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1. Large-scale assessment of polyglutamine repeat expansions in Parkinson disease

Author

Wang, L, Aasly, J, Annesi, G, Bardien, S, Bozi, M, Brice, A, Carr, J, Chung, S, Clarke, C, Crosiers, D, Deutschländer, A, Eckstein, G, Farrer, M, Goldwurm, S, Garraux, G, Hadjigeorgiou, G, Hicks, A, Hattori, N, Klein, C, Jeon, B, Kim, Y, Lesage, S, Lin, J, Lynch, T, Lichtner, P, Lang, A, Mok, V, Jasinska-Myga, B, Mellick, G, Morrison, K, Opala, G, Pihlstrøm, L, Pramstaller, P, Park, S, Quattrone, A, Rogaeva, E, Ross, O, Stefanis, L, Stockton, J, Silburn, P, Theuns, J, Tan, E, Tomiyama, H, Toft, M, Van Broeckhoven, C, Uitti, R, Wirdefeldt, K, Wszolek, Z, Xiromerisiou, G, Yueh, K, Zhao, Y, Gasser, T, Maraganore, D, Krüger, R, Sharma, M, Boyle, RS, Sellbach, A, O'Sullivan, JD, Sutherland, GT, Siebert, GA, Dissanayaka, NN, Pickut, B, Engelborghs, S, Meeus, B, De Deyn, PP, Cras, P, Lang, AE, Tzourio, C, Amouyel, P, Loriot, MA, Mutez, E, Duflot, A, Legendre, JP, Waucquier, N, Riess, O, Berg, D, Schulte, C, Djarmati, A, Hagenah, J, Lohman, K, Auburger, G, Hilker, R, van de Loo, S, Dardiotis, E, Tsimourtou, V, Ralli, S, Kountra, P, Patramani, G, Vogiatzi, C, Funayama, M, Yoshino, H, Li, Y, Imamichi, Y, Toda, T, Satake, W, Valente, EM, Ferraris, A, Dallapiccola, B, Ialongo, T, Brighina, L, Corradi, B, Ferrarese, C, Piolti, MR, Tarantino, P, Annesi, F, Gagliardi, M, Jeon, BS, Klodowska-Duda, G, Boczarska-Jedynak, M, Tan, EK, Belin, AC, Olson, L, Galter, D, Westerlund, M, Sydow, O, Nilsson, C, Puschmann, A, Lin, JJ, Maraganore, DM, Ahlskog, J, de Andrade, M, Lesnick, TG, Rocca, WA, Checkowa, H, Ross, OA, Wszolek, ZK, Uitti, RJ, Pathologic Biochemistry and Physiology, GEO-PD Consortium, Wang, L, Aasly, J, Annesi, G, Bardien, S, Bozi, M, Brice, A, Carr, J, Chung, S, Clarke, C, Crosiers, D, Deutschländer, A, Eckstein, G, Farrer, M, Goldwurm, S, Garraux, G, Hadjigeorgiou, G, Hicks, A, Hattori, N, Klein, C, Jeon, B, Kim, Y, Lesage, S, Lin, J, Lynch, T, Lichtner, P, Lang, A, Mok, V, Jasinska-Myga, B, Mellick, G, Morrison, K, Opala, G, Pihlstrøm, L, Pramstaller, P, Park, S, Quattrone, A, Rogaeva, E, Ross, O, Stefanis, L, Stockton, J, Silburn, P, Theuns, J, Tan, E, Tomiyama, H, Toft, M, Van Broeckhoven, C, Uitti, R, Wirdefeldt, K, Wszolek, Z, Xiromerisiou, G, Yueh, K, Zhao, Y, Gasser, T, Maraganore, D, Krüger, R, Sharma, M, Boyle, R, Sellbach, A, O'Sullivan, J, Sutherland, G, Siebert, G, Dissanayaka, N, Pickut, B, Engelborghs, S, Meeus, B, De Deyn, P, Cras, P, Tzourio, C, Amouyel, P, Loriot, M, Mutez, E, Duflot, A, Legendre, J, Waucquier, N, Riess, O, Berg, D, Schulte, C, Djarmati, A, Hagenah, J, Lohman, K, Auburger, G, Hilker, R, van de Loo, S, Dardiotis, E, Tsimourtou, V, Ralli, S, Kountra, P, Patramani, G, Vogiatzi, C, Funayama, M, Yoshino, H, Li, Y, Imamichi, Y, Toda, T, Satake, W, Valente, E, Ferraris, A, Dallapiccola, B, Ialongo, T, Brighina, L, Corradi, B, Ferrarese, C, Piolti, M, Tarantino, P, Annesi, F, Gagliardi, M, Klodowska-Duda, G, Boczarska-Jedynak, M, Belin, A, Olson, L, Galter, D, Westerlund, M, Sydow, O, Nilsson, C, Puschmann, A, Ahlskog, J, de Andrade, M, Lesnick, T, Rocca, W, and Checkowa, H

Subjects
Male, Age at onset, confidence interval, Genetic Epidemiology of Parkinson's Disease, Parkinson disease, spinocerebellar ataxia, Nerve Tissue Proteins, Disease, Biology, Parkinson Disease/epidemiology, Trinucleotide Repeat Expansion/genetics, Gene Frequency, Ataxins/genetics, Humans, Nerve Tissue Proteins/genetics, Genetic Predisposition to Disease, Risk factor, Allele frequency, Nuclear Protein, Aged, risk, Genetics, Medicine(all), Nuclear Proteins, Parkinson Disease, Ataxin, Odds ratio, Middle Aged, Phenotype, Nuclear Proteins/genetics, Genetic epidemiology, Ataxins, Gene Frequency/genetics, Nerve Tissue Protein, Peptide, Cohort, Female, Neurology (clinical), Human medicine, Trinucleotide repeat expansion, Peptides, Trinucleotide Repeat Expansion, Peptides/genetics, Human
Abstract

Objectives: We aim to clarify the pathogenic role of intermediate size repeat expansions of SCA2, SCA3, SCA6, and SCA17 as risk factors for idiopathic Parkinson disease (PD). Methods: We invited researchers from the Genetic Epidemiology of Parkinson9s Disease Consortium to participate in the study. There were 12,346 cases and 8,164 controls genotyped, for a total of 4 repeats within the SCA2, SCA3, SCA6, and SCA17 genes. Fixed- and random-effects models were used to estimate the summary risk estimates for the genes. We investigated between-study heterogeneity and heterogeneity between different ethnic populations. Results: We did not observe any definite pathogenic repeat expansions for SCA2, SCA3, SCA6, and SCA17 genes in patients with idiopathic PD from Caucasian and Asian populations. Furthermore, overall analysis did not reveal any significant association between intermediate repeats and PD. The effect estimates (odds ratio) ranged from 0.93 to 1.01 in the overall cohort for the SCA2, SCA3, SCA6, and SCA17 loci. Conclusions: Our study did not support a major role for definite pathogenic repeat expansions in SCA2, SCA3, SCA6, and SCA17 genes for idiopathic PD. Thus, results of this large study do not support diagnostic screening of SCA2, SCA3, SCA6, and SCA17 gene repeats in the common idiopathic form of PD. Likewise, this largest multicentered study performed to date excludes the role of intermediate repeats of these genes as a risk factor for PD.

Published
2015
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2. Project Arrivée: Countermapping Super-diversity in Brussels and Ghent with Architecture Students

Author

Pak, B, Meeus, B, Grasl, T, Martens, B, Wurzer, G, Grasl, Thomas, Martens, Bob, and Wurzer, Gabriel

Abstract

In this paper we report on a research study in Brussels and Ghent on the affordances of geographic web platforms for countermapping. We use the term “affordance” to describe the “action possibilities latent in the environment in relation to agents and their capabilities” as introduced by Gibson (1986). Countermapping is a practice that actively challenges the dominant images of particular places (Peluso, 1995; Hodgson & Schroeder, 2002). Maps and visualizations with themes such as high densities of crime, poverty, foreigners and immigration reinforce these dominant discourses and the presumed isomorphism of particular Belgian urban neighbourhoods and crime, poverty and foreigners. Our countermapping project in this context aims at challenging dominant discourses that describe particular Belgian immigrant neighbourhoods as ‘no-go areas’, ‘ghetto’s’, ‘disadvantaged’ or ‘a foreign country’ (Schuermans et al., 2014). In order to develop a deeper understanding of these neighborhoods, there is a need for developing and testing alternative analysis and mapping strategies and tools. A new generation of geographical web (Geoweb 2.0) applications emerged during the last decade as a strong alternative to expert-led top-down production and analysis practices. Their availability and ease of use enabled novel modes of counter-mapping (Leszczynski, 2012: 544). Through these technologies, a large number of people became potential ‘sensors’ as well as ‘produsers’ of geographic information (Haklay et al. 2010)(Bruns, 2010). The possibility of facilitating collective production at a historically unprecedented scale enabled harnessing the power of masses or ‘crowdsourcing’ location-based intersubjective information (Goodchild, 2009). In this sense, Geoweb 2.0 is well-positioned for the collective countermapping of the particular urban ‘arrival neighborhoods’. In line with the aims above the research questions of our study are: • Can Geoweb 2.0 applications afford the countermapping of urban ‘arrival neighborhoods’? • What can we learn from countermaps created as a result? • What are the key factors to be considered for the facilitation of better Geoweb 2.0 supported countermapping practices? no issn publicationstatus: published ispartof: pages:369-378 ispartof: eCAADe 2015 - 33rd Annual Conference 16th-18th September 2015 pages:369-378 ispartof: International Conference on Education and Research in Computer Aided Architectural Design in Europe (eCAADe) location:Vienna date:16 Sep - 18 Sep 2015 status: published

Published
2015

8. PARK11 gene GIGYF2 in sporadic Parkinson disease in a Belgian population

Author

Meeus, B., Nuytemans, K., Crosiers, D., Engelborghs, Sebastiaan, Pals, P., Pickut, B., Peeters, K., Mattheijssens, M., Corsmit, E., Cras, P., De Deyn, P.p., Theuns, J., Van Broeckhoven, C., Clinical sciences, and Neurology

Subjects
Parkinson disease, Medicine(all), Belgium
Published
2009

9. DLB locus on chromosome 2q35-q36 represents a separate genetic entity

Author

Meeus, B., Nuytemans, K., Crosiers, D., Engelborghs, S., Pickut, B., Peeters, K., Mattheijssens, M., Corsmit, E., De Deyn, P. P., Van Broeckhoven, C., Theuns, J., Clinical sciences, Neuroprotection & Neuromodulation, and Neurology

Subjects
Medicine(all), separate genetic entity
Published
2009

10. Non-replication of association for six polymorphisms from meta-analysis of genome-wide association studies of Parkinson's disease: large-scale collaborative study

Author

Evangelou, E, Maraganore, D, Annesi, G, Brighina, L, Brice, A, Elbaz, A, Ferrarese, C, Hadjigeorgiou, G, Krueger, R, Lambert, J, Lesage, S, Markopoulou, K, Mellick, G, Meeus, B, Pedersen, N, Quattrone, A, Van Broeckhoven, C, Sharma, M, Silburn, P, Tan, E, Wirdefeldt, K, Ioannidis, J, Genetic Epidemiology of Parkinson's Disease, C, Maraganore, DM, FERRARESE, CARLO, Hadjigeorgiou, GM, Mellick, GD, Pedersen, NL, Silburn, PA, Ioannidis, JPA, Genetic Epidemiology of Parkinson's Disease Consortium, Evangelou, E, Maraganore, D, Annesi, G, Brighina, L, Brice, A, Elbaz, A, Ferrarese, C, Hadjigeorgiou, G, Krueger, R, Lambert, J, Lesage, S, Markopoulou, K, Mellick, G, Meeus, B, Pedersen, N, Quattrone, A, Van Broeckhoven, C, Sharma, M, Silburn, P, Tan, E, Wirdefeldt, K, Ioannidis, J, Genetic Epidemiology of Parkinson's Disease, C, Maraganore, DM, FERRARESE, CARLO, Hadjigeorgiou, GM, Mellick, GD, Pedersen, NL, Silburn, PA, Ioannidis, JPA, and Genetic Epidemiology of Parkinson's Disease Consortium

Abstract

Early genome-wide association (GWA) studies on Parkinson's disease (PD) have not been able to yield conclusive, replicable signals of association, perhaps due to limited sample size. We aimed to investigate whether association signals derived from the meta-analysis of the first two GWA investigations might be replicable in different populations. We examined six single-nucleotide polymorphisms (SNPs) (rs1000291, rs1865997, rs2241743, rs2282048, rs2313982, and rs3018626) that had reached nominal significance with at least two of three different strategies proposed in a previous analysis of the original GWA studies. Investigators from the "Genetic Epidemiology of Parkinson's Disease" (GEOPD) consortium were invited to join in this study. Ten teams contributed replication data from 3,458 PD cases and 3,719 controls. The data from the two previously published GWAs (599 PD cases, 592 controls and 443 sibling pairs) were considered as well. All data were synthesized using both fixed and random effects models. The summary allelic odds ratios were ranging from 0.97 to 1.09 by random effects, when all data were included. The summary estimates of the replication data sets (excluding the original GWA data) were very close to 1.00 (range 0.98-1.09) and none of the effects were nominally statistically significant. The replication data sets had significantly different results than the GWA data. Our data do not support evidence that any of these six SNPs reflect susceptibility markers for PD. Much stronger signals of statistical significance in GWA platforms are needed to have substantial chances of replication. Specifically in PD genetics, this would require much largerGWA studies and perhaps novel analytical techniques.

Published
2010

11. Aandacht voor ruimte én tijd

Author

Meeus, B., Schuermans, N., Vermeiren, K., Meeus, B., Schuermans, N., and Vermeiren, K.

Abstract

In deze Agora gaan we op zoek naar het ruimtelijk aspect van tijd en het temporele aspect van de ruimte. Tijd en ruimte zijn onlosmakelijk met elkaar verbonden. Een bijdrage vanuit KU Leuven.

Published
2010

14. Dementia with Lewy Bodies: A Role for Dementia and Parkinson's Disease Genes?

Author

Meeus, B., Verstraeten, A., Nuytemans, K., Crosiers, D., Engelborghs, S., Den Broeck, M., Brys, J., Mattheijssens, M., Peeters, K., Corsmit, E., Elinck, E., Pickut, B., Cras, P., Rik Vandenberghe, Deyn, P. P., Broeckhoven, C., Theuns, J., Clinical sciences, Neuroprotection & Neuromodulation, and Neurology

Subjects
Medicine(all), Alzheimer's disease, Lewy bodies, dementia

17. From forced migration to forced arrival: the campization of refugee accommodation in European cities

Author

René Kreichauf, Meeus, B, Arnaut, K, B, van Heur, Brussels Interdisciplinary Research centre on Migration and Minorities, Faculty of Sciences and Bioengineering Sciences, Geography, and Cosmopolis Centre for Urban Research

Subjects
Sociology and Political Science, Refugee camps, Refugee, Geography, Planning and Development, 0507 social and economic geography, Urban studies, Social Sciences(all), Temporality, Asylum, Arrival infrastructures, Socio-spatial exclusion, Standard of living, Campization, lcsh:Urban groups. The city. Urban sociology, lcsh:Social Sciences, Politics, Urban planning, lcsh:HT51-1595, Political science, 050602 political science & public administration, lcsh:HT101-395, Demography, business.industry, 05 social sciences, Forced migration, 0506 political science, lcsh:HT201-221, lcsh:H, Political economy, lcsh:Communities. Classes. Races, Original Article, Statistics, Probability and Uncertainty, business, 050703 geography, Law, Accommodation, lcsh:City population. Including children in cities, immigration
Abstract

In the aftermath of large refugee arrivals in 2015, EU regulations and national asylum laws were tightened, especially those regarding reception and accommodation. The current contribution introduces the concept of “campization” to explain the impact of law and policy changes on the socio-spatial configuration and functions of refugee accommodation in European capital regions. Based on qualitative research concerning case studies for Athens, Berlin, and Copenhagen, I argue that refugee accommodation has increasingly been transformed into large, camp-like structures with lowered living standards and a closed character. This is shown by the structural, functional, and socio-spatial characteristics of the accommodation in the three case studies, as well as the political and administrative objectives that determine the campization of accommodation. The contribution lastly highlights changing notions and forms of containment, exclusion, and temporality as part of campization, and links this process to current trends in asylum and urban development.

Published
2018

18. Non-Replication of Association for Six Polymorphisms From Meta-Analysis of Genome-Wide Association Studies of Parkinson's Disease: Large-Scale Collaborative Study

Author

Peter A. Silburn, Grazia Annesi, Aldo Quattrone, Christine Van Broeckhoven, Evangelos Evangelou, Nancy L. Pedersen, George D. Mellick, Alexis Brice, Demetrius M. Maraganore, Eng-King Tan, Jean-Charles Lambert, Karin Wirdefeldt, Carlo Ferrarese, Rejko Krueger, Alexis Elbaz, Katerina Markopoulou, Laura Brighina, Georgios M. Hadjigeorgiou, John P. A. Ioannidis, Suzanne Lesage, Bram Meeus, Manu Sharma, Clinical and Molecular Epidemiology Unit, Department of Hygiene and Epidemiology, University of Ioannina, Institute of Microbiology, Université de Lausanne = University of Lausanne (UNIL), Department of Neurology, Mayo Clinic College of Medicine, Institute of Neurological Sciences, National Research Council [Italy] (CNR), Section of Neurology, Università degli Studi di Milano-Bicocca = University of Milano-Bicocca (UNIMIB)-San Gerardo Hospital of Monza, Neurologie et thérapeutique expérimentale, Université Pierre et Marie Curie - Paris 6 (UPMC)-IFR70-Institut National de la Santé et de la Recherche Médicale (INSERM), Neuroépidémiologie, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratory of Neurogenetics, Deparment of Neurology, University of Thessaly [Volos] (UTH), Institute of Biomedical Research & Technology, CERETETH, University Hospital Tuebingen-Hertie Institute for Clinical Brain Research, Epidémiologie des maladies chroniques : impact des interactions gène environnement sur la santé des populations, Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille, Droit et Santé, Eskitis Institute for Cell and Molecular Therapies, Griffith University [Brisbane], Neurodegenerative Brain Diseases Group, VIB, Laboratory of Neurogenetics, Born-Bunge Institute [Anvers], University of Antwerp (UA), Department of Medical Epidemiology and Biostatistics (MEB), Karolinska Institutet [Stockholm], Institute of Neurology, Università degli Studi 'Magna Graecia' di Catanzaro = University of Catanzaro (UMG), Duke-NUS Medical School [Singapore], Singapore General Hospital-National Neuroscience Institute, Biomedical Research Institute, Foundation for Research and Technology - Hellas (FORTH), Institute for Clinical Research and Health Policy Studies, Tufts Universiy, Inserm, MSA, Agence Nationale de la Recherche, Agence Francaise de Securite Sanitaire de l'Environnement et du Travail, France Parkinson, FIRB 2003 GENOPOLIS Project, National Institutes of Health (NIH) 2R01 ES10751 ES10758 AG 08724, Michael J. Fox Grants, Swedish Medical Research Council, Swedish Society of Medicine, Parkinson Foundation in Sweden, VIB Genetic Service Facility, The Biobank of the Institute Born-Bunge, Fund for Scientific Research Flanders Institute for Science and Technology - Flanders (IWT-V), Foundation for Alzheimer Research (SAO/FRMA), Interuniversity Attraction Poles Program P6/43 of the Belgian Science Policy Office, Belgium, Genetic Epidemiology of Parkinson's Disease (GEOPD) Consortium, Evangelou, E, Maraganore, D, Annesi, G, Brighina, L, Brice, A, Elbaz, A, Ferrarese, C, Hadjigeorgiou, G, Krueger, R, Lambert, J, Lesage, S, Markopoulou, K, Mellick, G, Meeus, B, Pedersen, N, Quattrone, A, Van Broeckhoven, C, Sharma, M, Silburn, P, Tan, E, Wirdefeldt, K, Ioannidis, J, Genetic Epidemiology of Parkinson's Disease, C, University of Ioannina Medical School, Université de Lausanne (UNIL), Università degli Studi di Milano-Bicocca [Milano] (UNIMIB)-San Gerardo Hospital, Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR70-Université Pierre et Marie Curie - Paris 6 (UPMC), Università degli Studi 'Magna Graecia' di Catanzaro [Catanzaro, Italie] (UMG), Theuns, Jessie, Crosiers, David, Pals, Philippe, Engelborghs, Sebastiaan, De Deyn, Peter Paul, Cras, Patrick, et al., Genetic Epidemiology of Parkinson's Disease Consortium, Sutherland, G.T., Siebert, G.A., Theuns, J., Crosiers, D., Pickut, B., Pals, P., Engelborghs, S., Nuytemans, K., De Deyn, P.P., Cras, P., Agid, Y., Bonnet, A.M., Borg, M., Brice, A., Broussolle, E., Damier, P., Destée, A., Dürr, A., Durif, F., Lesage, S., Lohmann, E., Pollak, P., Rascol, O., Tison, F., Tranchant, C., Viallet, F., Vidailhet, M., Tzourio, C., Amouyel, P., Loriot, M.A., Gasser, T., Riess, O., Berg, D., Schulte, C., Klein, C., Djarmati, A., Lohmann, K., Xiromerisiou, G., Dardiotis, E., Kountra, P., Hattori, N., Tomiyama, H., Funayama, M., Yoshino, H., Li, Y., Valente, E.M., Ferraris, A., Bentivoglio, A.R., Ialongo, T., Riva, C., Corradi, B., Opala, G., Jasinska-Myga, B., Klodowska-Duda, G., Boczarska-Jedyna, M., Belin, A., Olson, L., Galter, D., Westerlund, M., Sydow, O., Nilsson, C., Puschmann, A., Maraganore, D.M., Ahlskog, J.E., de Andrade, M., Lesnick, T.G., Rocca, W.A., Checkoway, H., Savasta, Marc, and Pathologic Biochemistry and Physiology

Subjects
medicine.medical_specialty, Parkinson Disease/*genetics, Parkinson's disease, Single-nucleotide polymorphism, Genome-wide association study, challenges, Polymorphism, Genetic, Biology, Article, 03 medical and health sciences, Cellular and Molecular Neuroscience, 0302 clinical medicine, Replication (statistics), MESH: Polymorphism, Genetic, medicine, Humans, Meta-analysi, [SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Genome-Wide Association Study, Parkinson Disease/genetics, uncertainty, Genetics (clinical), 030304 developmental biology, Medicine(all), Genetics, 0303 health sciences, Genome-wide association, MESH: Humans, axon guidance, pathway, Parkinson Disease, Odds ratio, Random effects model, meta-analysis, Psychiatry and Mental health, Genetic epidemiology, Meta-analysis, MESH: Genome-Wide Association Study, parkinson's disease, genome-wide association, Medical genetics, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Human medicine, heterogeneity, 030217 neurology & neurosurgery, MESH: Parkinson Disease
Abstract

Early genome-wide association (GWA) studies on Parkinson's disease (PD) have not been able to yield conclusive, replicable signals of association, perhaps due to limited sample size. We aimed to investigate whether association signals derived from the meta-analysis of the first two GWA investigations might be replicable in different populations. We examined six single-nucleotide polymorphisms (SNPs) (rs1000291, rs1865997, rs2241743, rs2282048, rs2313982, and rs3018626) that had reached nominal significance with at least two of three different strategies proposed in a previous analysis of the original GWA studies. Investigators from the "Genetic Epidemiology of Parkinson's Disease" (GEOPD) consortium were invited to join in this study. Ten teams contributed replication data from 3,458 PD cases and 3,719 controls. The data from the two previously published GWAs (599 PD cases, 592 controls and 443 sibling pairs) were considered as well. All data were synthesized using both fixed and random effects models. The summary allelic odds ratios were ranging from 0.97 to 1.09 by random effects, when all data were included. The summary estimates of the replication data sets (excluding the original GWA data) were very close to 1.00 (range 0.98-1.09) and none of the effects were nominally statistically significant. The replication data sets had significantly different results than the GWA data. Our data do not support evidence that any of these six SNPs reflect susceptibility markers for PD. Much stronger signals of statistical significance in GWA platforms are needed to have substantial chances of replication. Specifically in PD genetics, this would require much larger GWA studies and perhaps novel analytical techniques. (C) 2009 Wiley-Liss, Inc. American Journal of Medical Genetics Part B-Neuropsychiatric Genetics

Published
2010
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19. Sniffing out safety: canine detection and identification of SARS-CoV-2 infection from armpit sweat.

Author

Callewaert C, Pezavant M, Vandaele R, Meeus B, Vankrunkelsven E, Van Goethem P, Plumacker A, Misset B, Darcis G, Piret S, De Vleeschouwer L, Staelens F, Van Varenbergh K, Tombeur S, Ottevaere A, Montag I, Vandecandelaere P, Jonckheere S, Vandekerckhove L, Tobback E, Wieers G, Marot JC, Anseeuw K, D'Hoore L, Tuyls S, De Tavernier B, Catteeuw J, Lotfi A, Melnik A, Aksenov A, Grandjean D, Stevens M, Gasthuys F, and Guyot H

Abstract

Detection dogs were trained to detect SARS-CoV-2 infection based on armpit sweat odor. Sweat samples were collected using cotton pads under the armpits of negative and positive human patients, confirmed by qPCR, for periods of 15-30 min. Multiple hospitals and organizations throughout Belgium participated in this study. The sweat samples were stored at -20°C prior to being used for training purposes. Six dogs were trained under controlled atmosphere conditions for 2-3 months. After training, a 7-day validation period was conducted to assess the dogs' performances. The detection dogs exhibited an overall sensitivity of 81%, specificity of 98%, and an accuracy of 95%. After validation, training continued for 3 months, during which the dogs' performances remained the same. Gas chromatography/mass spectrometry (GC/MS) analysis revealed a unique sweat scent associated with SARS-CoV-2 positive sweat samples. This scent consisted of a wide variety of volatiles, including breakdown compounds of antiviral fatty acids, skin proteins and neurotransmitters/hormones. An acceptability survey conducted in Belgium demonstrated an overall high acceptability and enthusiasm toward the use of detection dogs for SARS-CoV-2 detection. Compared to qPCR and previous canine studies, the detection dogs have good performances in detecting SARS-CoV-2 infection in humans, using frozen sweat samples from the armpits. As a result, they can be used as an accurate pre-screening tool in various field settings alongside the PCR test., Competing Interests: CC is the founder of DrArmpit BV. AA and AM are founders of Arome Science Inc. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The reviewer A-LC is currently co-organizing a Research Topic with one of the authors DG., (Copyright © 2023 Callewaert, Pezavant, Vandaele, Meeus, Vankrunkelsven, Van Goethem, Plumacker, Misset, Darcis, Piret, De Vleeschouwer, Staelens, Van Varenbergh, Tombeur, Ottevaere, Montag, Vandecandelaere, Jonckheere, Vandekerckhove, Tobback, Wieers, Marot, Anseeuw, D’Hoore, Tuyls, De Tavernier, Catteeuw, Lotfi, Melnik, Aksenov, Grandjean, Stevens, Gasthuys and Guyot.)

Published
2023
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20. Guanosine triphosphate cyclohydrolase 1 promoter deletion causes dopa-responsive dystonia.

Author

Theuns J, Crosiers D, Debaene L, Nuytemans K, Meeus B, Sleegers K, Goossens D, Corsmit E, Elinck E, Peeters K, Mattheijssens M, Pickut B, Del-Favero J, Engelborghs S, De Deyn PP, Cras P, and Van Broeckhoven C

Subjects
Adult, Belgium, Chromosome Mapping, Dopamine Agents therapeutic use, Dystonia drug therapy, Dystonia etiology, Family Health, Female, Genetic Linkage, Genome-Wide Association Study, Humans, Levodopa therapeutic use, Male, Middle Aged, Young Adult, Dystonia genetics, GTP Cyclohydrolase genetics, Promoter Regions, Genetic genetics, Sequence Deletion genetics
Abstract

Background: Autosomal dominant dopa-responsive dystonia (AD-DRD) is caused by a biochemical defect primarily resulting from guanosine triphosphate cyclohydrolase 1 gene (GCH1) mutations. Few families have been reported without mutations in GCH1., Methods: Genome-wide linkage analysis and positional cloning to identify the genetic defect in a Belgian AD-DRD family was carried out., Results and Conclusion: In this study, we report on the identification and characterization of a novel 24-kb deletion spanning exon 1 and the 5' regulatory region of GCH1 causing a wide spectrum of motor and nonmotor symptoms in a large Belgian AD-DRD family. This large-scale deletion of regulatory sequences leads to decreased GCH1 activity in all carriers, most probably resulting from allelic loss of transcription. We mapped the breakpoints of this deletion to the nucleotide level, allowing the development of a straightforward polymerase chain reaction assay for fast, efficient detection of this large deletion, which will prove valuable for preimplantation genetic diagnosis., (Copyright © 2012 Movement Disorder Society.)

Published
2012
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21. The genetics of dementia with Lewy bodies: what are we missing?

Author

Meeus B, Theuns J, and Van Broeckhoven C

Subjects
Amyloid beta-Protein Precursor genetics, Amyloid beta-Protein Precursor metabolism, Brain metabolism, Brain pathology, Humans, Lewy Bodies metabolism, Lewy Bodies pathology, Lewy Body Disease metabolism, Lewy Body Disease pathology, Presenilins genetics, Presenilins metabolism, alpha-Synuclein genetics, alpha-Synuclein metabolism, Lewy Bodies genetics, Lewy Body Disease genetics
Abstract

Dementia with Lewy bodies is a complex brain disorder and a key member of the Lewy body disease spectrum. Its genetic etiology is unclear, and information is scattered. However, the results of molecular genetic studies imply a genetic and mechanistic overlap with Alzheimer disease, Parkinson disease with dementia, and Parkinson disease. In this review, we provide a comprehensive overview of the current studies on dementia with Lewy bodies heritability, genetic etiology, and genetic heterogeneity. We conclude with a critical discussion of the missing heritability in dementia with Lewy bodies and encourage scientists to further explore the underlying mechanisms of this disease.

Published
2012
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22. Contribution of VPS35 genetic variability to LBD in the Flanders-Belgian population.

Author

Verstraeten A, Wauters E, Crosiers D, Meeus B, Corsmit E, Elinck E, Mattheijssens M, Peeters K, Cras P, Pickut B, Vandenberghe R, Engelborghs S, De Deyn PP, Van Broeckhoven C, and Theuns J

Subjects
Aged, 80 and over, Belgium epidemiology, Genetic Markers genetics, Humans, Male, Middle Aged, Prevalence, Risk Factors, Genetic Predisposition to Disease epidemiology, Genetic Predisposition to Disease genetics, Genetic Variation genetics, Lewy Body Disease epidemiology, Lewy Body Disease genetics, Polymorphism, Single Nucleotide genetics, Vesicular Transport Proteins genetics
Abstract

VPS35 was recently identified as a novel autosomal dominant gene for Parkinson disease. In this study, we aimed to determine the contribution of simple and complex VPS35 variations to the genetic etiology of the spectrum of Lewy body disorders (LBD) in a Flanders-Belgian patient cohort (n = 677). We identified 3 novel missense variations in addition to 1 silent and 1 intronic variation predicted to activate a cryptic splice site, but no copy number variations. Despite the absence of these rare variations in the control group (n = 800), we could not attain convincing evidence for pathogenicity by segregation analysis or in silico predictions. Hence, our data do not support a major role for VPS35 variations in the genetic etiology of Lewy body disorders in the Flanders-Belgian population., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Published
2012
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23. DLB and PDD: a role for mutations in dementia and Parkinson disease genes?

Author

Meeus B, Verstraeten A, Crosiers D, Engelborghs S, Van den Broeck M, Mattheijssens M, Peeters K, Corsmit E, Elinck E, Pickut B, Vandenberghe R, Cras P, De Deyn PP, Van Broeckhoven C, and Theuns J

Subjects
Adult, Aged, Aged, 80 and over, Amyloid beta-Protein Precursor genetics, Case-Control Studies, Cohort Studies, DNA Copy Number Variations genetics, Female, Genetic Predisposition to Disease epidemiology, Humans, Lewy Body Disease epidemiology, Lewy Body Disease metabolism, Male, Parkinson Disease epidemiology, Parkinson Disease metabolism, Pedigree, Prospective Studies, Genetic Predisposition to Disease genetics, Lewy Body Disease genetics, Parkinson Disease genetics, Point Mutation genetics
Abstract

Based on the substantial overlap in clinical and pathological characteristics of dementia with Lewy bodies (DLB) and Parkinson disease with dementia (PDD) with Alzheimer disease (AD) and Parkinson disease (PD) we hypothesized that these disorders might share underlying genetic factors. The contribution of both sequence and copy number variants (CNVs) in known AD and PD genes to the genetic etiology of DLB and PDD however is currently unclear. Therefore, we performed a gene-based mutation analysis of all major AD and PD genes in 99 DLB and 75 PDD patients, including familial and sporadic forms, from Flanders, Belgium. Also, copy number variants in APP, SNCA, and PARK2 were determined. In the AD genes we detected proven pathogenic missense mutations in PSEN1 and PSEN2, and 2 novel missense variants in PSEN2 and MAPT. In the PD genes we identified 1 SNCA duplication, the LRRK2 R1441C founder mutation and 4 novel heterozygous missense variants with unknown pathogenicity. Our results suggest a contribution of established AD and PD genes to the genetic etiology of DLB and PDD though to a limited extent. They do support the hypothesis of a genetic overlap between members of the Lewy body disease spectrum, but additional genes still have to exist., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Published
2012
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24. Juvenile dystonia-parkinsonism and dementia caused by a novel ATP13A2 frameshift mutation.

Author

Crosiers D, Ceulemans B, Meeus B, Nuytemans K, Pals P, Van Broeckhoven C, Cras P, and Theuns J

Subjects
Child, Dementia complications, Dementia diagnosis, Dystonia complications, Dystonia diagnosis, Humans, Male, Parkinsonian Disorders complications, Parkinsonian Disorders diagnosis, Pedigree, Video Recording, Dementia genetics, Dystonia genetics, Frameshift Mutation genetics, Parkinsonian Disorders genetics, Proton-Translocating ATPases genetics
Published
2011
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25. GIGYF2 has no major role in Parkinson genetic etiology in a Belgian population.

Author

Meeus B, Nuytemans K, Crosiers D, Engelborghs S, Pals P, Pickut B, Peeters K, Mattheijssens M, Corsmit E, Cras P, De Deyn PP, Theuns J, and Van Broeckhoven C

Subjects
Adult, Aged, Belgium ethnology, DNA Mutational Analysis, Female, Humans, Male, Middle Aged, Carrier Proteins genetics, Mutation genetics, Parkinson Disease genetics
Abstract

Missense mutations were identified in the Grb10-Interacting GYF Protein-2 gene (GIGYF2), located in the chromosomal region 2q36-q37, in familial Parkinson disease (PD) patients of European descent. To determine the contribution of GIGYF2 mutations in an extended (N=305) Belgian series of both familial and sporadic PD patients, we sequenced all 32 coding and non-coding exons of GIGYF2. In three sporadic PD patients we identified two novel heterozygous missense mutations (c.1907A>G, p.Tyr636Cys and c.2501G>A, p.Arg834Gln), that were absent from control individuals (N=360). However, since we lack genetic as well as functional data supporting their pathogenic nature, we cannot exclude that these variants are benign polymorphisms. Together, our results do not support a role for GIGYF2 in the genetic etiology of Belgian PD., (Copyright © 2009 Elsevier Inc. All rights reserved.)

Published
2011
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26. Comprehensive genetic and mutation analysis of familial dementia with Lewy bodies linked to 2q35-q36.

Author

Meeus B, Nuytemans K, Crosiers D, Engelborghs S, Peeters K, Mattheijssens M, Elinck E, Corsmit E, De Deyn PP, Van Broeckhoven C, and Theuns J

Subjects
Adult, Aged, Aged, 80 and over, Chromosome Mapping methods, DNA Copy Number Variations genetics, DNA Mutational Analysis, Databases, Genetic, Female, Genetic Linkage physiology, Genotype, Humans, Male, Middle Aged, Nerve Tissue Proteins genetics, Tandem Repeat Sequences genetics, Chromosomes, Human, Pair 2 genetics, Family Health, Lewy Body Disease genetics, Lewy Body Disease pathology
Abstract

The second most frequent form of neurodegenerative dementia after Alzheimer's disease is dementia with Lewy bodies (DLB). Since informative DLB families are scarce, little is presently known about the molecular genetic etiology of DLB. We recently mapped the first locus for DLB on chromosome 2q35-q36 in a multiplex Belgian family, DR246, with autopsy-proven DLB pathology in a region of 9.2 Mb. Here, we describe the ascertainment of additional DR246 family members and significant finemapping of the DLB locus to 3.3 Mb based on informative meiotic recombinants. Extensive sequencing of the 42 positional candidate genes within the DLB region did not identify a simple pathogenic mutation that co-segregated with disease in family DR246. Also high resolution analysis of copy number variations in the DLB locus did not provide evidence for a complex mutation. In conclusion, we confirmed the DLB locus at 2q35-q36 as a genetic entity but candidate gene-based sequencing and copy number variation analysis did not identify the pathogenic mutation in family DR246. Other detection strategies will be needed to reveal the underlying mutation explaining the linkage of DLB to 2q35-q26. Possibly the disease mutation in this family acts through a more complex mechanism than generally envisaged for monogenic disorders. Nevertheless, identifying the first familial DLB gene is likely to contribute an entry point into the pathogenic cascades underlying DLB pathology.

Published
2010
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27. Relative contribution of simple mutations vs. copy number variations in five Parkinson disease genes in the Belgian population.

Author

Nuytemans K, Meeus B, Crosiers D, Brouwers N, Goossens D, Engelborghs S, Pals P, Pickut B, Van den Broeck M, Corsmit E, Cras P, De Deyn PP, Del-Favero J, Van Broeckhoven C, and Theuns J

Subjects
Belgium epidemiology, Case-Control Studies, DNA Mutational Analysis, Gene Frequency, Genetics, Population, Humans, Intracellular Signaling Peptides and Proteins genetics, Leucine-Rich Repeat Serine-Threonine Protein Kinase-2, Oncogene Proteins genetics, Protein Deglycase DJ-1, Protein Kinases genetics, Protein Serine-Threonine Kinases genetics, Ubiquitin-Protein Ligases genetics, alpha-Synuclein genetics, Gene Dosage, Mutation, Parkinson Disease genetics
Abstract

The relative contribution of simple mutations and copy number variations (CNVs) in SNCA, PARK2, PINK1, PARK7, and LRRK2 to the genetic etiology of Parkinson disease (PD) is still unclear because most studies did not completely analyze each gene. In a large group of Belgian PD patients (N = 310) and control individuals (N = 270), we determined the mutation frequency of both simple mutations and CNVs in these five PD genes, using direct sequencing, multiplex amplicon quantification (MAQ), and real-time PCR assays. Overall, we identified 14 novel heterozygous variants, of which 11 were absent in control individuals. We observed eight PARK2 (multiple) exon multiplications in PD patients and one exon deletion in a control individual. Furthermore, we identified one SNCA whole-gene duplication. The PARK2 and LRRK2 mutation frequencies in Belgian PD patients were similar to those reported in other studies. However, at this stage the true pathogenic nature of some heterozygous mutations in recessive genes remains elusive. Furthermore, though mutations is SNCA, PINK1, and PARK7 are rare, our identification of a SNCA duplication confirmed that screening of these genes remains meaningful., ((c) 2009 Wiley-Liss, Inc.)

Published
2009
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