N
Nathalie Brouwers
Researcher at University of Antwerp
Publications - 55
Citations - 3929
Nathalie Brouwers is an academic researcher from University of Antwerp. The author has contributed to research in topics: Single-nucleotide polymorphism & Secretion. The author has an hindex of 29, co-authored 53 publications receiving 3563 citations. Previous affiliations of Nathalie Brouwers include Pompeu Fabra University & Flanders Institute for Biotechnology.
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Journal ArticleDOI
APOE and Alzheimer disease: a major gene with semi-dominant inheritance
Emmanuelle Génin,Didier Hannequin,David Wallon,Kristel Sleegers,Mikko Hiltunen,Onofre Combarros,María J. Bullido,Sebastiaan Engelborghs,P.P. De Deyn,Claudine Berr,Florence Pasquier,Bruno Dubois,Gloria Tognoni,Nathalie Fievet,Nathalie Fievet,Nathalie Brouwers,Karolien Bettens,Beatrice Arosio,Eliecer Coto,M. Del Zompo,Ignacio Mateo,Jacques Epelbaum,Anna Frank-García,Seppo Helisalmi,Elisa Porcellini,Alberto Pilotto,Paola Forti,Raffaele Ferri,Elio Scarpini,Gabriele Siciliano,Vincenzo Solfrizzi,Sandro Sorbi,Gianfranco Spalletta,Fernando Valdivieso,Saila Vepsäläinen,Victoria Alvarez,P. Bosco,Michelangelo Mancuso,Francesco Panza,Benedetta Nacmias,Paola Bossù,Oliver Hanon,Paola Piccardi,Giorgio Annoni,Davide Seripa,Daniela Galimberti,Federico Licastro,Hilkka Soininen,J. F. Dartigues,Kamboh Mi,C. Van Broeckhoven,Jean-Charles Lambert,Jean-Charles Lambert,P. Amouyel,Dominique Campion +54 more
TL;DR: Apolipoprotein E (APOE) dependent lifetime risks (LTRs) for Alzheimer Disease (AD) are currently not accurately known and odds ratios alone are insufficient to assess these risks as mentioned in this paper.
Journal ArticleDOI
APP duplication is sufficient to cause early onset Alzheimer's dementia with cerebral amyloid angiopathy.
Kristel Sleegers,Nathalie Brouwers,Ilse Gijselinck,Jessie Theuns,Dirk Goossens,Jan Wauters,Jurgen Del-Favero,Marc Cruts,Cornelia M. van Duijn,Christine Van Broeckhoven +9 more
TL;DR: It is indicated that APP locus duplications explained <2% of familial, non-autosomal dominant Alzheimer's disease and are an infrequent cause of de novo mutation.
Journal ArticleDOI
Potent amyloidogenicity and pathogenicity of Aβ43
Takashi Saito,Takahiro Suemoto,Nathalie Brouwers,Kristel Sleegers,Satoru Funamoto,Naomi Mihira,Yukio Matsuba,Kazuyuki Yamada,Per Nilsson,Jiro Takano,Masaki Nishimura,Nobuhisa Iwata,Nobuhisa Iwata,Christine Van Broeckhoven,Yasuo Ihara,Takaomi C. Saido +15 more
TL;DR: The authors showed that Aβ43 showed a higher propensity to aggregate and was more neurotoxic than Aβ42, and other pathogenic presenilin mutations also caused overproduction of Aβ 43 in a manner correlating with Aβ 42 and with the age of disease onset.
Journal ArticleDOI
Molecular genetics of Alzheimer's disease: an update.
TL;DR: An overview of the current understanding in the field of AD genetics, covering both the rare monogenic forms as well as recent developments in the search for novel AD susceptibility genes is provided.
Journal ArticleDOI
Serum biomarker for progranulin‐associated frontotemporal lobar degeneration
Kristel Sleegers,Nathalie Brouwers,Nathalie Brouwers,Philip Van Damme,Sebastiaan Engelborghs,Ilse Gijselinck,Ilse Gijselinck,Julie van der Zee,Julie van der Zee,Karin Peeters,Karin Peeters,Maria Mattheijssens,Maria Mattheijssens,Marc Cruts,Marc Cruts,Rik Vandenberghe,Peter Paul De Deyn,Wim Robberecht,Christine Van Broeckhoven,Christine Van Broeckhoven +19 more
TL;DR: A biomarker allowing rapid detection of a loss of progranulin (PGRN) was tested and found to explain a considerable portion of the occurrence of frontotemporal lobar degeneration.