203 results on '"BrÅthen, Geir"'
Search Results
2. A systematic review of progranulin concentrations in biofluids in over 7,000 people—assessing the pathogenicity of GRN mutations and other influencing factors
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Swift, Imogen J., Rademakers, Rosa, Finch, NiCole, Baker, Matt, Ghidoni, Roberta, Benussi, Luisa, Binetti, Giuliano, Rossi, Giacomina, Synofzik, Matthis, Wilke, Carlo, Mengel, David, Graff, Caroline, Takada, Leonel T., Sánchez-Valle, Raquel, Antonell, Anna, Galimberti, Daniela, Fenoglio, Chiara, Serpente, Maria, Arcaro, Marina, Schreiber, Stefanie, Vielhaber, Stefan, Arndt, Philipp, Santana, Isabel, Almeida, Maria Rosario, Moreno, Fermín, Barandiaran, Myriam, Gabilondo, Alazne, Stubert, Johannes, Gómez-Tortosa, Estrella, Agüero, Pablo, Sainz, M. José, Gohda, Tomohito, Murakoshi, Maki, Kamei, Nozomu, Kittel-Schneider, Sarah, Reif, Andreas, Weigl, Johannes, Jian, Jinlong, Liu, Chuanju, Serrero, Ginette, Greither, Thomas, Theil, Gerit, Lohmann, Ebba, Gazzina, Stefano, Bagnoli, Silvia, Coppola, Giovanni, Bruni, Amalia, Quante, Mirja, Kiess, Wieland, Hiemisch, Andreas, Jurkutat, Anne, Block, Matthew S., Carlson, Aaron M., Bråthen, Geir, Sando, Sigrid Botne, Grøntvedt, Gøril Rolfseng, Lauridsen, Camilla, Heslegrave, Amanda, Heller, Carolin, Abel, Emily, Gómez-Núñez, Alba, Puey, Roger, Arighi, Andrea, Rotondo, Enmanuela, Jiskoot, Lize C., Meeter, Lieke H. H., Durães, João, Lima, Marisa, Tábuas-Pereira, Miguel, Lemos, João, Boeve, Bradley, Petersen, Ronald C., Dickson, Dennis W., Graff-Radford, Neill R., LeBer, Isabelle, Sellami, Leila, Lamari, Foudil, Clot, Fabienne, Borroni, Barbara, Cantoni, Valentina, Rivolta, Jasmine, Lleó, Alberto, Fortea, Juan, Alcolea, Daniel, Illán-Gala, Ignacio, Andres-Cerezo, Lucie, Van Damme, Philip, Clarimon, Jordi, Steinacker, Petra, Feneberg, Emily, Otto, Markus, van der Ende, Emma L., van Swieten, John C., Seelaar, Harro, Zetterberg, Henrik, Sogorb-Esteve, Aitana, and Rohrer, Jonathan D.
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- 2024
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3. Genome-wide analyses reveal a potential role for the MAPT, MOBP, and APOE loci in sporadic frontotemporal dementia
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Manzoni, Claudia, Kia, Demis A., Ferrari, Raffaele, Leonenko, Ganna, Costa, Beatrice, Saba, Valentina, Jabbari, Edwin, Tan, Manuela MX., Albani, Diego, Alvarez, Victoria, Alvarez, Ignacio, Andreassen, Ole A., Angiolillo, Antonella, Arighi, Andrea, Baker, Matt, Benussi, Luisa, Bessi, Valentina, Binetti, Giuliano, Blackburn, Daniel J., Boada, Merce, Boeve, Bradley F., Borrego-Ecija, Sergi, Borroni, Barbara, Bråthen, Geir, Brooks, William S., Bruni, Amalia C., Caroppo, Paola, Bandres-Ciga, Sara, Clarimon, Jordi, Colao, Rosanna, Cruchaga, Carlos, Danek, Adrian, de Boer, Sterre CM., de Rojas, Itziar, di Costanzo, Alfonso, Dickson, Dennis W., Diehl-Schmid, Janine, Dobson-Stone, Carol, Dols-Icardo, Oriol, Donizetti, Aldo, Dopper, Elise, Durante, Elisabetta, Ferrari, Camilla, Forloni, Gianluigi, Frangipane, Francesca, Fratiglioni, Laura, Kramberger, Milica G., Galimberti, Daniela, Gallucci, Maurizio, García-González, Pablo, Ghidoni, Roberta, Giaccone, Giorgio, Graff, Caroline, Graff-Radford, Neill R., Grafman, Jordan, Halliday, Glenda M., Hernandez, Dena G., Hjermind, Lena E., Hodges, John R., Holloway, Guy, Huey, Edward D., Illán-Gala, Ignacio, Josephs, Keith A., Knopman, David S., Kristiansen, Mark, Kwok, John B., Leber, Isabelle, Leonard, Hampton L., Libri, Ilenia, Lleo, Alberto, Mackenzie, Ian R., Madhan, Gaganjit K., Maletta, Raffaele, Marquié, Marta, Maver, Ales, Menendez-Gonzalez, Manuel, Milan, Graziella, Miller, Bruce L., Morris, Christopher M., Morris, Huw R., Nacmias, Benedetta, Newton, Judith, Nielsen, Jørgen E., Nilsson, Christer, Novelli, Valeria, Padovani, Alessandro, Pal, Suvankar, Pasquier, Florence, Pastor, Pau, Perneczky, Robert, Peterlin, Borut, Petersen, Ronald C., Piguet, Olivier, Pijnenburg, Yolande AL., Puca, Annibale A., Rademakers, Rosa, Rainero, Innocenzo, Reus, Lianne M., Richardson, Anna MT., Riemenschneider, Matthias, Rogaeva, Ekaterina, Rogelj, Boris, Rollinson, Sara, Rosen, Howard, Rossi, Giacomina, Rowe, James B., Rubino, Elisa, Ruiz, Agustin, Salvi, Erika, Sanchez-Valle, Raquel, Sando, Sigrid Botne, Santillo, Alexander F., Saxon, Jennifer A., Schlachetzki, Johannes CM., Scholz, Sonja W., Seelaar, Harro, Seeley, William W., Serpente, Maria, Sorbi, Sandro, Sordon, Sabrina, St George-Hyslop, Peter, Thompson, Jennifer C., Van Broeckhoven, Christine, Van Deerlin, Vivianna M., Van der Lee, Sven J., Van Swieten, John, Tagliavini, Fabrizio, van der Zee, Julie, Veronesi, Arianna, Vitale, Emilia, Waldo, Maria Landqvist, Yokoyama, Jennifer S., Nalls, Mike A., Momeni, Parastoo, Singleton, Andrew B., Hardy, John, and Escott-Price, Valentina
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- 2024
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4. Longitudinal cerebrospinal fluid measurements show glial hypo- and hyperactivation in predementia Alzheimer’s disease
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Nordengen, Kaja, Kirsebom, Bjørn-Eivind, Richter, Grit, Pålhaugen, Lene, Gísladóttir, Berglind, Siafarikas, Nikias, Nakling, Arne, Rongve, Arvid, Bråthen, Geir, Grøntvedt, Gøril Rolfseng, Gonzalez, Fernando, Waterloo, Knut, Sharma, Kulbhushan, Karikari, Thomas, Vromen, Eleonora M., Tijms, Betty M., Visser, Pieter J., Selnes, Per, Kramberger, Milicia G., Winblad, Bengt, Blennow, Kaj, and Fladby, Tormod
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- 2023
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5. New insights into the genetic etiology of Alzheimer’s disease and related dementias
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Bellenguez, Céline, Küçükali, Fahri, Jansen, Iris E., Kleineidam, Luca, Moreno-Grau, Sonia, Amin, Najaf, Naj, Adam C., Campos-Martin, Rafael, Grenier-Boley, Benjamin, Andrade, Victor, Holmans, Peter A., Boland, Anne, Damotte, Vincent, van der Lee, Sven J., Costa, Marcos R., Kuulasmaa, Teemu, Yang, Qiong, de Rojas, Itziar, Bis, Joshua C., Yaqub, Amber, Prokic, Ivana, Chapuis, Julien, Ahmad, Shahzad, Giedraitis, Vilmantas, Aarsland, Dag, Garcia-Gonzalez, Pablo, Abdelnour, Carla, Alarcón-Martín, Emilio, Alcolea, Daniel, Alegret, Montserrat, Alvarez, Ignacio, Álvarez, Victoria, Armstrong, Nicola J., Tsolaki, Anthoula, Antúnez, Carmen, Appollonio, Ildebrando, Arcaro, Marina, Archetti, Silvana, Pastor, Alfonso Arias, Arosio, Beatrice, Athanasiu, Lavinia, Bailly, Henri, Banaj, Nerisa, Baquero, Miquel, Barral, Sandra, Beiser, Alexa, Pastor, Ana Belén, Below, Jennifer E., Benchek, Penelope, Benussi, Luisa, Berr, Claudine, Besse, Céline, Bessi, Valentina, Binetti, Giuliano, Bizarro, Alessandra, Blesa, Rafael, Boada, Mercè, Boerwinkle, Eric, Borroni, Barbara, Boschi, Silvia, Bossù, Paola, Bråthen, Geir, Bressler, Jan, Bresner, Catherine, Brodaty, Henry, Brookes, Keeley J., Brusco, Luis Ignacio, Buiza-Rueda, Dolores, Bûrger, Katharina, Burholt, Vanessa, Bush, William S., Calero, Miguel, Cantwell, Laura B., Chene, Geneviève, Chung, Jaeyoon, Cuccaro, Michael L., Carracedo, Ángel, Cecchetti, Roberta, Cervera-Carles, Laura, Charbonnier, Camille, Chen, Hung-Hsin, Chillotti, Caterina, Ciccone, Simona, Claassen, Jurgen A. H. R., Clark, Christopher, Conti, Elisa, Corma-Gómez, Anaïs, Costantini, Emanuele, Custodero, Carlo, Daian, Delphine, Dalmasso, Maria Carolina, Daniele, Antonio, Dardiotis, Efthimios, Dartigues, Jean-François, de Deyn, Peter Paul, de Paiva Lopes, Katia, de Witte, Lot D., Debette, Stéphanie, Deckert, Jürgen, del Ser, Teodoro, Denning, Nicola, DeStefano, Anita, Dichgans, Martin, Diehl-Schmid, Janine, Diez-Fairen, Mónica, Rossi, Paolo Dionigi, Djurovic, Srdjan, Duron, Emmanuelle, Düzel, Emrah, Dufouil, Carole, Eiriksdottir, Gudny, Engelborghs, Sebastiaan, Escott-Price, Valentina, Espinosa, Ana, Ewers, Michael, Faber, Kelley M., Fabrizio, Tagliavini, Nielsen, Sune Fallgaard, Fardo, David W., Farotti, Lucia, Fenoglio, Chiara, Fernández-Fuertes, Marta, Ferrari, Raffaele, Ferreira, Catarina B., Ferri, Evelyn, Fin, Bertrand, Fischer, Peter, Fladby, Tormod, Fließbach, Klaus, Fongang, Bernard, Fornage, Myriam, Fortea, Juan, Foroud, Tatiana M., Fostinelli, Silvia, Fox, Nick C., Franco-Macías, Emlio, Bullido, María J., Frank-García, Ana, Froelich, Lutz, Fulton-Howard, Brian, Galimberti, Daniela, García-Alberca, Jose Maria, García-González, Pablo, Garcia-Madrona, Sebastian, Garcia-Ribas, Guillermo, Ghidoni, Roberta, Giegling, Ina, Giorgio, Giaccone, Goate, Alison M., Goldhardt, Oliver, Gomez-Fonseca, Duber, González-Pérez, Antonio, Graff, Caroline, Grande, Giulia, Green, Emma, Grimmer, Timo, Grünblatt, Edna, Grunin, Michelle, Gudnason, Vilmundur, Guetta-Baranes, Tamar, Haapasalo, Annakaisa, Hadjigeorgiou, Georgios, Haines, Jonathan L., Hamilton-Nelson, Kara L., Hampel, Harald, Hanon, Olivier, Hardy, John, Hartmann, Annette M., Hausner, Lucrezia, Harwood, Janet, Heilmann-Heimbach, Stefanie, Helisalmi, Seppo, Heneka, Michael T., Hernández, Isabel, Herrmann, Martin J., Hoffmann, Per, Holmes, Clive, Holstege, Henne, Vilas, Raquel Huerto, Hulsman, Marc, Humphrey, Jack, Biessels, Geert Jan, Jian, Xueqiu, Johansson, Charlotte, Jun, Gyungah R., Kastumata, Yuriko, Kauwe, John, Kehoe, Patrick G., Kilander, Lena, Ståhlbom, Anne Kinhult, Kivipelto, Miia, Koivisto, Anne, Kornhuber, Johannes, Kosmidis, Mary H., Kukull, Walter A., Kuksa, Pavel P., Kunkle, Brian W., Kuzma, Amanda B., Lage, Carmen, Laukka, Erika J., Launer, Lenore, Lauria, Alessandra, Lee, Chien-Yueh, Lehtisalo, Jenni, Lerch, Ondrej, Lleó, Alberto, Longstreth, Jr, William, Lopez, Oscar, de Munain, Adolfo Lopez, Love, Seth, Löwemark, Malin, Luckcuck, Lauren, Lunetta, Kathryn L., Ma, Yiyi, Macías, Juan, MacLeod, Catherine A., Maier, Wolfgang, Mangialasche, Francesca, Spallazzi, Marco, Marquié, Marta, Marshall, Rachel, Martin, Eden R., Montes, Angel Martín, Rodríguez, Carmen Martínez, Masullo, Carlo, Mayeux, Richard, Mead, Simon, Mecocci, Patrizia, Medina, Miguel, Meggy, Alun, Mehrabian, Shima, Mendoza, Silvia, Menéndez-González, Manuel, Mir, Pablo, Moebus, Susanne, Mol, Merel, Molina-Porcel, Laura, Montrreal, Laura, Morelli, Laura, Moreno, Fermin, Morgan, Kevin, Mosley, Thomas, Nöthen, Markus M., Muchnik, Carolina, Mukherjee, Shubhabrata, Nacmias, Benedetta, Ngandu, Tiia, Nicolas, Gael, Nordestgaard, Børge G., Olaso, Robert, Orellana, Adelina, Orsini, Michela, Ortega, Gemma, Padovani, Alessandro, Paolo, Caffarra, Papenberg, Goran, Parnetti, Lucilla, Pasquier, Florence, Pastor, Pau, Peloso, Gina, Pérez-Cordón, Alba, Pérez-Tur, Jordi, Pericard, Pierre, Peters, Oliver, Pijnenburg, Yolande A. L., Pineda, Juan A., Piñol-Ripoll, Gerard, Pisanu, Claudia, Polak, Thomas, Popp, Julius, Posthuma, Danielle, Priller, Josef, Puerta, Raquel, Quenez, Olivier, Quintela, Inés, Thomassen, Jesper Qvist, Rábano, Alberto, Rainero, Innocenzo, Rajabli, Farid, Ramakers, Inez, Real, Luis M., Reinders, Marcel J. T., Reitz, Christiane, Reyes-Dumeyer, Dolly, Ridge, Perry, Riedel-Heller, Steffi, Riederer, Peter, Roberto, Natalia, Rodriguez-Rodriguez, Eloy, Rongve, Arvid, Allende, Irene Rosas, Rosende-Roca, Maitée, Royo, Jose Luis, Rubino, Elisa, Rujescu, Dan, Sáez, María Eugenia, Sakka, Paraskevi, Saltvedt, Ingvild, Sanabria, Ángela, Sánchez-Arjona, María Bernal, Sanchez-Garcia, Florentino, Juan, Pascual Sánchez, Sánchez-Valle, Raquel, Sando, Sigrid B., Sarnowski, Chloé, Satizabal, Claudia L., Scamosci, Michela, Scarmeas, Nikolaos, Scarpini, Elio, Scheltens, Philip, Scherbaum, Norbert, Scherer, Martin, Schmid, Matthias, Schneider, Anja, Schott, Jonathan M., Selbæk, Geir, Seripa, Davide, Serrano, Manuel, Sha, Jin, Shadrin, Alexey A., Skrobot, Olivia, Slifer, Susan, Snijders, Gijsje J. L., Soininen, Hilkka, Solfrizzi, Vincenzo, Solomon, Alina, Song, Yeunjoo, Sorbi, Sandro, Sotolongo-Grau, Oscar, Spalletta, Gianfranco, Spottke, Annika, Squassina, Alessio, Stordal, Eystein, Tartan, Juan Pablo, Tárraga, Lluís, Tesí, Niccolo, Thalamuthu, Anbupalam, Thomas, Tegos, Tosto, Giuseppe, Traykov, Latchezar, Tremolizzo, Lucio, Tybjærg-Hansen, Anne, Uitterlinden, Andre, Ullgren, Abbe, Ulstein, Ingun, Valero, Sergi, Valladares, Otto, Broeckhoven, Christine Van, Vance, Jeffery, Vardarajan, Badri N., van der Lugt, Aad, Dongen, Jasper Van, van Rooij, Jeroen, van Swieten, John, Vandenberghe, Rik, Verhey, Frans, Vidal, Jean-Sébastien, Vogelgsang, Jonathan, Vyhnalek, Martin, Wagner, Michael, Wallon, David, Wang, Li-San, Wang, Ruiqi, Weinhold, Leonie, Wiltfang, Jens, Windle, Gill, Woods, Bob, Yannakoulia, Mary, Zare, Habil, Zhao, Yi, Zhang, Xiaoling, Zhu, Congcong, Zulaica, Miren, Farrer, Lindsay A., Psaty, Bruce M., Ghanbari, Mohsen, Raj, Towfique, Sachdev, Perminder, Mather, Karen, Jessen, Frank, Ikram, M. Arfan, de Mendonça, Alexandre, Hort, Jakub, Tsolaki, Magda, Pericak-Vance, Margaret A., Amouyel, Philippe, Williams, Julie, Frikke-Schmidt, Ruth, Clarimon, Jordi, Deleuze, Jean-François, Rossi, Giacomina, Seshadri, Sudha, Andreassen, Ole A., Ingelsson, Martin, Hiltunen, Mikko, Sleegers, Kristel, Schellenberg, Gerard D., van Duijn, Cornelia M., Sims, Rebecca, van der Flier, Wiesje M., Ruiz, Agustín, Ramirez, Alfredo, and Lambert, Jean-Charles
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- 2022
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6. Bidirectionality of antiseizure and antipsychotic treatment: A population-based study
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Revdal, Eline, Morken, Gunnar, Bakken, Inger Johanne, Bråthen, Geir, Landmark, Cecilie Johannesen, and Brodtkorb, Eylert
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- 2022
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7. Plasma apolipoprotein E levels in longitudinally followed patients with mild cognitive impairment and Alzheimer’s disease
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Giannisis, Andreas, Al-Grety, Asma, Carlsson, Henrik, Patra, Kalicharan, Twohig, Daniel, Sando, Sigrid Botne, Lauridsen, Camilla, Berge, Guro, Grøntvedt, Gøril Rolfseng, Bråthen, Geir, White, Linda R., Kultima, Kim, and Nielsen, Henrietta M.
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- 2022
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8. CSF neurofilament light may predict progression from amnestic mild cognitive impairment to Alzheimer's disease dementia
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Lim, Bryant, Grøntvedt, Gøril Rolfseng, Bathala, Pradeepthi, Kale, Shraddha S., Campbell, Christopher T., Stengelin, Martin, Sando, Sigrid Botne, Prassas, Ioannis, Diamandis, Eleftherios P., and Bråthen, Geir
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- 2021
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9. A genome-wide association study with 1,126,563 individuals identifies new risk loci for Alzheimer’s disease
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Wightman, Douglas P., Jansen, Iris E., Savage, Jeanne E., Shadrin, Alexey A., Bahrami, Shahram, Holland, Dominic, Rongve, Arvid, Børte, Sigrid, Winsvold, Bendik S., Drange, Ole Kristian, Martinsen, Amy E., Skogholt, Anne Heidi, Willer, Cristen, Bråthen, Geir, Bosnes, Ingunn, Nielsen, Jonas Bille, Fritsche, Lars G., Thomas, Laurent F., Pedersen, Linda M., Gabrielsen, Maiken E., Johnsen, Marianne Bakke, Meisingset, Tore Wergeland, Zhou, Wei, Proitsi, Petroula, Hodges, Angela, Dobson, Richard, Velayudhan, Latha, Heilbron, Karl, Auton, Adam, Sealock, Julia M., Davis, Lea K., Pedersen, Nancy L., Reynolds, Chandra A., Karlsson, Ida K., Magnusson, Sigurdur, Stefansson, Hreinn, Thordardottir, Steinunn, Jonsson, Palmi V., Snaedal, Jon, Zettergren, Anna, Skoog, Ingmar, Kern, Silke, Waern, Margda, Zetterberg, Henrik, Blennow, Kaj, Stordal, Eystein, Hveem, Kristian, Zwart, John-Anker, Athanasiu, Lavinia, Selnes, Per, Saltvedt, Ingvild, Sando, Sigrid B., Ulstein, Ingun, Djurovic, Srdjan, Fladby, Tormod, Aarsland, Dag, Selbæk, Geir, Ripke, Stephan, Stefansson, Kari, Andreassen, Ole A., and Posthuma, Danielle
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- 2021
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10. Author Correction: A genome-wide association study with 1,126,563 individuals identifies new risk loci for Alzheimer’s disease
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Wightman, Douglas P., Jansen, Iris E., Savage, Jeanne E., Shadrin, Alexey A., Bahrami, Shahram, Holland, Dominic, Rongve, Arvid, Børte, Sigrid, Winsvold, Bendik S., Drange, Ole Kristian, Martinsen, Amy E., Skogholt, Anne Heidi, Willer, Cristen, Bråthen, Geir, Bosnes, Ingunn, Nielsen, Jonas Bille, Fritsche, Lars G., Thomas, Laurent F., Pedersen, Linda M., Gabrielsen, Maiken E., Johnsen, Marianne Bakke, Meisingset, Tore Wergeland, Zhou, Wei, Proitsi, Petroula, Hodges, Angela, Dobson, Richard, Velayudhan, Latha, Heilbron, Karl, Auton, Adam, Sealock, Julia M., Davis, Lea K., Pedersen, Nancy L., Reynolds, Chandra A., Karlsson, Ida K., Magnusson, Sigurdur, Stefansson, Hreinn, Thordardottir, Steinunn, Jonsson, Palmi V., Snaedal, Jon, Zettergren, Anna, Skoog, Ingmar, Kern, Silke, Waern, Margda, Zetterberg, Henrik, Blennow, Kaj, Stordal, Eystein, Hveem, Kristian, Zwart, John-Anker, Athanasiu, Lavinia, Selnes, Per, Saltvedt, Ingvild, Sando, Sigrid B., Ulstein, Ingun, Djurovic, Srdjan, Fladby, Tormod, Aarsland, Dag, Selbæk, Geir, Ripke, Stephan, Stefansson, Kari, Andreassen, Ole A., and Posthuma, Danielle
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- 2022
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11. Repeat expansions in AR, ATXN1, ATXN2 and HTT in Norwegian patients diagnosed with amyotrophic lateral sclerosis.
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Novy, Camilla, Busk, Øyvind L, Tysnes, Ole-Bjørn, Landa, Sigve S, Aanjesen, Tori N, Alstadhaug, Karl B, Bjerknes, Tale L, Bjørnå, Ingrid K, Bråthen, Geir, Dahl, Elin, Demic, Natasha, Fahlström, Maria, Flemmen, Heidi Ø, Hallerstig, Erika, HogenEsch, Ineke, Kampman, Margitta T, Kleveland, Grethe, Kvernmo, Helene B, Ljøstad, Unn, and Maniaol, Angelina
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- 2024
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12. The seizure precipitating effect of alcohol: A prospective observational cross-over study
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Samsonsen, Christian, Myklebust, Harald, Strindler, Tåle, Bråthen, Geir, Helde, Grethe, and Brodtkorb, Eylert
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- 2018
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13. Cerebrospinal fluid neurogranin/β-site APP-cleaving enzyme 1 predicts cognitive decline in preclinical Alzheimer's disease
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Kirsebom, Bjørn-Eivind, Nordengen, Kaja, Selnes, Per, Waterloo, Knut, Torsetnes, Silje Bøen, Gísladóttir, Berglind, Brix, Britta, Vanmechelen, Eugeen, Bråthen, Geir, Hessen, Erik, Aarsland, Dag, and Fladby, Tormod
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- 2018
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14. C9orf72, AAO and ancestry help discriminating behavioural from language variants in FTLD cohorts
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Costa, Beatrice, Manzoni, Claudia, Bernal-Quiros, Manuel, Kia, Demis A, Aguilar, Miquel, Alvarez, Ignacio, Alvarez, Victoria, Andreassen, Ole, Anfossi, Maria, Bagnoli, Silvia, Benussi, Luisa, Bernardi, Livia, Binetti, Giuliano, Blackburn, Daniel, Boada, Mercè, Borroni, Barbara, Bowns, Lucy, Bråthen, Geir, Bruni, Amalia C, Chiang, Huei-Hsin, Clarimon, Jordi, Colville, Shuna, Conidi, Maria E, Cope, Tom E, Cruchaga, Carlos, Cupidi, Chiara, Di Battista, Maria Elena, Diehl-Schmid, Janine, Diez-Fairen, Monica, Dols-Icardo, Oriol, Durante, Elisabetta, Flisar, Dušan, Frangipane, Francesca, Galimberti, Daniela, Gallo, Maura, Gallucci, Maurizio, Ghidoni, Roberta, Graff, Caroline, Grafman, Jordan H, Grossman, Murray, Hardy, John, Hernández, Isabel, Holloway, Guy JT, Huey, Edward D, Illán-Gala, Ignacio, Karydas, Anna, Khoshnood, Behzad, Kramberger, Milica G, Kristiansen, Mark, Lewis, Patrick A, Lleó, Alberto, Madhan, Gaganjit K, Maletta, Raffaele, Maver, Aleš, Menendez-Gonzalez, Manuel, Milan, Graziella, Miller, Bruce, Mol, Merel O, Momeni, Parastoo, Moreno-Grau, Sonia, Morris, Chris M, Nacmias, Benedetta, Nilsson, Christer, Novelli, Valeria, Öijerstedt, Linn, Padovani, Alessandro, Pal, Suvankar, Panchbhaya, Yasmin, Pastor, Pau, Peterlin, Borut, Piaceri, Irene, Pickering-Brown, Stuart, Pijnenburg, Yolande AL, Puca, Annibale A, Rainero, Innocenzo, Rendina, Antonella, Richardson, Anna MT, Rogaeva, Ekaterina, Rogelj, Boris, Rollinson, Sara, Rossi, Giacomina, Rossmeier, Carola, Rowe, James B, Rubino, Elisa, Ruiz, Agustín, Sanchez-Valle, Raquel, Sando, Sigrid B, Santillo, Alexander F, Saxon, Jennifer, Scarpini, Elio, Serpente, Maria, Smirne, Nicoletta, Sorbi, Sandro, Suh, EunRan, Tagliavini, Fabrizio, Thompson, Jennifer C, Trojanowski, John Q, Van Deerlin, Vivianna M, Van der Zee, Julie, Van Broeckhoven, Christine, van Rooij, Jeroen, Van Swieten, John C, Veronesi, Arianna, Vitale, Emilia, Waldö, Maria L, Woodward, Cathy, Yokoyama, Jennifer, Escott-Price, Valentina, Polke, James M, and Ferrari, Raffaele
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- 2020
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15. Genome-wide meta-analysis identifies new loci and functional pathways influencing Alzheimer’s disease risk
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Jansen, Iris E., Savage, Jeanne E., Watanabe, Kyoko, Bryois, Julien, Williams, Dylan M., Steinberg, Stacy, Sealock, Julia, Karlsson, Ida K., Hägg, Sara, Athanasiu, Lavinia, Voyle, Nicola, Proitsi, Petroula, Witoelar, Aree, Stringer, Sven, Aarsland, Dag, Almdahl, Ina S., Andersen, Fred, Bergh, Sverre, Bettella, Francesco, Bjornsson, Sigurbjorn, Brækhus, Anne, Bråthen, Geir, de Leeuw, Christiaan, Desikan, Rahul S., Djurovic, Srdjan, Dumitrescu, Logan, Fladby, Tormod, Hohman, Timothy J., Jonsson, Palmi V., Kiddle, Steven J., Rongve, Arvid, Saltvedt, Ingvild, Sando, Sigrid B., Selbæk, Geir, Shoai, Maryam, Skene, Nathan G., Snaedal, Jon, Stordal, Eystein, Ulstein, Ingun D., Wang, Yunpeng, White, Linda R., Hardy, John, Hjerling-Leffler, Jens, Sullivan, Patrick F., van der Flier, Wiesje M., Dobson, Richard, Davis, Lea K., Stefansson, Hreinn, Stefansson, Kari, Pedersen, Nancy L., Ripke, Stephan, Andreassen, Ole A., and Posthuma, Danielle
- Published
- 2019
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16. Author Correction: A genome-wide association study with 1,126,563 individuals identifies new risk loci for Alzheimer’s disease
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Wightman, Douglas P., Jansen, Iris E., Savage, Jeanne E., Shadrin, Alexey A., Bahrami, Shahram, Holland, Dominic, Rongve, Arvid, Børte, Sigrid, Winsvold, Bendik S., Drange, Ole Kristian, Martinsen, Amy E., Skogholt, Anne Heidi, Willer, Cristen, Bråthen, Geir, Bosnes, Ingunn, Nielsen, Jonas Bille, Fritsche, Lars G., Thomas, Laurent F., Pedersen, Linda M., Gabrielsen, Maiken E., Johnsen, Marianne Bakke, Meisingset, Tore Wergeland, Zhou, Wei, Proitsi, Petroula, Hodges, Angela, Dobson, Richard, Velayudhan, Latha, Heilbron, Karl, Auton, Adam, Sealock, Julia M., Davis, Lea K., Pedersen, Nancy L., Reynolds, Chandra A., Karlsson, Ida K., Magnusson, Sigurdur, Stefansson, Hreinn, Thordardottir, Steinunn, Jonsson, Palmi V., Snaedal, Jon, Zettergren, Anna, Skoog, Ingmar, Kern, Silke, Waern, Margda, Zetterberg, Henrik, Blennow, Kaj, Stordal, Eystein, Hveem, Kristian, Zwart, John-Anker, Athanasiu, Lavinia, Selnes, Per, Saltvedt, Ingvild, Sando, Sigrid B., Ulstein, Ingun, Djurovic, Srdjan, Fladby, Tormod, Aarsland, Dag, Selbæk, Geir, Ripke, Stephan, Stefansson, Kari, Andreassen, Ole A., and Posthuma, Danielle
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- 2021
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17. C9orf72, age at onset, and ancestry help discriminate behavioral from language variants in FTLD cohorts
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Costa, Beatrice, Manzoni, Claudia, Bernal-Quiros, Manuel, Kia, Demis A., Aguilar, Miquel, Alvarez, Ignacio, Alvarez, Victoria, Andreassen, Ole, Anfossi, Maria, Bagnoli, Silvia, Benussi, Luisa, Bernardi, Livia, Binetti, Giuliano, Blackburn, Daniel, Boada, Mercè, Borroni, Barbara, Bowns, Lucy, Bråthen, Geir, Bruni, Amalia C., Chiang, Huei-Hsin, Clarimon, Jordi, Colville, Shuna, Conidi, Maria E., Cope, Tom E., Cruchaga, Carlos, Cupidi, Chiara, Di Battista, Maria Elena, Diehl-Schmid, Janine, Diez-Fairen, Monica, Dols-Icardo, Oriol, Durante, Elisabetta, Flisar, Dušan, Frangipane, Francesca, Galimberti, Daniela, Gallo, Maura, Gallucci, Maurizio, Ghidoni, Roberta, Graff, Caroline, Grafman, Jordan H., Grossman, Murray, Hardy, John, Hernández, Isabel, Holloway, Guy J.T., Huey, Edward D., Illán-Gala, Ignacio, Karydas, Anna, Khoshnood, Behzad, Kramberger, Milica G., Kristiansen, Mark, Lewis, Patrick A., Lleó, Alberto, Madhan, Gaganjit K., Maletta, Raffaele, Maver, Aleš, Menendez-Gonzalez, Manuel, Milan, Graziella, Miller, Bruce, Mol, Merel O., Momeni, Parastoo, Moreno-Grau, Sonia, Morris, Chris M., Nacmias, Benedetta, Nilsson, Christer, Novelli, Valeria, Öijerstedt, Linn, Padovani, Alessandro, Pal, Suvankar, Panchbhaya, Yasmin, Pastor, Pau, Peterlin, Borut, Piaceri, Irene, Pickering-Brown, Stuart, Pijnenburg, Yolande A.L., Puca, Annibale A., Rainero, Innocenzo, Rendina, Antonella, Richardson, Anna M.T., Rogaeva, Ekaterina, Rogelj, Boris, Rollinson, Sara, Rossi, Giacomina, Rossmeier, Carola, Rowe, James B., Rubino, Elisa, Ruiz, Agustín, Sanchez-Valle, Raquel, Sando, Sigrid B., Santillo, Alexander F., Saxon, Jennifer, Scarpini, Elio, Serpente, Maria, Smirne, Nicoletta, Sorbi, Sandro, Suh, EunRan, Tagliavini, Fabrizio, Thompson, Jennifer C., Trojanowski, John Q., Van Deerlin, Vivianna M., Van der Zee, Julie, Van Broeckhoven, Christine, van Rooij, Jeroen, Van Swieten, John C., Veronesi, Arianna, Vitale, Emilia, Waldö, Maria L., Woodward, Cathy, Yokoyama, Jennifer, Escott-Price, Valentina, Polke, James M., and Ferrari, Raffaele
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- 2020
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18. A multinational study distinguishing Alzheimer's and healthy patients using cerebrospinal fluid tau/Aβ42 cutoff with concordance to amyloid positron emission tomography imaging
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Mo, Yi, Stromswold, Julie, Wilson, Kimberly, Holder, Daniel, Sur, Cyrille, Laterza, Omar, Savage, Mary J., Struyk, Arie, Scheltens, Philip, Teunissen, Charlotte E., Burke, James, Macaulay, S. Lance, Bråthen, Geir, Sando, Sigrid Botne, White, Linda R., Weiss, Christy, Cowes, Arturo, Bush, Michele M., DeSilva, Ganga, Darby, David G., Rainey-Smith, Stephanie R., Surls, Jackie, Sagini, Eileen, Tanen, Michael, Altman, Amy, Luthman, Johan, and Egan, Michael F.
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- 2017
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19. Stroke risk after transient ischemic attack in a Norwegian prospective cohort
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Ildstad, Fredrik, Ellekjær, Hanne, Wethal, Torgeir, Lydersen, Stian, Sund, Janne Kutschera, Fjærtoft, Hild, Schüler, Stephan, Horn, Jens Wilhelm, Bråthen, Geir, Midtsæther, Ann-Grete, Morsund, Åse Hagen, Lillebø, Marja-Liisa, Seljeseth, Yngve Müller, and Indredavik, Bent
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- 2019
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20. The impact of sleep loss on the facilitation of seizures: A prospective case-crossover study
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Samsonsen, Christian, Sand, Trond, Bråthen, Geir, Helde, Grethe, and Brodtkorb, Eylert
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- 2016
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21. Treatment non-adherence in pseudo-refractory epilepsy
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Brodtkorb, Eylert, Samsonsen, Christian, Sund, Janne Kutschera, Bråthen, Geir, Helde, Grethe, and Reimers, Arne
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- 2016
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22. Regression-based norms for the FAS phonemic fluency test for ages 40–84 based on a Norwegian sample
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Lorentzen, Ingrid Myrvoll, Espenes, Jacob, Hessen, Erik, Waterloo, Knut, Bråthen, Geir, Timón, Santiago, Aarsland, Dag, Fladby, Tormod, Bjørn-Eivind, Kirsebom, Kirsebom, Bjørn-Eivind, and Waterloo, Knut
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VDP::Samfunnsvitenskap: 200::Psykologi: 260::Andre psykologiske fag: 279 ,Neuropsychology ,VDP::Social science: 200::Psychology: 260::Other psychology disciplines: 279 - Abstract
The FAS phonemic fluency test is a commonly used neuropsychological test of executive function and processing speed. Although Norwegian discrete norms have been developed for the FAS test, American regression-based norms are frequently used by clinicians in Norway. However, language and cultural differences impact performance on the FAS test, and using foreign norms may not be appropriate. Moreover, while discrete norming relies on stratified subgroups of demographics, regression-based norming uses the entire sample to estimate the influence of demographics on performance and may thus improve normative estimates. Here we develop regression-based norms for the FAS phonemic fluency test based on n = 204 healthy Norwegian controls between the ages 40−84 from the Norwegian Dementia Disease Initiation cohort (DDI). We compare the proposed regression norms to published Norwegian discrete norms and American regression-based norms in an independent sample of n = 182 cognitively healthy adults reporting subjective cognitive decline (SCD). We found that years of education was the only significant predictor of FAS performance in our normative sample, accounting for 14.9% of the variance. Both the proposed regression-based norms and previously published discrete norms adequately adjusted for demographics in the independent sample. In contrast, the American norms underestimated the effect of education and overestimated the effect of age. While both the proposed Norwegian regression norms and the previously published discrete norms are suitable for use in Norway, the proposed regression norms may be less vulnerable to sub-stratification sample characteristics posed by discrete norming procedures, and thereby improve normative estimation.
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- 2023
23. Cerebrospinal fluid neuronal pentraxin receptor as a biomarker of long-term progression of Alzheimer's disease: a 24-month follow-up study
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Lim, Bryant, Sando, Sigrid Botne, Grøntvedt, Gøril Rolfseng, Bråthen, Geir, and Diamandis, Eleftherios P.
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- 2020
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24. GBA and APOE ε4 associate with sporadic dementia with Lewy bodies in European genome wide association study
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Rongve, Arvid, Witoelar, Aree, Ruiz, Agustín, Athanasiu, Lavinia, Abdelnour, Carla, Clarimon, Jordi, Heilmann-Heimbach, Stefanie, Hernández, Isabel, Moreno-Grau, Sonia, de Rojas, Itziar, Morenas-Rodríguez, Estrella, Fladby, Tormod, Sando, Sigrid B., Bråthen, Geir, Blanc, Frédéric, Bousiges, Olivier, Lemstra, Afina W., van Steenoven, Inger, Londos, Elisabet, Almdahl, Ina S., Pålhaugen, Lene, Eriksen, Jon A., Djurovic, Srdjan, Stordal, Eystein, Saltvedt, Ingvild, Ulstein, Ingun D., Bettella, Francesco, Desikan, Rahul S., Idland, Ane-Victoria, Toft, Mathias, Pihlstrøm, Lasse, Snaedal, Jon, Tárraga, Lluís, Boada, Mercè, Lleó, Alberto, Stefánsson, Hreinn, Stefánsson, Kári, Ramírez, Alfredo, Aarsland, Dag, and Andreassen, Ole A.
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- 2019
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25. Meta-analysis of Alzheimer’s disease on 9,751 samples from Norway and IGAP study identifies four risk loci
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Witoelar, Aree, Rongve, Arvid, Almdahl, Ina S., Ulstein, Ingun D., Engvig, Andreas, White, Linda R., Selbæk, Geir, Stordal, Eystein, Andersen, Fred, Brækhus, Anne, Saltvedt, Ingvild, Engedal, Knut, Hughes, Timothy, Bergh, Sverre, Bråthen, Geir, Bogdanovic, Nenad, Bettella, Francesco, Wang, Yunpeng, Athanasiu, Lavinia, Bahrami, Shahram, Le Hellard, Stephanie, Giddaluru, Sudheer, Dale, Anders M., Sando, Sigrid B., Steinberg, Stacy, Stefansson, Hreinn, Snaedal, Jon, Desikan, Rahul S., Stefansson, Kari, Aarsland, Dag, Djurovic, Srdjan, Fladby, Tormod, and Andreassen, Ole A.
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- 2018
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26. The relevance of cerebrospinal fluid α-synuclein levels to sporadic and familial Alzheimer’s disease
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Twohig, Daniel, Rodriguez-Vieitez, Elena, Sando, Sigrid B., Berge, Guro, Lauridsen, Camilla, Møller, Ina, Grøntvedt, Gøril R., Bråthen, Geir, Patra, Kalicharan, Bu, Guojun, Benzinger, Tammie L. S., Karch, Celeste M., Fagan, Anne, Morris, John C., Bateman, Randall J., Nordberg, Agneta, White, Linda R., Nielsen, Henrietta M., and for the Dominantly Inherited Alzheimer Network (DIAN)
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- 2018
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27. The Norwegian Cognitive impairment after stroke study (Nor-COAST): study protocol of a multicentre, prospective cohort study
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Thingstad, Pernille, Askim, Torunn, Beyer, Mona K., Bråthen, Geir, Ellekjær, Hanne, Ihle-Hansen, Hege, Knapskog, Anne Brita, Lydersen, Stian, Munthe-Kaas, Ragnhild, Næss, Halvor, Pendlebury, Sarah T., Seljeseth, Yngve Muller, and Saltvedt, Ingvild
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- 2018
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28. Author Correction: Genome-wide meta-analysis identifies new loci and functional pathways influencing Alzheimer’s disease risk
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Jansen, Iris E., Savage, Jeanne E., Watanabe, Kyoko, Bryois, Julien, Williams, Dylan M., Steinberg, Stacy, Sealock, Julia, Karlsson, Ida K., Hägg, Sara, Athanasiu, Lavinia, Voyle, Nicola, Proitsi, Petroula, Witoelar, Aree, Stringer, Sven, Aarsland, Dag, Almdahl, Ina S., Andersen, Fred, Bergh, Sverre, Bettella, Francesco, Bjornsson, Sigurbjorn, Brækhus, Anne, Bråthen, Geir, de Leeuw, Christiaan, Desikan, Rahul S., Djurovic, Srdjan, Dumitrescu, Logan, Fladby, Tormod, Hohman, Timothy J., Jonsson, Palmi V., Kiddle, Steven J., Rongve, Arvid, Saltvedt, Ingvild, Sando, Sigrid B., Selbæk, Geir, Shoai, Maryam, Skene, Nathan G., Snaedal, Jon, Stordal, Eystein, Ulstein, Ingun D., Wang, Yunpeng, White, Linda R., Hardy, John, Hjerling-Leffler, Jens, Sullivan, Patrick F., van der Flier, Wiesje M., Dobson, Richard, Davis, Lea K., Stefansson, Hreinn, Stefansson, Kari, Pedersen, Nancy L., Ripke, Stephan, Andreassen, Ole A., and Posthuma, Danielle
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- 2020
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29. Lamotrigine and its N2-glucuronide during pregnancy: The significance of renal clearance and estradiol
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Reimers, Arne, Helde, Grethe, Bråthen, Geir, and Brodtkorb, Eylert
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- 2011
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30. Stable cerebrospinal fluid neurogranin and ß-site amyloid precursor protein cleaving enzyme 1 levels differentiate predementia Alzheimer's disease patients.
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Kirsebom, Bjørn-Eivind, Richter, Grit, Nordengen, Kaja, Aarsland, Dag, Bråthen, Geir, Tijms, Betty M., Jelle Visser, Pieter, Nilsson, Johanna, Selnes, Per, Kramberger, Milica G., Winblad, Bengt, Waterloo, Knut, Gísladóttir, Berglind, Blennow, Kaj, and Fladby, Tormod
- Published
- 2022
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31. Clinical trials in pediatric ALS: a TRICALS feasibility study.
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Kliest, Tessa, Van Eijk, Ruben P.A., Al-Chalabi, Ammar, Albanese, Alberto, Andersen, Peter M., Amador, Maria Del Mar, BrÅthen, Geir, Brunaud-Danel, Veronique, Brylev, Lev, Camu, William, De Carvalho, Mamede, Cereda, Cristina, Cetin, Hakan, Chaverri, Delia, Chiò, Adriano, Corcia, Philippe, Couratier, Philippe, De Marchi, Fabiola, Desnuelle, Claude, and Van Es, Michael A.
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CLINICAL trials ,AMYOTROPHIC lateral sclerosis ,FEASIBILITY studies ,CHILD patients ,PEDIATRIC therapy - Abstract
Background: Pediatric investigation plans (PIPs) describe how adult drugs can be studied in children. In 2015, PIPs for Amyotrophic Lateral Sclerosis (ALS) became mandatory for European marketing-authorization of adult treatments, unless a waiver is granted by the European Medicines Agency (EMA). Objective: To assess the feasibility of clinical studies on the effect of therapy in children (<18 years) with ALS in Europe. Methods: The EMA database was searched for submitted PIPs in ALS. A questionnaire was sent to 58 European ALS centers to collect the prevalence of pediatric ALS during the past ten years, the recruitment potential for future pediatric trials, and opinions of ALS experts concerning a waiver for ALS. Results: Four PIPs were identified; two were waived and two are planned for the future. In total, 49 (84.5%) centers responded to the questionnaire. The diagnosis of 44,858 patients with ALS was reported by 46 sites; 39 of the patients had an onset < 18 years (prevalence of 0.008 cases per 100,000 or 0.087% of all diagnosed patients). The estimated recruitment potential (47 sites) was 26 pediatric patients within five years. A majority of ALS experts (75.5%) recommend a waiver should apply for ALS due to the low prevalence of pediatric ALS. Conclusions: ALS with an onset before 18 years is extremely rare and may be a distinct entity from adult ALS. Conducting studies on the effect of disease-modifying therapy in pediatric ALS may involve lengthy recruitment periods, high costs, ethical/legal implications, challenges in trial design and limited information. [ABSTRACT FROM AUTHOR]
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- 2022
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32. The EEG response to photic stimulation is not increased in alcohol-related seizures
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Sand, Trond, Bjørk, Marte, Bråthen, Geir, Brodtkorb, Eylert, Michler, Ralf Peter, and Bovim, Gunnar
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- 2010
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33. Nonadherence to treatment causing acute hospitalizations in people with epilepsy: An observational, prospective study
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Samsonsen, Christian, Reimers, Arne, Bråthen, Geir, Helde, Grethe, and Brodtkorb, Eylert
- Published
- 2014
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34. The validity of questionnaire-based diagnoses: the third Nord-Trøndelag Health Study 2006–2008
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Hagen, Knut, Zwart, John-Anker, Aamodt, Anne Hege, Nilsen, Kristian Bernhard, Bråthen, Geir, Helde, Grethe, Stjern, Marit, Tronvik, Erling A., and Stovner, Lars Jacob
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- 2010
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35. A face-to-face interview of participants in HUNT 3: the impact of the screening question on headache prevalence
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Hagen, Knut, Zwart, John-Anker, Aamodt, Anne Hege, Nilsen, Kristian Berhard, Bråthen, Geir, Helde, Grethe, Stjern, Marit, Tronvik, Erling A., and Stovner, Lars Jacob
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- 2008
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36. Author Correction: GBA and APOE ε4 associate with sporadic dementia with Lewy bodies in European genome wide association study (Scientific Reports, (2019), 9, 1, (7013), 10.1038/s41598-019-43458-2)
- Author
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Rongve, Arvid, Witoelar, Aree, Ruiz, Agustín, Athanasiu, Lavinia, Abdelnour, Carla, Clarimon, Jordi, Heilmann-Heimbach, Stefanie, Hernández, Isabel, Moreno-Grau, Sonia, de Rojas, Itziar, Morenas-Rodríguez, Estrella, Fladby, Tormod, Sando, Sigrid B., Bråthen, Geir, Blanc, Frédéric, Bousiges, Olivier, Lemstra, Afina W., van Steenoven, Inger, Londos, Elisabet, Almdahl, Ina S., Pålhaugen, Lene, Eriksen, Jon A., Djurovic, Srdjan, Stordal, Eystein, Saltvedt, Ingvild, Ulstein, Ingun D., Bettella, Francesco, Desikan, Rahul S., Idland, Ane-Victoria, Toft, Mathias, Pihlstrøm, Lasse, Snaedal, Jon, Tárraga, Lluís, Boada, Mercè, Lleó, Alberto, Stefánsson, Hreinn, Stefánsson, K. ri, Ramírez, Alfredo, Aarsland, Dag, and Andreassen, Ole A.
- Abstract
“The authors would like to thank the Norwegian Dementia Genetics Network (DemGene), the European DLB Consortium (E-DLB), Dementia Genetics Spanish Consortium (DEGESCO) and Genomic Research at Fundació ACE (GR@ACE) Consortium. Fundació ACE would like to thank patients and controls who participated in this project. We are indebted to private donors for their support of Fundació ACE research programs. Fundació ACE collaborates with the Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED, Spain) and is one of the participating centers of the Dementia Genetics Spanish Consortium (DEGESCO). The study was founded by the Research Council of Norway, Norwegian Regional Health Authorities and Norwegian Health Association and 237250/EU/JPND (APGeM). The Cohort 2 results were generated with the assistance of financial support of grants PI13/02434 and PI16/01861. Acción Estratégica en Salud, integrated in the Spanish National R + D + I Plan and financed by ISCIII (Instituto de Salud Carlos III)-Subdirección General de Evaluación and the Fondo Europeo de Desarrollo Regional (FEDER- “Una manera de Hacer Europa”). GR@ACE project has been funded by Fundación bancaria “La Caixa”, Grifols SA, Fundació ACE. The funding sources did not in any way affect the results or presentation of the results.” should read: “The authors would like to thank the Norwegian Dementia Genetics Network (DemGene), the European DLB Consortium (E-DLB), Dementia Genetics Spanish Consortium (DEGESCO) and Genomic Research at Fundació ACE (GR@ACE) Consortium. Fundació ACE would like to thank patients and controls who participated in this project. We are indebted to private donors for their support of Fundació ACE research programs. Fundació ACE collaborates with the Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED, Spain) and is one of the participating centers of the Dementia Genetics Spanish Consortium (DEGESCO). The study was founded by the Research Council of Norway, Norwegian Regional Health Authorities and Norwegian Health Association and 237250/EU/JPND (APGeM). The Cohort 2 results were generated with the assistance of financial support of grants PI13/02434 and PI16/01861. Acción Estratégica en Salud, integrated in the Spanish National R + D + I Plan and financed by ISCIII (Instituto de Salud Carlos III)-Subdirección General de Evaluación and the Fondo Europeo de Desarrollo Regional (FEDER- “Una manera de Hacer Europa”). GR@ACE project has been funded by Fundación bancaria “La Caixa”, Grifols SA, Fundació ACE. The funding sources did not in any way affect the results or presentation of the results. This paper represents independent research partly funded by the National Institute for Health Research (NIHR) Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King’s College London. The views expressed are those of the author and not necessarily those of the NIHR or the Department of Health and Social Care”.
- Published
- 2019
37. Quantitative EEG in Patients With Alcohol-Related Seizures
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Sand, Trond, Bjrk, Marte, Bråthen, Geir, Michler, Ralf P., Brodtkorb, Eylert, and Bovim, Gunnar
- Published
- 2010
- Full Text
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38. Time to Diagnosis in Young Onset Alzheimer's Disease: A Population-Based Study from Central Norway.
- Author
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Kvello-Alme, Marte, Bråthen, Geir, White, Linda R., and Sando, Sigrid Botne
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- *
ALZHEIMER'S disease , *DELAYED diagnosis , *MEDICAL personnel , *CEREBROSPINAL fluid examination , *COGNITION disorders , *ALZHEIMER'S disease diagnosis , *DISEASE progression , *PUBLIC health surveillance , *RESEARCH , *RESEARCH methodology , *MEDICAL cooperation , *EVALUATION research , *COMPARATIVE studies - Abstract
Background: Young onset dementia is associated with a longer time to diagnosis compared to late onset dementia. Earlier publications have indicated that atypical presentation is a key contributing factor to the diagnostic delay. Our hypothesis was that even the most common presentation of Alzheimer's disease is associated with a substantial diagnostic delay in patients < 65 years.Objective: To determine the time to diagnosis, and time lags in the diagnostic pathway in typical young onset Alzheimer's disease in central Norway.Methods: The main sources of patients were the databases at the Department of Neurology, University Hospital of Trondheim (St. Olav's Hospital), and Department of Psychiatry, Levanger Hospital. Other sources included key persons in the communities, collaborating hospital departments examining patients with suspected cognitive impairment, and review of hospital records of all three hospitals in the area. Information on the time lags, and the clinical assessment, including the use of biomarkers, was collected from hospital notes. Caregivers were interviewed by telephone.Results: Time from first symptom to diagnosis in typical young onset Alzheimer's disease was 5.5 years (n = 223, SD 2.8). Time from onset to contact with healthcare services (usually a general practitioner) was 3.4 years (SD 2.3). Time from contact with healthcare services to the first visit at a hospital was 10.3 months (SD 15.5). Time from first visit at a hospital to diagnosis was 14.8 months (SD 22.6). The analysis of cerebrospinal fluid core biomarkers was performed after 8.3 months (SD 20.9).Conclusion: Typical Alzheimer's disease is associated with a substantial diagnostic delay in younger patients. Raising public awareness, and education of healthcare professionals on the aspects of young onset Alzheimer's disease is warranted. CSF core biomarkers should be performed earlier in the hospital evaluation process. [ABSTRACT FROM AUTHOR]- Published
- 2021
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39. An easily performed group education programme for patients with uncontrolled epilepsy—a pilot study
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HELDE, GRETHE, BRODTKORB, EYLERT, BRÅTHEN, GEIR, and BOVIM, GUNNAR
- Published
- 2003
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40. Validity of carbohydrate deficient transferrin and other markers as diagnostic aids in the detection of alcohol related seizures
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Bråthen, Geir, Bjerve, Kristian S, Brodtkorb, Eylert, and Bovim, Gunnar
- Published
- 2000
41. Early functional changes associated with alpha-synuclein proteinopathy in engineered human neural networks.
- Author
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Valderhaug, Vibeke D., Heiney, Kristine, Ramstad, Ola Huse, Bråthen, Geir, Wei-Li Kuan, Nichele, Stefano, Sandvig, Axel, and Sandvig, Ioanna
- Subjects
PARKINSON'S disease ,ALPHA-synuclein ,SUBSTANTIA nigra ,PATHOLOGICAL physiology ,UNITS of measurement - Abstract
A patterned spread of proteinopathy represents a common characteristic of many neurodegenerative diseases. In Parkinson's disease (PD), misfolded forms of a-synuclein proteins accumulate in hallmark pathological inclusions termed Lewy bodies and Lewy neurites. Such protein aggregates seem to affect selectively vulnerable neuronal populations in the substantia nigra and to propagate within interconnected neuronal networks. Research findings suggest that these proteinopathic inclusions are present at very early time points in disease development, even before clear behavioral symptoms of dysfunction arise. In this study, we investigate the early pathophysiology developing after induced formation of such PD-related a-synuclein inclusions in a physiologically relevant in vitro setup using engineered human neural networks. We monitor the neural network activity using multielectrode arrays (MEAs) for a period of 3 wk following proteinopathy induction to identify associated changes in network function, with a special emphasis on the measure of network criticality. Self-organized criticality represents the critical point between resilience against perturbation and adaptational flexibility, which appears to be a functional trait in self-organizing neural networks, both in vitro and in vivo. We show that although developing pathology at early onset is not clearly manifest in standard measurements of network function, it may be discerned by investigating differences in network criticality states. [ABSTRACT FROM AUTHOR]
- Published
- 2021
- Full Text
- View/download PDF
42. Assessment of kallikrein 6 as a cross-sectional and longitudinal biomarker for Alzheimer's disease
- Author
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Patra, Kalicharan, Soosaipillai, Antoninus, Sando, Sigrid Botne, Lauridsen, Camilla, Berge, Guro, Møller, Ina, Grøntvedt, Gøril Rolfseng, Bråthen, Geir, Begcevic, Ilijana, Moussaud, Simon, Minthon, Lennart, Hansson, Oskar, Diamandis, Eleftherios P., White, Linda Rosemary, and Nielsen, Henrietta M.
- Abstract
Background Kallikrein 6 (KLK6) is known to be an age-related protease expressed at high levels in the central nervous system. It was previously shown to be involved in proteolysis of extracellular proteins implicated in neurodegenerative diseases such as Alzheimer’s disease (AD), prompting validation of KLK6 as a potential biomarker of disease. However, analyses of both plasma and cerebrospinal fluid (CSF) levels of KLK6 in patients with AD have been inconclusive. We present a detailed analysis of KLK6 in plasma and CSF in two separate cohorts in a cross-sectional and a longitudinal clinical setting. Methods The cross-sectional cohort included control subjects without dementia and patients with AD, and the longitudinal cohort included patients with MCI and patients with AD followed over a 2-year period. Plasma and CSF levels of KLK6 were quantified by use of a previously developed and validated enzyme-linked immunosorbent assay. Statistical analyses were performed to compare KLK6 levels between diagnostic groups and to identify potential associations between KLK6 level, age, apolipoprotein E (APOE) genotype, total apoE level and the classical CSF AD biomarkers. Results In the cross-sectional setting, KLK6 levels in plasma but not in CSF were significantly higher in the AD group than in control subjects. CSF but not plasma KLK6 levels were positively correlated with age in both the cross-sectional and longitudinal settings. In both cohorts, the CSF KLK6 levels were significantly and positively correlated with the CSF levels of core AD biomarkers. Total plasma and CSF apoE levels were positively associated with KLK6 in the cross-sectional study. Finally, during the 2-year monitoring period of the longitudinal cohort, CSF KLK6 levels increased with disease progression over time in the investigated patient groups. Conclusions In two separate cohorts we have confirmed the previously reported correlation between age and CSF levels of KLK6. Increased plasma KLK6 levels in patients with AD with a more advanced disease stage suggest KLK6 as a potential biomarker in patients with AD with more severe dementia. Significant correlations between KLK6 levels and core CSF AD biomarkers suggest molecular links between KLK6 and AD-related pathological processes. © The Author(s). 2018. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
- Published
- 2018
43. Symptoms of epilepsy and organic brain dysfunctions in patients with acute, brief depression combined with other fluctuating psychiatric symptoms: a controlled study from an acute psychiatric department
- Author
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Linaker Olav M, Morken Gunnar, Vaaler Arne E, Sand Trond, Kvistad Kjell A, and Bråthen Geir
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Psychiatry ,RC435-571 - Abstract
Abstract Background In psychiatric acute departments some patients present with brief depressive periods accompanied with fluctuating arrays of other psychiatric symptoms like psychosis, panic or mania. For the purpose of the present study we call this condition Acute Unstable Depressive Syndrome (AUDS). The aims of the present study were to compare clinical signs of organic brain dysfunctions and epilepsy in patients with AUDS and Major Depressive Episode (MDE). Methods Out of 1038 consecutive patients admitted to a psychiatric acute ward, 16 patients with AUDS and 16 age- and gender-matched MDE patients were included in the study. Using standardized instruments and methods we recorded clinical data, EEG and MRI. Results A history of epileptic seizures and pathologic EEG activity was more common in the AUDS group than in the MDE group (seizures, n = 6 vs. 0, p = 0.018; pathologic EEG activity, n = 8 vs. 1, p = 0.015). Five patients in the AUDS group were diagnosed as having epilepsy, whereas none of those with MDE had epilepsy (p = 0.043). There were no differences between the groups regarding pathological findings in neurological bedside examination and cerebral MRI investigation. Conclusion Compared to patients admitted with mood symptoms fulfilling DSM 4 criteria of a major depressive disorder, short-lasting atypical depressive symptoms seem to be associated with a high frequency of epileptic and pathologic EEG activity in patients admitted to psychiatric acute departments. Trial registration NCT00201474
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- 2009
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44. Quantitative EEG findings in patients with acute, brief depression combined with other fluctuating psychiatric symptoms: a controlled study from an acute psychiatric department
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Linaker Olav M, Bråthen Geir, Sand Trond, Bjørk Marte, Morken Gunnar, Nilsen Brigt M, and Vaaler Arne
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Psychiatry ,RC435-571 - Abstract
Abstract Background Patients with brief depressive episodes and concurrent rapidly fluctuating psychiatric symptoms do not fit current diagnostic criteria and they can be difficult to diagnose and treat in an acute psychiatric setting. We wanted to study whether these patients had signs of more epileptic or organic brain dysfunction than patients with depression without additional symptomatology. Methods Sixteen acutely admitted patients diagnosed with a brief depressive episode as well as another concurrent psychiatric diagnosis were included. Sixteen patients with major depression served as controls. Three electroencephalographic studies (EEG) were visually interpreted and the background activity was also analysed with quantitative electroencephalography (QEEG). Results The group with brief depression and concurrent symptoms had multiple abnormal features in their standard EEG compared to patients with major depression, but they did not show significantly more epileptiform activity. They also had significantly higher temporal QEEG delta amplitude and interhemispheric temporal delta asymmetry. Conclusion Organic brain dysfunction may be involved in the pathogenesis of patients with brief depressive episodes mixed with rapidly fluctuating psychiatric symptoms. This subgroup of depressed patients should be investigated further in order to clarify the pathophysiology and to establish the optimal evaluation scheme and treatment in an acute psychiatric setting.
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- 2008
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45. Incidence of Young Onset Dementia in Central Norway: A Population-Based Study.
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Kvello-Alme, Marte, Bråthen, Geir, White, Linda R, and Sando, Sigrid Botne
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Background: The epidemiology of young onset dementia is little researched compared to late onset dementia. Information on incidence rates is vital for medical professionals, and for government planning purposes.Objective: To determine the incidence of young onset dementia in a defined catchment area of central Norway.Methods: The target area was Trøndelag county in central Norway with a total population of 449,796 inhabitants per January 1, 2016. We applied multiple case ascertainment strategies with sources from both primary and secondary healthcare facilities. Included patients received a diagnosis of dementia according to DSM-IV in the ages 30 to 64 years during the years 2015-2017. Subtypes of dementia were diagnosed according to standardized criteria. Incidence rates for dementia and Alzheimer's disease with dementia were calculated according to age and sex.Results: A total of 89 incident cases were included. Incidence rates for dementia were 14.8 and 25.0 per 100,000 person-years for the age range 30-64 and 45-64, respectively. Corresponding incidence rates for Alzheimer's disease were 6.7 and 11.8. Alzheimer's disease represented half of all dementias. A majority of patients above the age of 50 had neurodegenerative disease, whereas non-degenerative disorders were more prevalent in younger patients.Conclusion: Young onset dementia is a significant contributor to the overall occurrence of dementia in central Norway, and Alzheimer's disease is by far the most common diagnosis. [ABSTRACT FROM AUTHOR]- Published
- 2020
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46. The Amyloid, Tau, and Neurodegeneration (A/T/N) Classification Applied to a Clinical Research Cohort with Long-Term Follow-Up.
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Grøntvedt, Gøril Rolfseng, Lauridsen, Camilla, Berge, Guro, White, Linda R., Salvesen, Øyvind, Bråthen, Geir, and Sando, Sigrid Botne
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AMNESTIC mild cognitive impairment ,AMYLOID ,ALZHEIMER'S disease ,NEURODEGENERATION ,CEREBROSPINAL fluid ,DISEASE progression ,RESEARCH ,NERVE tissue proteins ,PROGNOSIS ,EVALUATION research ,COMPARATIVE studies ,PEPTIDES ,LONGITUDINAL method ,AMNESIA - Abstract
Background: The unbiased amyloid, tau, and neurodegeneration (A/T/N) classification is designed to characterize individuals in the Alzheimer continuum and is currently little explored in clinical cohorts.Objective: A retrospective comparison of the A/T/N classification system with the results of a two-year clinical study, with extended follow-up up to 10 years after inclusion.Methods: Patients (n = 102) clinically diagnosed as Alzheimer's disease (AD) with dementia or amnestic mild cognitive impairment (MCI), and 61 cognitively healthy control individuals were included. Baseline cerebrospinal fluid core biomarkers for AD (Aβ42, phosphorylated tau, and total tau) were applied to the A/T/N classification using the final clinical diagnosis at extended follow-up as the gold standard.Results: A + T + N+ was a strong predictor for AD dementia, even among cognitively healthy individuals. Amnestic MCI was heterogenous, considering both clinical outcome and distribution within A/T/N. Some individuals with amnestic MCI progressed to clinical AD dementia within all four major A/T/N groups. The highest proportion of progression was among triple positive cases, but progression was also common in individuals with suspected non-Alzheimer pathophysiology (A-T + N+), and those with triple negative status. A-T-N- individuals who were cognitively healthy overwhelmingly remained cognitively intact over time, but in amnestic MCI the clinical outcome was heterogenous, including AD dementia, other dementias, and recovery.Conclusion: The A/T/N framework accentuates biomarkers over clinical status. However, when selecting individuals for research, a combination of the two may be necessary since the prognostic value of the A/T/N framework depends on clinical status. [ABSTRACT FROM AUTHOR]- Published
- 2020
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47. Efficacy of Vestibular Rehabilitation Following Acute Vestibular Neuritis: A Randomized Controlled Trial.
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Tokle, Guri, Mørkved, Siv, Bråthen, Geir, Goplen, Frederik Kragerud, Salvesen, Øyvind, Arnesen, Haakon, Holmeslet, Berit, Nordahl, Stein Helge Glad, and Wilhelmsen, Kjersti Thulin
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- 2020
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48. Experiential seizures related to the hippocampal-parahippocampal spatial representation system
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Revdal, Eline, Arntsen, Vibeke, Doan, Thanh Pierre, Kvello-Alme, Marte, Kvistad, Kjell Arne, Bråthen, Geir, and Brodtkorb, Eylert
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- 2020
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49. Plasma Apolipoprotein E Monomer and Dimer Profile and Relevance to Alzheimer's Disease.
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Patra, Kalicharan, Giannisis, Andreas, Edlund, Anna K., Sando, Sigrid Botne, Lauridsen, Camilla, Berge, Guro, Grøntvedt, Gøril Rolfseng, Bråthen, Geir, White, Linda R., Nielsen, Henrietta M., and Nacmias, Benedatta
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APOLIPOPROTEIN E ,ALZHEIMER'S disease ,MONOMERS ,MILD cognitive impairment ,HIGH density lipoproteins ,CHOLESTERYL ester transfer protein - Abstract
The APOEɛ4 gene variant is the strongest genetic risk factor for Alzheimer's disease (AD), whereas APOEɛ3 conventionally is considered as 'risk neutral' although APOEɛ3-carriers also develop AD. Previous studies have shown that the apolipoprotein E3 (apoE3) isoform occurs as monomers, homodimers and heterodimers with apolipoprotein A-II in human body fluids and brain tissue, but the relevance of a plasma apoE3 monomer/dimer profile to AD is unknown. Here we assessed the distribution of monomers, homodimers and heterodimers in plasma from control subjects and patients with mild cognitive impairment (MCI) and AD with either a homozygous APOEɛ3 (n = 31 control subjects, and n = 14 MCI versus n = 5 AD patients) or APOEɛ4 genotype (n = 1 control subject, n = 21 MCI and n = 7 AD patients). Total plasma apoE levels were lower in APOEɛ4-carriers and overall correlated significantly to CSF Aβ42, p(Thr181)-tau and t-tau levels. Apolipoprotein E dimers were only observed in the APOEɛ3-carriers and associated with total plasma apoE levels, negatively correlated to apoE monomers, but were unrelated to plasma homocysteine levels. Importantly, the APOEɛ3-carrying AD patients versus controls exhibited a significant decrease in apoE homodimers (17.8±9.6% versus 26.7±6.3%, p = 0.025) paralleled by an increase in apoE monomers (67.8±18.3% versus 48.5±11.2%, p = 0.008). In the controls, apoE monomers and heterodimers were significantly associated with plasma triglycerides; the apoE heterodimers were also associated with levels of high-density lipoprotein cholesterol. The physiological relevance of apoE dimer formation needs to be further investigated, though the distribution of apoE in monomers and dimers appears to be of relevance to AD in APOEɛ3 subjects. [ABSTRACT FROM AUTHOR]
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- 2019
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50. The Prevalence and Subtypes of Young Onset Dementia in Central Norway: A Population-Based Study.
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Knopman, David, Kvello-Alme, Marte, Bråthen, Geir, White, Linda R., and Sando, Sigrid Botne
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DEMENTIA ,ALZHEIMER'S disease ,ETIOLOGY of diseases ,WATERSHEDS ,DISEASE prevalence - Abstract
Background: Young onset dementia poses several challenges for the individual, health care, and society that are not normally relevant for late onset dementia, but is little researched.Objective: To determine the prevalence and subtypes of young onset dementia in a defined catchment area in central Norway.Methods: The main sources of patient identification were the databases at the Department of Neurology, University Hospital of Trondheim (St. Olav's Hospital), and Department of Psychiatry, Levanger Hospital. Both departments are the main sites for referral of young onset dementia (onset before age 65 years) in the county, covering approximately 90% of the catchment area of the study. Other sources included key persons in the communities, collaborating hospital departments examining dementia, and review of hospital records of all three hospitals in the area. Included patients met the DSM-IV criteria for dementia. The prevalence of dementias was calculated by sex and age.Results: All patients identified with dementia and onset before 65 years on census date were included in the study (n = 390). Patients younger than 65 on census date were included in the calculation of prevalence, giving a result of 76.3 per 100 000 persons at risk in the age category of 30-65 years, and 163.1 per 100,000 for the category 45-64 years. Etiology was heterogeneous, but the main subtype of dementia was Alzheimer's disease.Conclusions: Young onset dementia affects a significant number of people in central Norway. Prevalence figures are higher than previously reported from England and Japan, but are similar to a more recent study from Australia. [ABSTRACT FROM AUTHOR]- Published
- 2019
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