hanne, Teunissen, Charlotte E., Verhey, Frans R.J., Vos, Stephanie J.B., van Waalwijk van Doorn, Linda J.C., Waldemar, Gunhild, Wallin, Åsa K., Wiltfang, Jens, Vandenberghe, Rik, Brooks, David J., Fladby, Tormod, Rowe, Christopher C., Drzezga, Alexander, Verbeek, Marcel M., Sarazin, Marie, Wolk, David A., Fleisher, Adam S., Klunk, William E., Na, Duk L., Sánchez-Juan, Pascual, Lee, Dong Young, Nordberg, Agneta, Tsolaki, Magda, Camus, Vincent, Rinne, Juha O., Fagan, Anne M., Zetterberg, Henrik, Blennow, Kaj, Rabinovici, Gil D., Hansson, Oskar, van Berckel, Bart N.M., van der Flier, Wiesje M., Scheltens, Philip, Visser, Pieter Jelle, and Ossenkoppele, Rik

Published
2018
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31. Structural and functional brain connectivity in presymptomatic familial frontotemporal dementia

Author

Dopper, Elise GP, Rombouts, Serge ARB, Jiskoot, Lize C, Heijer, Tom den, de Graaf, J Roos A, de Koning, Inge, Hammerschlag, Anke R, Seelaar, Harro, Seeley, William W, Veer, Ilya M, van Buchem, Mark A, Rizzu, Patrizia, and van Swieten, John C

Subjects
Alzheimer's Disease, Aging, Dementia, Neurodegenerative, Rare Diseases, Biomedical Imaging, Prevention, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Acquired Cognitive Impairment, Brain Disorders, Neurosciences, Frontotemporal Dementia (FTD), Clinical Research, Neurological, Adult, Aged, Brain Chemistry, Case-Control Studies, Female, Frontal Lobe, Frontotemporal Dementia, Genetic Predisposition to Disease, Humans, Male, Middle Aged, Mutation, Nerve Net, Risk, Structure-Activity Relationship, Clinical Sciences, Cognitive Sciences, Neurology & Neurosurgery
Abstract

ObjectiveWe aimed to investigate whether cognitive deficits and structural and functional connectivity changes can be detected before symptom onset in a large cohort of carriers of microtubule-associated protein tau and progranulin mutations.MethodsIn this case-control study, 75 healthy individuals (aged 20-70 years) with 50% risk for frontotemporal dementia (FTD) underwent DNA screening, neuropsychological assessment, and structural and functional MRI. We used voxel-based morphometry and tract-based spatial statistics for voxelwise analyses of gray matter volume and diffusion tensor imaging measures. Using resting-state fMRI scans, we assessed whole-brain functional connectivity to frontoinsula, anterior midcingulate cortex (aMCC), and posterior cingulate cortex.ResultsAlthough carriers (n = 37) and noncarriers (n = 38) had similar neuropsychological performance, worse performance on Stroop III, Ekman faces, and Happé cartoons correlated with higher age in carriers, but not controls. Reduced fractional anisotropy and increased radial diffusivity throughout frontotemporal white matter tracts were found in carriers and correlated with higher age. Reductions in functional aMCC connectivity were found in carriers compared with controls, and connectivity between frontoinsula and aMCC seeds and several brain regions significantly decreased with higher age in carriers but not controls. We found no significant differences or age correlations in posterior cingulate cortex connectivity. No differences in regional gray matter volume were found.ConclusionsThis study convincingly demonstrates that alterations in structural and functional connectivity develop before the first symptoms of FTD arise. These findings suggest that diffusion tensor imaging and resting-state fMRI may have the potential to become sensitive biomarkers for early FTD in future clinical trials.

Published
2013

33. Neuroimaging in Dementia

Author

Barkhof, Frederik, van Buchem, Mark A., Hodler, Jürg, editor, Kubik-Huch, Rahel A., editor, and von Schulthess, Gustav K., editor

Published
2016
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34. Predicting progression to dementia in persons with mild cognitive impairment using cerebrospinal fluid markers

Author

Handels, Ron L.H., Vos, Stephanie J.B., Kramberger, Milica G., Jelic, Vesna, Blennow, Kaj, van Buchem, Mark, van der Flier, Wiesje, Freund-Levi, Yvonne, Hampel, Harald, Olde Rikkert, Marcel, Oleksik, Ania, Pirtosek, Zvezdan, Scheltens, Philip, Soininen, Hilkka, Teunissen, Charlotte, Tsolaki, Magda, Wallin, Asa K., Winblad, Bengt, Verhey, Frans R.J., and Visser, Pieter Jelle

Published
2017
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37. Decreased cerebral perfusion in Duchenne muscular dystrophy patients

Author

Doorenweerd, Nathalie, Dumas, Eve M., Ghariq, Eidrees, Schmid, Sophie, Straathof, Chiara S.M., Roest, Arno A.W., Wokke, Beatrijs H., van Zwet, Erik W., Webb, Andrew G., Hendriksen, Jos G.M., van Buchem, Mark A., Verschuuren, Jan J.G.M., Asllani, Iris, Niks, Erik H., van Osch, Matthias J.P., and Kan, Hermien E.

Published
2017
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39. A holistic approach to implementing artificial intelligence in radiology.

Author

Kim, Bomi, Romeijn, Stephan, van Buchem, Mark, Mehrizi, Mohammad Hosein Rezazade, and Grootjans, Willem

Abstract

Objective: Despite the widespread recognition of the importance of artificial intelligence (AI) in healthcare, its implementation is often limited. This article aims to address this implementation gap by presenting insights from an in-depth case study of an organisation that approached AI implementation with a holistic approach. Materials and methods: We conducted a longitudinal, qualitative case study of the implementation of AI in radiology at a large academic medical centre in the Netherlands for three years. Collected data consists of 43 days of work observations, 30 meeting observations, 18 interviews and 41 relevant documents. Abductive reasoning was used for systematic data analysis, which revealed three change initiative themes responding to specific AI implementation challenges. Results: This study identifies challenges of implementing AI in radiology at different levels and proposes a holistic approach to tackle those challenges. At the technology level, there is the issue of multiple narrow AI applications with no standard use interface; at the workflow level, AI results allow limited interaction with radiologists; at the people and organisational level, there are divergent expectations and limited experience with AI. The case of Southern illustrates that organisations can reap more benefits from AI implementation by investing in long-term initiatives that holistically align both social and technological aspects of clinical practice. Conclusion: This study highlights the importance of a holistic approach to AI implementation that addresses challenges spanning technology, workflow, and organisational levels. Aligning change initiatives between these different levels has proven to be important to facilitate wide-scale implementation of AI in clinical practice. Critical relevance statement: Adoption of artificial intelligence is crucial for future-ready radiological care. This case study highlights the importance of a holistic approach that addresses technological, workflow, and organisational aspects, offering practical insights and solutions to facilitate successful AI adoption in clinical practice. Key points: 1. Practical and actionable insights into successful AI implementation in radiology are lacking. 2. Aligning technology, workflow, organisational aspects is crucial for a successful AI implementation 3. Holistic approach aids organisations to create sustainable value through AI implementation. [ABSTRACT FROM AUTHOR]

Published
2024
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47. Genetic and lifestyle risk factors for MRI-defined brain infarcts in a population-based setting

Author

Chauhan, Ganesh, Adams, Hieab H.H., Satizabal, Claudia L., Bis, Joshua C., Teumer, Alexander, Sargurupremraj, Muralidharan, Hofer, Edith, Trompet, Stella, Hilal, Saima, Smith, Albert Vernon, Jian, Xueqiu, Malik, Rainer, Traylor, Matthew, Pulit, Sara L., Amouyel, Philippe, Mazoyer, Bernard, Zhu, Yi-Cheng, Kaffashian, Sara, Schilling, Sabrina, Beecham, Gary W., Montine, Thomas J., Schellenberg, Gerard D., Kjartansson, Olafur, Guðnason, Vilmundur, Knopman, David S., Griswold, Michael E., Windham, B. Gwen, Gottesman, Rebecca F., Mosley, Thomas H., Schmidt, Reinhold, Saba, Yasaman, Schmidt, Helena, Takeuchi, Fumihiko, Yamaguchi, Shuhei, Nabika, Toru, Kato, Norihiro, Rajan, Kumar B., Aggarwal, Neelum T., De Jager, Philip L., Evans, Denis A., Psaty, Bruce M., Rotter, Jerome I., Rice, Kenneth, Lopez, Oscar L., Liao, Jiemin, Chen, Christopher, Cheng, Ching-Yu, Wong, Tien Y., Ikram, Mohammad K., van der Lee, Sven J., Amin, Najaf, Chouraki, Vincent, DeStefano, Anita L., Aparicio, Hugo J., Romero, Jose R., Maillard, Pauline, DeCarli, Charles, Wardlaw, Joanna M., Hernández, Maria del C. Valdés, Luciano, Michelle, Liewald, David, Deary, Ian J., Starr, John M., Bastin, Mark E., Muñoz Maniega, Susana, Slagboom, P. Eline, Beekman, Marian, Deelen, Joris, Uh, Hae-Won, Lemmens, Robin, Brodaty, Henry, Wright, Margaret J., Ames, David, Boncoraglio, Giorgio B., Hopewell, Jemma C., Beecham, Ashley H., Blanton, Susan H., Wright, Clinton B., Sacco, Ralph L., Wen, Wei, Thalamuthu, Anbupalam, Armstrong, Nicola J., Chong, Elizabeth, Schofield, Peter R., Kwok, John B., van der Grond, Jeroen, Stott, David J., Ford, Ian, Jukema, J. Wouter, Vernooij, Meike W., Hofman, Albert, Uitterlinden, André G., van der Lugt, Aad, Wittfeld, Katharina, Grabe, Hans J., Hosten, Norbert, von Sarnowski, Bettina, Völker, Uwe, Levi, Christopher, Jimenez-Conde, Jordi, Sharma, Pankaj, Sudlow, Cathie L.M., Rosand, Jonathan, Woo, Daniel, Cole, John W., Meschia, James F., Slowik, Agnieszka, Thijs, Vincent, Lindgren, Arne, Melander, Olle, Grewal, Raji P., Rundek, Tatjana, Rexrode, Kathy, Rothwell, Peter M., Arnett, Donna K., Jern, Christina, Johnson, Julie A., Benavente, Oscar R., Wasssertheil-Smoller, Sylvia, Lee, Jin-Moo, Wong, Quenna, Mitchell, Braxton D., Rich, Stephen S., McArdle, Patrick F., Geerlings, Mirjam I., van der Graaf, Yolanda, de Bakker, Paul I.W., Asselbergs, Folkert W., Srikanth, Velandai, Thomson, Russell, McWhirter, Rebekah, Moran, Chris, Callisaya, Michele, Phan, Thanh, Rutten-Jacobs, Loes C.A., Bevan, Steve, Tzourio, Christophe, Mather, Karen A., Sachdev, Perminder S., van Duijn, Cornelia M., Worrall, Bradford B., Dichgans, Martin, Kittner, Steven J., Markus, Hugh S., Ikram, Mohammad A., Fornage, Myriam, Launer, Lenore J., Seshadri, Sudha, Longstreth, W.T., Jr, Debette, Stéphanie, Almgren, Peter, Anderson, Christopher D., Arnett, Donna K., Attia, John, Ay, Hakan, Benavente, Oscar R., Bevan, Steve, Brown, Robert D., Bustamante, Mariana, Cheng, Yu-Ching, Cole, John W., Cotlarciuc, Ioana, Cruchaga, Carlos, de Bakker, Paul IW., Delavaran, Hossein, Dichgans, Martin, Engström, Gunnar, Fornage, Myriam, Grewal, Raji P., Heitsch, Laura, Holliday, Elizabeth, Ibanez, Laure, Ilinca, Andreea, Irvin, Marguerite R., Jackson, Rebecca D., Jern, Christina, Jimenez-Conde, Jordi, Johnson, Julie A., Jood, Katarina, Kissela, Brett M., Kittner, Steven J., Kleindorfer, Dawn O., Labovitz, Daniel, Laurie, Cathy C., Lee, Jin-Moo, Lemmens, Robin, Levi, Christopher, Li, Linxin, Lindgren, Arne G., Maguire, Jane, Markus, Hugh S., McArdle, Patrick F., Melander, Olle, Meschia, James F., Mitchell, Braxton D., Müller-Nurasyid, Martina, Norrving, Bo, Peddareddygari, Leema Reddy, Pera, Joanna, Pulit, Sara L., Rexrode, Kathryn, Ribasés, Marta, Roquer, Jaume, Rost, Natalia S., Rothwell, Peter M., Rundek, Tatjana, Sacco, Ralph L., Schmidt, Reinhold, Sharma, Pankaj, Slowik, Agnieszka, Soriano-Tárraga, Carolina, Stanne, Tara, Stauch, Konstantin, Stine, O C., Sudlow, Cathie LM., Thijs, Vincent N.S., Wasssertheil-Smoller, Sylvia, Weir, David, Williams, Stephen R., Wong, Quenna, Woo, Daniel, Worrall, Bradford B., Xu, Huichun, Seshadri, Sudha, Hyacinth, Hyacinth I, Marini, Sandro, Nyquist, Paul, Lewis, Cathryn, Hansen, Bjorn, Norrving, Bo, Rosand, Jonathan, Biffi, Alessandro, Kourkoulis, Christina, Anderson, Chris, Giese, Anne-Katrin, Sacco, Ralph, Sharma, Pankaj, Chung, Jong-Won, Kim, Gyeong-Moon, Lubitz, Steven, Bourcier, Romain, Howson, Joanna, Granata, Alessandra, Drazyk, Anna, Markus, Hugh, Wardlaw, Joanna, Mitchell, Braxton, Cole, John, Hopewell, Jemma, Walters, Robin, Turnbull, Iain, Worrall, Bradford, Bis, Josh, Reiner, Alex, Dhar, Raj, Heitsch, Laura, Lee, Jin-Moo, Prasad, Kameshwar, Sarnowski, Chloé, Aparicio, Hugo Javier, Yang, Qiong, Chasman, Daniel, Rexrode, Kathryn, Phuah, Chia-Ling, Liu, Guiyou, Elkind, Mitchell, Lange, Leslie, Rost, Natalia, James, Michael, Stewart, Jill, Vojinovic, Dina, Thijs, Vincent, Parati, Eugenio, Boncoraglio, Giorgio, Zand, Ramin, Bijlenga, Philippe, Selim, Magdy, Grond-Ginsbach, Caspar, Strbian, Daniel, Tomppo, Liisa, Sallinen, Hanne, Pfeiffer, Dorothea, Torres, Nuria, Barboza, Miguel, Laarman, Melanie, Carriero, Roberta, Holliday, Elizabeth, Jimenez-Conde, Jordi, Soriano, Carolina, Gill, Dipender, Debette, Stephanie, Mishra, Aniket, Wu, Jer-Yuarn, Ko, Tai-Ming, Bione, Silvia, Jood, Katarina, Tatlisumak, Turgut, Holmegaard, Lukas, Yue, Suo, bersano, Anna, Pera, Joanna, Slowik, Agnieszka, Levi, Christopher, Schlicht, Kristina, Lemmens, Robin, Ninomiya, Toshiharu, Oberstein, Saskia Lesnik, Lee, Tsong-Hai, Malik, Rainer, Dichgans, Martin, Lindgren, Arne, 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Published
2019
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49. White matter hyperintensity shape is associated with long‐term dementia risk.

Author

Keller, Jasmin Annica, Sigurdsson, Sigurdur, Klaassen, Kelly, Hirschler, Lydiane, van Buchem, Mark A., Launer, Lenore J., van Osch, Matthias J. P., Gudnason, Vilmundur, and de Bresser, Jeroen

Abstract

INTRODUCTION: We aimed to investigate the association between white matter hyperintensity (WMH) shape and volume and the long‐term dementia risk in community‐dwelling older adults. METHODS: Three thousand seventy‐seven participants (mean age: 75.6 ± 5.2 years) of the Age Gene/Environment Susceptibility (AGES)‐Reykjavik study underwent baseline 1.5T brain magnetic resonance imaging and were followed up for dementia (mean follow‐up: 9.9 ± 2.6 years). RESULTS: More irregular shape of periventricular/confluent WMH (lower solidity (hazard ratio (95% confidence interval) 1.34 (1.17 to 1.52), p <.001) and convexity 1.38 (1.28 to 1.49), p <.001); higher concavity index 1.43 (1.32 to 1.54), p <.001) and fractal dimension 1.45 (1.32 to 1.58), p <.001)), higher total WMH volume (1.68 (1.54 to 1.87), p <.001), higher periventricular/confluent WMH volume (1.71 (1.55 to 1.89), p <.001), and higher deep WMH volume (1.17 (1.08 to 1.27), p <.001) were associated with an increased long‐term dementia risk. DISCUSSION: WMH shape markers may in the future be useful in determining patient prognosis and may aid in patient selection for future preventive treatments in community‐dwelling older adults. [ABSTRACT FROM AUTHOR]

Published
2023
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