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1. Progress toward standardized diagnosis of vascular cognitive impairment: Guidelines from the Vascular Impairment of Cognition Classification Consensus Study

Author

Taragano, F.E., Kril, J., Cavalieri, M., Jellinger, K.A., Kovacs, G.G., Engelborghs, S., Lafosse, C., Bertolucci, P.H., Brucki, S., Caramelli, P., de Toledo Ferraz Alves, T.C., Bocti, C., Fulop, T., Hogan, D.B., Hsiung, G.R., Kirk, A., Leach, L., Robillard, A., Sahlas, D.J., Guo, Q., Tian, J., Hokkanen, L., Jokinen, H., Benisty, S., Deramecourt, V., Hauw, J., Lenoir, H., Tsatali, M., Tsolaki, M., Sundar, U., Coen, R.F., Korczyn, A.D., Altieri, M., Baldereschi, M., Caltagirone, C., Caravaglios, G., Di Carlo, A., Di Piero, V., Gainotti, G., Galluzzi, S., Logroscino, G., Mecocci, P., Moretti, D.V., Padovani, A., Fukui, T., Ihara, M., Mizuno, T., Kim, S.Y., Akinyemi, R., Baiyewu, O., Ogunniyi, A., Szczudlik, A., Bastos-Leite, A.J., Firmino, H., Massano, J., Verdelho, A., Kruglov, L.S., Ikram, M.K., Kandiah, N., Arana, E., Barroso-Ribal, J., Calatayud, T., Cruz-Jentoft, A.J., López-Pousa, S., Martinez-Lage, P., Mataro, M., Börjesson-Hanson, A., Englund, E., Laukka, E.J., Qiu, C., Viitanen, M., Biessels, G.J., de Leeuw, F.-E., den Heijer, T., Exalto, L.G., Kappelle, L.J., Prins, N.D., Richard, E., Schmand, B., van den Berg, E., van der Flier, W.M., Bilgic, B., Allan, L.M., Archer, J., Attems, J., Bayer, A., Blackburn, D., Brayne, C., Bullock, R., Connelly, P.J., Farrant, A., Fish, M., Harkness, K., Ince, P.G., Langhorne, P., Mann, J., Matthews, F.E., Mayer, P., Pendlebury, S.T., Perneczky, R., Peters, R., Smithard, D., Stephan, B.C., Swartz, J.E., Todd, S., Werring, D.J., Wijayasiri, S.N., Wilcock, G., Zamboni, G., Au, R., Borson, S., Bozoki, A., Browndyke, J.N., Corrada, M.M., Crane, P.K., Diniz, B.S., Etcher, L., Fillit, H., Greenberg, S.M., Grinberg, L.T., Hurt, S.W., Lamar, M., Mielke, M., Ott, B.R., Perry, G., Powers, W.J., Ramos-Estebanez, C., Reed, B., Roberts, R.O., Romero, J.R., Saykin, A.J., Seshadri, S., Silbert, L., Stern, Y., Zarow, C., Skrobot, Olivia A., Black, Sandra E., Chen, Christopher, DeCarli, Charles, Erkinjuntti, Timo, Ford, Gary A., Kalaria, Rajesh N., O'Brien, John, Pantoni, Leonardo, Pasquier, Florence, Roman, Gustavo C., Wallin, Anders, Sachdev, Perminder, Skoog, Ingmar, Ben-Shlomo, Yoav, Passmore, Anthony P., Love, Seth, and Kehoe, Patrick G.

Published
2018
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2. The Vascular Impairment of Cognition Classification Consensus Study

Author

Taragano, F.E., Kril, J., Cavalieri, M., Jellinger, K.A., Kovacs, G.G., Engelborghs, S., Lafosse, C., Bertolucci, P.H., Brucki, S., Caramelli, P., de Toledo Ferraz Alves, T.C., Bocti, C., Fulop, T., Hogan, D.B., Hsiung, G.R., Kirk, A., Leach, L., Robillard, A., Sahlas, D.J., Guo, Q., Tian, J., Hokkanen, L., Jokinen, H., Benisty, S., Deramecourt, V., Hauw, J., Lenoir, H., Tsatali, M., Tsolaki, M., Sundar, U., Coen, R.F., Korczyn, A.D., Altieri, M., Baldereschi, M., Caltagirone, C., Caravaglios, G., Di Carlo, A., DI Piero, V., Gainotti, G., Galluzzi, S., Logroscino, G., Mecocci, P., Moretti, D.V., Padovani, A., Fukui, T., Ihara, M., Mizuno, T., Kim, S.Y., Akinyemi, R., Baiyewu, O., Ogunniyi, A., Szczudlik, A., Bastos-Leite, A.J., Firmino, H., Massano, J., Verdelho, A., Kruglov, L.S., Ikram, M.K., Kandiah, N., Arana, E., Barroso-Ribal, J., Calatayud, T., Cruz-Jentoft, A.J., López-Pousa, S., Martinez-Lage, P., Mataro, M., Börjesson-Hanson, A., Englund, E., Laukka, E.J., Qiu, C., Viitanen, M., Biessels, G.J., de Leeuw, F.-E., den Heijer, T., Exalto, L.G., Kappelle, L.J., Prins, N.D., Richard, E., Schmand, B., van den Berg, E., van der Flier, W.M., Bilgic, B., Allan, L.M., Archer, J., Attems, J., Bayer, A., Blackburn, D., Brayne, C., Bullock, R., Connelly, P.J., Farrant, A., Fish, M., Harkness, K., Ince, P.G., Langhorne, P., Mann, J., Matthews, F.E., Mayer, P., Pendlebury, S.T., Perneczky, R., Peters, R., Smithard, D., Stephan, B.C., Swartz, J.E., Todd, S., Werring, D.J., Wijayasiri, S.N., Wilcock, G., Zamboni, G., Au, R., Borson, S., Bozoki, A., Browndyke, J.N., Corrada, M.M., Crane, P.K., Diniz, B.S., Etcher, L., Fillit, H., Greenberg, S.M., Grinberg, L.T., Hurt, S.W., Lamar, M., Mielke, M., Ott, B.R., Perry, G., Powers, W.J., Ramos-Estebanez, C., Reed, B., Roberts, R.O., Romero, J.R., Saykin, A.J., Seshadri, S., Silbert, L., Stern, Y., Zarow, C., Skrobot, Olivia A., O'Brien, John, Black, Sandra, Chen, Christopher, DeCarli, Charles, Erkinjuntti, Timo, Ford, Gary A., Kalaria, Rajesh N., Pantoni, Leonardo, Pasquier, Florence, Roman, Gustavo C., Wallin, Anders, Sachdev, Perminder, Skoog, Ingmar, Ben-Shlomo, Yoav, Passmore, Anthony P., Love, Seth, and Kehoe, Patrick G.

Published
2017
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3. Stroke genetics informs drug discovery and risk prediction across ancestries

Author

Mishra, A, Malik, R, Hachiya, T, Jurgenson, T, Namba, S, Posner, DC, Kamanu, FK, Koido, M, Le Grand, Q, Shi, M, He, Y, Georgakis, MK, Caro, I, Krebs, K, Liaw, Y-C, Vaura, FC, Lin, K, Winsvold, BS, Srinivasasainagendra, V, Parodi, L, Bae, H-J, Chauhan, G, Chong, MR, Tomppo, L, Akinyemi, R, Roshchupkin, GV, Habib, N, Jee, YH, Thomassen, JQ, Abedi, V, Carcel-Marquez, J, Nygaard, M, Leonard, HL, Yang, C, Yonova-Doing, E, Knol, MJ, Lewis, AJ, Judy, RL, Ago, T, Amouyel, P, Armstrong, ND, Bakker, MK, Bartz, TM, Bennett, DA, Bis, JC, Bordes, C, Borte, S, Cain, A, Ridker, PM, Cho, K, Chen, Z, Cruchaga, C, Cole, JW, de Jager, PL, de Cid, R, Endres, M, Ferreira, LE, Geerlings, MI, Gasca, NC, Gudnason, V, Hata, J, He, J, Heath, AK, Ho, Y-L, Havulinna, AS, Hopewell, JC, Hyacinth, HI, Inouye, M, Jacob, MA, Jeon, CE, Jern, C, Kamouchi, M, Keene, KL, Kitazono, T, Kittner, SJ, Konuma, T, Kumar, A, Lacaze, P, Launer, LJ, Lee, K-J, Lepik, K, Li, J, Li, L, Manichaikul, A, Markus, HS, Marston, NA, Meitinger, T, Mitchell, BD, Montellano, FA, Morisaki, T, Mosley, TH, Nalls, MA, Nordestgaard, BG, O'Donnell, MJ, Okada, Y, Onland-Moret, NC, Ovbiagele, B, Peters, A, Psaty, BM, Rich, SS, Rosand, J, Sabatine, MS, Sacco, RL, Saleheen, D, Sandset, EC, Salomaa, V, Sargurupremraj, M, Sasaki, M, Satizabal, CL, Schmidt, CO, Shimizu, A, Smith, NL, Sloane, KL, Sutoh, Y, Sun, YV, Tanno, K, Tiedt, S, Tatlisumak, T, Torres-Aguila, NP, Tiwari, HK, Tregouet, D-A, Trompet, S, Tuladhar, AM, Tybjaerg-Hansen, A, van Vugt, M, Vibo, R, Verma, SS, Wiggins, KL, Wennberg, P, Woo, D, Wilson, PWF, Xu, H, Yang, Q, Yoon, K, Millwood, IY, Gieger, C, Ninomiya, T, Grabe, HJ, Jukema, JW, Rissanen, IL, Strbian, D, Kim, YJ, Chen, P-H, Mayerhofer, E, Howson, JMM, Irvin, MR, Adams, H, Wassertheil-Smoller, S, Christensen, K, Ikram, MA, Rundek, T, Worrall, BB, Lathrop, GM, Riaz, M, Simonsick, EM, Korv, J, Franca, PHC, Zand, R, Prasad, K, Frikke-Schmidt, R, de Leeuw, F-E, Liman, T, Haeusler, KG, Ruigrok, YM, Heuschmann, PU, Longstreth, WT, Jung, KJ, Bastarache, L, Pare, G, Damrauer, SM, Chasman, DI, Rotter, JI, Anderson, CD, Zwart, J-A, Niiranen, TJ, Fornage, M, Liaw, Y-P, Seshadri, S, Fernandez-Cadenas, I, Walters, RG, Ruff, CT, Owolabi, MO, Huffman, JE, Milani, L, Kamatani, Y, Dichgans, M, Debette, S, Lee, J-M, Cheng, Y-C, Meschia, JF, Chen, WM, Sale, MM, Zonderman, AB, Evans, MK, Wilson, JG, Correa, A, Traylor, M, Lewis, CM, Reiner, A, Haessler, J, Langefeld, CD, Gottesman, RF, Yaffe, K, Liu, YM, Kooperberg, C, Lange, LA, Furie, KL, Arnett, DK, Benavente, OR, Grewal, RP, Peddareddygari, LR, Hveem, K, Lindstrom, S, Wang, L, Smith, EN, Gordon, W, Vlieg, AVH, de Andrade, M, Brody, JA, Pattee, JW, Brumpton, BM, Suchon, P, Chen, M-H, Frazer, KA, Turman, C, Germain, M, MacDonald, J, Braekkan, SK, Armasu, SM, Pankratz, N, Jackson, RD, Nielsen, JB, Giulianin, F, Puurunen, MK, Ibrahim, M, Heckbert, SR, Bammler, TK, McCauley, BM, Taylor, KD, Pankow, JS, Reiner, AP, Gabrielsen, ME, Deleuze, J-F, O'Donnell, CJ, Kim, J, McKnight, B, Kraft, P, Hansen, J-B, Rosendaal, FR, Heit, JA, Tang, W, Morange, P-E, Johnson, AD, Kabrhel, C, van Dijk, EJ, Koudstaal, PJ, Luijckx, G-J, Nederkoorn, PJ, van Oostenbrugge, RJ, Visser, MC, Wermer, MJH, Kappelle, LJ, Esko, T, Metspalu, A, Magi, R, Nelis, M, Levi, CR, Maguire, J, Jimenez-Conde, J, Sharma, P, Sudlow, CLM, Rannikmae, K, Schmidt, R, Slowik, A, Pera, J, Thijs, VNS, Lindgren, AG, Ilinca, A, Melander, O, Engstrom, G, Rexrode, KM, Rothwell, PM, Stanne, TM, Johnson, JA, Danesh, J, Butterworth, AS, Heitsch, L, Boncoraglio, GB, Kubo, M, Pezzini, A, Rolfs, A, Giese, A-K, Weir, D, Ross, OA, Lemmons, R, Soderholm, M, Cushman, M, Jood, K, McDonough, CW, Bell, S, Linkohr, B, Lee, T-H, Putaala, J, Lopez, OL, Carty, CL, Jian, X, Schminke, U, Cullell, N, Delgado, P, Ibanez, L, Krupinski, J, Lioutas, V, Matsuda, K, Montaner, J, Muino, E, Roquer, J, Sarnowski, C, Sattar, N, Sibolt, G, Teumer, A, Rutten-Jacobs, L, Kanai, M, Gretarsdottir, S, Rost, NS, Yusuf, S, Almgren, P, Ay, H, Bevan, S, Brown, RD, Carrera, C, Buring, JE, Chen, W-M, Cotlarciuc, I, de Bakker, PIW, DeStefano, AL, den Hoed, M, Duan, Q, Engelter, ST, Falcone, GJ, Gustafsson, S, Hassan, A, Holliday, EG, Howard, G, Hsu, F-C, Ingelsson, E, Harris, TB, Kissela, BM, Kleindorfer, DO, Langenberg, C, Leys, D, Lin, W-Y, Lorentzen, E, Magnusson, PK, McArdle, PF, Pulit, SL, Rice, K, Sakaue, S, Sapkota, BR, Tanislav, C, Thorleifsson, G, Thorsteinsdottir, U, Tzourio, C, van Duijn, CM, Walters, M, Wareham, NJ, Amin, N, Aparicio, HJ, Attia, J, Beiser, AS, Berr, C, Bustamante, M, Caso, V, Choi, SH, Chowhan, A, Dartigues, J-F, Delavaran, H, Dorr, M, Ford, I, Gurpreet, WS, Hamsten, A, Hozawa, A, Ingelsson, M, Iwasaki, M, Kaffashian, S, Kalra, L, Kjartansson, O, Kloss, M, Labovitz, DL, Laurie, CC, Lind, L, Lindgren, CM, Makoto, H, Minegishi, N, Morris, AP, Mueller-Nurasyid, M, Norrving, B, Ogishima, S, Parati, EA, Pedersen, NL, Perola, M, Jousilahti, P, Pileggi, S, Rabionet, R, Riba-Llena, I, Ribases, M, Romero, JR, Rudd, AG, Sarin, A-P, Sarju, R, Satoh, M, Sawada, N, Sigurdsson, A, Smith, A, Stine, OC, Stott, DJ, Strauch, K, Takai, T, Tanaka, H, Touze, E, Tsugane, S, Uitterlinden, AG, Valdimarsson, EM, van der Lee, SJ, Wakai, K, Williams, SR, Wolfe, CDA, Wong, Q, Yamaji, T, Sanghera, DK, Stefansson, K, Martinez-Majander, N, Sobue, K, Soriano-Tarraga, C, Volzke, H, Akpa, O, Sarfo, FS, Akpalu, A, Obiako, R, Wahab, K, Osaigbovo, G, Owolabi, L, Komolafe, M, Jenkins, C, Arulogun, O, Ogbole, G, Adeoye, AM, Akinyemi, J, Agunloye, A, Fakunle, AG, Uvere, E, Olalere, A, Adebajo, OJ, Chen, J, Clarke, R, Collins, R, Guo, Y, Wang, C, Lv, J, Peto, R, Chen, Y, Fairhurst-Hunter, Z, Hill, M, Pozarickij, A, Schmidt, D, Stevens, B, Turnbull, I, Yu, C, Nagai, A, Murakami, Y, Shiroma, EJ, Sigurdsson, S, Ghanbari, M, Boerwinkle, E, Fongang, B, Wang, R, Ikram, MK, Volker, U, de Laat, KF, van Norden, AGW, de Kort, PL, Vermeer, SE, Brouwers, PJAM, Gons, RAR, den Heijer, T, van Dijk, GW, van Rooij, FGW, Aamodt, AH, Skogholt, AH, Willer, CJ, Heuch, I, Hagen, K, Fritsche, LG, Pedersen, LM, Ellekjaer, H, Zhou, W, Martinsen, AE, Kristoffersen, ES, Thomas, LF, Kleinschnitz, C, Frantz, S, Ungethum, K, Gallego-Fabrega, C, Lledos, M, Llucia-Carol, L, Sobrino, T, Campos, F, Castillo, J, Freijo, M, Arenillas, JF, Obach, V, Alvarez-Sabin, J, Molina, CA, Ribo, M, Munoz-Narbona, L, Lopez-Cancio, E, Millan, M, Diaz-Navarro, R, Vives-Bauza, C, Serrano-Heras, G, Segura, T, Dhar, R, Delgado-Mederos, R, Prats-Sanchez, L, Camps-Renom, P, Blay, N, Sumoy, L, Marti-Fabregas, J, Schnohr, P, Jensen, GB, Benn, M, Afzal, S, Kamstrup, PR, van Setten, J, van der Laan, SW, Vonk, JMJ, Kim, B-J, Curtze, S, Tiainen, M, Kinnunen, J, Menon, V, Sung, YJ, Saillour-Glenisson, F, Gravel, S, Mishra, A, Malik, R, Hachiya, T, Jurgenson, T, Namba, S, Posner, DC, Kamanu, FK, Koido, M, Le Grand, Q, Shi, M, He, Y, Georgakis, MK, Caro, I, Krebs, K, Liaw, Y-C, Vaura, FC, Lin, K, Winsvold, BS, Srinivasasainagendra, V, Parodi, L, Bae, H-J, Chauhan, G, Chong, MR, Tomppo, L, Akinyemi, R, Roshchupkin, GV, Habib, N, Jee, YH, Thomassen, JQ, Abedi, V, Carcel-Marquez, J, Nygaard, M, Leonard, HL, Yang, C, Yonova-Doing, E, Knol, MJ, Lewis, AJ, Judy, RL, Ago, T, Amouyel, P, Armstrong, ND, Bakker, MK, Bartz, TM, Bennett, DA, Bis, JC, Bordes, C, Borte, S, Cain, A, Ridker, PM, Cho, K, Chen, Z, Cruchaga, C, Cole, JW, de Jager, PL, de Cid, R, Endres, M, Ferreira, LE, Geerlings, MI, Gasca, NC, Gudnason, V, Hata, J, He, J, Heath, AK, Ho, Y-L, Havulinna, AS, Hopewell, JC, Hyacinth, HI, Inouye, M, Jacob, MA, Jeon, CE, Jern, C, Kamouchi, M, Keene, KL, Kitazono, T, Kittner, SJ, Konuma, T, Kumar, A, Lacaze, P, Launer, LJ, Lee, K-J, Lepik, K, Li, J, Li, L, Manichaikul, A, Markus, HS, Marston, NA, Meitinger, T, Mitchell, BD, Montellano, FA, Morisaki, T, Mosley, TH, Nalls, MA, Nordestgaard, BG, O'Donnell, MJ, Okada, Y, Onland-Moret, NC, Ovbiagele, B, Peters, A, Psaty, BM, Rich, SS, Rosand, J, Sabatine, MS, Sacco, RL, Saleheen, D, Sandset, EC, Salomaa, V, Sargurupremraj, M, Sasaki, M, Satizabal, CL, Schmidt, CO, Shimizu, A, Smith, NL, Sloane, KL, Sutoh, Y, Sun, YV, Tanno, K, Tiedt, S, Tatlisumak, T, Torres-Aguila, NP, Tiwari, HK, Tregouet, D-A, Trompet, S, Tuladhar, AM, Tybjaerg-Hansen, A, van Vugt, M, Vibo, R, Verma, SS, Wiggins, KL, Wennberg, P, Woo, D, Wilson, PWF, Xu, H, Yang, Q, Yoon, K, Millwood, IY, Gieger, C, Ninomiya, T, Grabe, HJ, Jukema, JW, Rissanen, IL, Strbian, D, Kim, YJ, Chen, P-H, Mayerhofer, E, Howson, JMM, Irvin, MR, Adams, H, Wassertheil-Smoller, S, Christensen, K, Ikram, MA, Rundek, T, Worrall, BB, Lathrop, GM, Riaz, M, Simonsick, EM, Korv, J, Franca, PHC, Zand, R, Prasad, K, Frikke-Schmidt, R, de Leeuw, F-E, Liman, T, Haeusler, KG, Ruigrok, YM, Heuschmann, PU, Longstreth, WT, Jung, KJ, Bastarache, L, Pare, G, Damrauer, SM, Chasman, DI, Rotter, JI, Anderson, CD, Zwart, J-A, Niiranen, TJ, Fornage, M, Liaw, Y-P, Seshadri, S, Fernandez-Cadenas, I, Walters, RG, Ruff, CT, Owolabi, MO, Huffman, JE, Milani, L, Kamatani, Y, Dichgans, M, Debette, S, Lee, J-M, Cheng, Y-C, Meschia, JF, Chen, WM, Sale, MM, Zonderman, AB, Evans, MK, Wilson, JG, Correa, A, Traylor, M, Lewis, CM, Reiner, A, Haessler, J, Langefeld, CD, Gottesman, RF, Yaffe, K, Liu, YM, Kooperberg, C, Lange, LA, Furie, KL, Arnett, DK, Benavente, OR, Grewal, RP, Peddareddygari, LR, Hveem, K, Lindstrom, S, Wang, L, Smith, EN, Gordon, W, Vlieg, AVH, de Andrade, M, Brody, JA, Pattee, JW, Brumpton, BM, Suchon, P, Chen, M-H, Frazer, KA, Turman, C, Germain, M, MacDonald, J, Braekkan, SK, Armasu, SM, Pankratz, N, Jackson, RD, Nielsen, JB, Giulianin, F, Puurunen, MK, Ibrahim, M, Heckbert, SR, Bammler, TK, McCauley, BM, Taylor, KD, Pankow, JS, Reiner, AP, Gabrielsen, ME, Deleuze, J-F, O'Donnell, CJ, Kim, J, McKnight, B, Kraft, P, Hansen, J-B, Rosendaal, FR, Heit, JA, Tang, W, Morange, P-E, Johnson, AD, Kabrhel, C, van Dijk, EJ, Koudstaal, PJ, Luijckx, G-J, Nederkoorn, PJ, van Oostenbrugge, RJ, Visser, MC, Wermer, MJH, Kappelle, LJ, Esko, T, Metspalu, A, Magi, R, Nelis, M, Levi, CR, Maguire, J, Jimenez-Conde, J, Sharma, P, Sudlow, CLM, Rannikmae, K, Schmidt, R, Slowik, A, Pera, J, Thijs, VNS, Lindgren, AG, Ilinca, A, Melander, O, Engstrom, G, Rexrode, KM, Rothwell, PM, Stanne, TM, Johnson, JA, Danesh, J, Butterworth, AS, Heitsch, L, Boncoraglio, GB, Kubo, M, Pezzini, A, Rolfs, A, Giese, A-K, Weir, D, Ross, OA, Lemmons, R, Soderholm, M, Cushman, M, Jood, K, McDonough, CW, Bell, S, Linkohr, B, Lee, T-H, Putaala, J, Lopez, OL, Carty, CL, Jian, X, Schminke, U, Cullell, N, Delgado, P, Ibanez, L, Krupinski, J, Lioutas, V, Matsuda, K, Montaner, J, Muino, E, Roquer, J, Sarnowski, C, Sattar, N, Sibolt, G, Teumer, A, Rutten-Jacobs, L, Kanai, M, Gretarsdottir, S, Rost, NS, Yusuf, S, Almgren, P, Ay, H, Bevan, S, Brown, RD, Carrera, C, Buring, JE, Chen, W-M, Cotlarciuc, I, de Bakker, PIW, DeStefano, AL, den Hoed, M, Duan, Q, Engelter, ST, Falcone, GJ, Gustafsson, S, Hassan, A, Holliday, EG, Howard, G, Hsu, F-C, Ingelsson, E, Harris, TB, Kissela, BM, Kleindorfer, DO, Langenberg, C, Leys, D, Lin, W-Y, Lorentzen, E, Magnusson, PK, McArdle, PF, Pulit, SL, Rice, K, Sakaue, S, Sapkota, BR, Tanislav, C, Thorleifsson, G, Thorsteinsdottir, U, Tzourio, C, van Duijn, CM, Walters, M, Wareham, NJ, Amin, N, Aparicio, HJ, Attia, J, Beiser, AS, Berr, C, Bustamante, M, Caso, V, Choi, SH, Chowhan, A, Dartigues, J-F, Delavaran, H, Dorr, M, Ford, I, Gurpreet, WS, Hamsten, A, Hozawa, A, Ingelsson, M, Iwasaki, M, Kaffashian, S, Kalra, L, Kjartansson, O, Kloss, M, Labovitz, DL, Laurie, CC, Lind, L, Lindgren, CM, Makoto, H, Minegishi, N, Morris, AP, Mueller-Nurasyid, M, Norrving, B, Ogishima, S, Parati, EA, Pedersen, NL, Perola, M, Jousilahti, P, Pileggi, S, Rabionet, R, Riba-Llena, I, Ribases, M, Romero, JR, Rudd, AG, Sarin, A-P, Sarju, R, Satoh, M, Sawada, N, Sigurdsson, A, Smith, A, Stine, OC, Stott, DJ, Strauch, K, Takai, T, Tanaka, H, Touze, E, Tsugane, S, Uitterlinden, AG, Valdimarsson, EM, van der Lee, SJ, Wakai, K, Williams, SR, Wolfe, CDA, Wong, Q, Yamaji, T, Sanghera, DK, Stefansson, K, Martinez-Majander, N, Sobue, K, Soriano-Tarraga, C, Volzke, H, Akpa, O, Sarfo, FS, Akpalu, A, Obiako, R, Wahab, K, Osaigbovo, G, Owolabi, L, Komolafe, M, Jenkins, C, Arulogun, O, Ogbole, G, Adeoye, AM, Akinyemi, J, Agunloye, A, Fakunle, AG, Uvere, E, Olalere, A, Adebajo, OJ, Chen, J, Clarke, R, Collins, R, Guo, Y, Wang, C, Lv, J, Peto, R, Chen, Y, Fairhurst-Hunter, Z, Hill, M, Pozarickij, A, Schmidt, D, Stevens, B, Turnbull, I, Yu, C, Nagai, A, Murakami, Y, Shiroma, EJ, Sigurdsson, S, Ghanbari, M, Boerwinkle, E, Fongang, B, Wang, R, Ikram, MK, Volker, U, de Laat, KF, van Norden, AGW, de Kort, PL, Vermeer, SE, Brouwers, PJAM, Gons, RAR, den Heijer, T, van Dijk, GW, van Rooij, FGW, Aamodt, AH, Skogholt, AH, Willer, CJ, Heuch, I, Hagen, K, Fritsche, LG, Pedersen, LM, Ellekjaer, H, Zhou, W, Martinsen, AE, Kristoffersen, ES, Thomas, LF, Kleinschnitz, C, Frantz, S, Ungethum, K, Gallego-Fabrega, C, Lledos, M, Llucia-Carol, L, Sobrino, T, Campos, F, Castillo, J, Freijo, M, Arenillas, JF, Obach, V, Alvarez-Sabin, J, Molina, CA, Ribo, M, Munoz-Narbona, L, Lopez-Cancio, E, Millan, M, Diaz-Navarro, R, Vives-Bauza, C, Serrano-Heras, G, Segura, T, Dhar, R, Delgado-Mederos, R, Prats-Sanchez, L, Camps-Renom, P, Blay, N, Sumoy, L, Marti-Fabregas, J, Schnohr, P, Jensen, GB, Benn, M, Afzal, S, Kamstrup, PR, van Setten, J, van der Laan, SW, Vonk, JMJ, Kim, B-J, Curtze, S, Tiainen, M, Kinnunen, J, Menon, V, Sung, YJ, Saillour-Glenisson, F, and Gravel, S

Abstract

Previous genome-wide association studies (GWASs) of stroke - the second leading cause of death worldwide - were conducted predominantly in populations of European ancestry1,2. Here, in cross-ancestry GWAS meta-analyses of 110,182 patients who have had a stroke (five ancestries, 33% non-European) and 1,503,898 control individuals, we identify association signals for stroke and its subtypes at 89 (61 new) independent loci: 60 in primary inverse-variance-weighted analyses and 29 in secondary meta-regression and multitrait analyses. On the basis of internal cross-ancestry validation and an independent follow-up in 89,084 additional cases of stroke (30% non-European) and 1,013,843 control individuals, 87% of the primary stroke risk loci and 60% of the secondary stroke risk loci were replicated (P < 0.05). Effect sizes were highly correlated across ancestries. Cross-ancestry fine-mapping, in silico mutagenesis analysis3, and transcriptome-wide and proteome-wide association analyses revealed putative causal genes (such as SH3PXD2A and FURIN) and variants (such as at GRK5 and NOS3). Using a three-pronged approach4, we provide genetic evidence for putative drug effects, highlighting F11, KLKB1, PROC, GP1BA, LAMC2 and VCAM1 as possible targets, with drugs already under investigation for stroke for F11 and PROC. A polygenic score integrating cross-ancestry and ancestry-specific stroke GWASs with vascular-risk factor GWASs (integrative polygenic scores) strongly predicted ischaemic stroke in populations of European, East Asian and African ancestry5. Stroke genetic risk scores were predictive of ischaemic stroke independent of clinical risk factors in 52,600 clinical-trial participants with cardiometabolic disease. Our results provide insights to inform biology, reveal potential drug targets and derive genetic risk prediction tools across ancestries.

Published
2022

5. Progress toward standardized diagnosis of vascular cognitive impairment

Author

Skrobot, Olivia A., Black, Sandra E., Chen, Christopher, DeCarli, Charles, Erkinjuntti, Timo, Ford, Gary A., Kalaria, Rajesh N., O'Brien, John, Pantoni, Leonardo, Pasquier, Florence, Roman, Gustavo C., Wallin, Anders, Sachdev, Perminder, Skoog, Ingmar, Ben-Shlomo, Yoav, Passmore, Anthony P., Love, Seth, Kehoe, Patrick G., Taragano, F.E., Kril, J., Cavalieri, M., Jellinger, K.A., Kovacs, G.G., Engelborghs, S., Lafosse, C., Bertolucci, P.H., Brucki, S., Caramelli, P., de Toledo Ferraz Alves, T.C., Bocti, C., Fulop, T., Hogan, D.B., Hsiung, G.R., Kirk, A., Leach, L., Robillard, A., Sahlas, D.J., Guo, Q., Tian, J., Hokkanen, L., Jokinen, H., Benisty, S., Deramecourt, V., Hauw, J., Lenoir, H., Tsatali, M., Tsolaki, M., Sundar, U., Coen, R.F., Korczyn, A.D., Altieri, M., Baldereschi, M., Caltagirone, C., Caravaglios, G., Di Carlo, A., Di Piero, V., Gainotti, G., Galluzzi, S., Logroscino, G., Mecocci, P., Moretti, D.V., Padovani, A., Fukui, T., Ihara, M., Mizuno, T., Kim, S.Y., Akinyemi, R., Baiyewu, O., Ogunniyi, A., Szczudlik, A., Bastos-Leite, A.J., Firmino, H., Massano, J., Verdelho, A., Kruglov, L.S., Ikram, M.K., Kandiah, N., Arana, E., Barroso-Ribal, J., Calatayud, T., Cruz-Jentoft, A.J., López-Pousa, S., Martinez-Lage, P., Mataro, M., Börjesson-Hanson, A., Englund, E., Laukka, E.J., Qiu, C., Viitanen, M., Biessels, G.J., de Leeuw, F.-E., den Heijer, T., Exalto, L.G., Kappelle, L.J., Prins, N.D., Richard, E., Schmand, B., van den Berg, E., van der Flier, W.M., Bilgic, B., Allan, L.M., Archer, J., Attems, J., Bayer, A., Blackburn, D., Brayne, C., Bullock, R., Connelly, P.J., Farrant, A., Fish, M., Harkness, K., Ince, P.G., Langhorne, Peter, Mann, J., Matthews, F.E., Mayer, P., Pendlebury, S.T., Perneczky, R., Peters, R., Smithard, D., Stephan, B.C., Swartz, J.E., Todd, S., Werring, D.J., Wijayasiri, S.N., Wilcock, G., Zamboni, G., Au, R., Borson, S., Bozoki, A., Browndyke, J.N., Corrada, M.M., Crane, P.K., Diniz, B.S., Etcher, L., Fillit, H., Greenberg, S.M., Grinberg, L.T., Hurt, S.W., Lamar, M., Mielke, M., Ott, B.R., Perry, G., Powers, W.J., Ramos-Estebanez, C., Reed, B., Roberts, R.O., Romero, J.R., Saykin, A.J., Seshadri, S., Silbert, L., Stern, Y., Zarow, C., Epidemiology, Neurology, General Practice, VICCCS Grp, Clinicum, Neurologian yksikkö, Department of Neurosciences, University of Helsinki, Department of Physics, HUS Neurocenter, Amsterdam Neuroscience - Neurodegeneration, APH - Personalized Medicine, and APH - Methodology

Subjects
0301 basic medicine, Neurology, Delphi Technique, Epidemiology, Delphi method, Delphi, Vascular dementia, 3124 Neurology and psychiatry, 0302 clinical medicine, SMALL VESSEL DISEASE, Neuropsychological assessment, Stroke, medicine.diagnostic_test, Health Policy, Neuropsychology, CLINICAL-CRITERIA, Brain, Cognition, 3. Good health, ALZHEIMERS-DISEASE, Settore MED/26 - NEUROLOGIA, Psychiatry and Mental health, Vascular cognitive impairment, NINDS-AIREN, ACUTE STROKE, STROKE, Clinical psychology, medicine.medical_specialty, Clinical Neurology, MINI-MENTAL-STATE, Guidelines, ATROPHY, 03 medical and health sciences, Cellular and Molecular Neuroscience, WHITE-MATTER CHANGES, Developmental Neuroscience, Vascular, medicine, Journal Article, Dementia, Humans, Intensive care medicine, business.industry, Dementia, Vascular, 3112 Neurosciences, medicine.disease, Criteria, 030104 developmental biology, consensus, Consensus, Neurology (clinical), Geriatrics and Gerontology, Psychiatry and Mental Health, CEREBRAL-BLOOD-FLOW, Human medicine, business, 030217 neurology & neurosurgery
Abstract

Hanna Jokinen tutkimusryhmän jäsenenä (VICCCS Grp) Introduction: Progress in understanding and management of vascular cognitive impairment (VCI) has been hampered by lack of consensus on diagnosis, reflecting the use of multiple different assessment protocols. A large multinational group of clinicians and researchers participated in a two-phase Vascular Impairment of Cognition Classification Consensus Study (VICCCS) to agree on principles (VICCCS-1) and protocols (VICCCS-2) for diagnosis of VCI. We present VICCCS-2. Methods: We used VICCCS-1 principles and published diagnostic guidelines as points of reference for an online Delphi survey aimed at achieving consensus on clinical diagnosis of VCI. Results: Six survey rounds comprising 65-79 participants agreed guidelines for diagnosis of VICCCS-revised mild and major forms of VCI and endorsed the National Institute of Neurological Disorders-Canadian Stroke Network neuropsychological assessment protocols and recommendations for imaging. Discussion: The VICCCS-2 suggests standardized use of the National Institute of Neurological Disorders-Canadian Stroke Network recommendations on neuropsychological and imaging assessment for diagnosis of VCI so as to promote research collaboration. (C) 2017 the Alzheimer's Association. Published by Elsevier Inc. All rights reserved.

Published
2018
Full Text
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11. Early recognition and treatment of neuropsychiatric symptoms to improve quality of life in early Alzheimer's disease: protocol of the BEAT-IT study

Author

Eikelboom, Willem, Singleton, E, van den Berg, Esther, Coesmans, Michiel, Mattace Raso, F.U.S., Van Bruchem - Visser, Rozemarijn, Goudzwaard, Jeannette, de Jong, Frank jan, Koopmanschap, Marc, den Heijer, T, Driesen, JJM, Vroegindeweij, L, Thomeer, EC, Hoogers, SE, Dijkstra, AA, Zuidema, SU, Pijnenburg, YAL, Scheltens, P, van Swieten, J.C., Ossenkoppele, R, Papma, Janne, Eikelboom, Willem, Singleton, E, van den Berg, Esther, Coesmans, Michiel, Mattace Raso, F.U.S., Van Bruchem - Visser, Rozemarijn, Goudzwaard, Jeannette, de Jong, Frank jan, Koopmanschap, Marc, den Heijer, T, Driesen, JJM, Vroegindeweij, L, Thomeer, EC, Hoogers, SE, Dijkstra, AA, Zuidema, SU, Pijnenburg, YAL, Scheltens, P, van Swieten, J.C., Ossenkoppele, R, and Papma, Janne

Published
2019

13. Progress toward standardized diagnosis of vascular cognitive impairment: Guidelines from the Vascular Impairment of Cognition Classification Consensus Study

Author

Skrobot, Olivia A., Black, Sandra E., Chen, Christopher, DeCarli, Charles, Erkinjuntti, Timo, Ford, Gary A., Kalaria, Rajesh N., O'Brien, John, Pantoni, Leonardo, Pasquier, Florence, Roman, Gustavo C., Wallin, Anders, Sachdev, Perminder, Skoog, Ingmar, VICCCS Group, Taragano, F. E., Kril, J., Cavalieri, M., Jellinger, K. A., Kovacs, G. G., Engelborghs, S., Lafosse, C., Bertolucci, P. H., Brucki, S., Caramelli, P., De Toledo Ferraz Alves, T. C., Bocti, C., Fulop, T., Hogan, D. B., Hsiung, G. R., Kirk, A., Leach, L., Robillard, A., Sahlas, D. J., Guo, Q., Tian, J., Hokkanen, L., Jokinen, H., Benisty, S., Deramecourt, V., Hauw, J., Lenoir, H., Tsatali, M., Tsolaki, M., Sundar, U., Coen, R. F., Korczyn, A. D., Altieri, M., Baldereschi, M., Caltagirone, C., Caravaglios, G., Di Carlo, A., Di Piero, V., Gainotti, G., Galluzzi, S., Logroscino, G., Mecocci, P., Moretti, D. V., Padovani, A., Fukui, T., Ihara, M., Mizuno, T., Kim, S. Y., Akinyemi, R., Baiyewu, O., Ogunniyi, A., Szczudlik, A., Bastos-Leite, A. J., Firmino, H., Massano, J., Verdelho, A., Kruglov, L. S., Ikram, M. K., Kandiah, N., Arana, E., Barroso-Ribal, J., Calatayud, T., Cruz-Jentoft, A. J., López-Pousa, S., Martinez-Lage, P., Mataro, M., Börjesson-Hanson, A., Englund, E., Laukka, E. J., Qiu, C., Viitanen, M., Biessels, G. J., De Leeuw, F.-E., Den Heijer, T., Exalto, L. G., Kappelle, L. J., Prins, N. D., Richard, E., Schmand, B., Van Den Berg, E., Van Der Flier, W. M., Bilgic, B., Allan, L. M., Archer, J., Attems, J., Bayer, A., Blackburn, D., Brayne, C., Bullock, R., Connelly, P. J., Farrant, A., Fish, M., Harkness, K., Ince, P. G., Langhorne, P., Mann, J., Matthews, F. E., Mayer, P., Pendlebury, S. T., Perneczky, R., Peters, R., Smithard, D., Stephan, B. C., Swartz, J. E., Todd, S., Werring, D. J., Wijayasiri, S. N., Wilcock, G., Zamboni, G., Au, R., Borson, S., Bozoki, A., Browndyke, J. N., Corrada, M. M., Crane, P. K., Diniz, B. S., Etcher, L., Fillit, H., Greenberg, S. M., Grinberg, L. T., Hurt, S. W., Lamar, M., Mielke, M., Ott, B. R., Perry, G., Powers, W. J., Ramos-Estebanez, C., Reed, B., Roberts, R. O., Romero, J. R., Saykin, A. J., Seshadri, S., Silbert, L., Stern, Yaakov, Zarow, C., Ben-Shlomo, Yoav, Passmore, Anthony P., Love, Seth, and Kehoe, Patrick G.

Subjects
Cognition disorders, Cognition disorders--Diagnosis, FOS: Clinical medicine, Neurosciences
Abstract

Introduction: Progress in understanding and management of vascular cognitive impairment (VCI) has been hampered by lack of consensus on diagnosis, reflecting the use of multiple different assessment protocols. A large multinational group of clinicians and researchers participated in a two-phase Vascular Impairment of Cognition Classification Consensus Study (VICCCS) to agree on principles (VICCCS-1) and protocols (VICCCS-2) for diagnosis of VCI. We present VICCCS-2. Methods: We used VICCCS-1 principles and published diagnostic guidelines as points of reference for an online Delphi survey aimed at achieving consensus on clinical diagnosis of VCI. Results: Six survey rounds comprising 65–79 participants agreed guidelines for diagnosis of VICCCS-revised mild and major forms of VCI and endorsed the National Institute of Neurological Disorders–Canadian Stroke Network neuropsychological assessment protocols and recommendations for imaging. Discussion: The VICCCS-2 suggests standardized use of the National Institute of Neurological Disorders–Canadian Stroke Network recommendations on neuropsychological and imaging assessment for diagnosis of VCI so as to promote research collaboration.

Published
2018
Full Text
View/download PDF

15. Progress toward standardized diagnosis of vascular cognitive impairment: Guidelines from the Vascular Impairment of Cognition Classification Consensus Study

Author

Skrobot, O. A., Black, S. E., Chen, C., Decarli, C., Erkinjuntti, T., Ford, G. A., Kalaria, R. N., O'Brien, J., Pantoni, L., Pasquier, F., Roman, G. C., Wallin, A., Sachdev, P., Skoog, I., Taragano, F. E., Kril, J., Cavalieri, M., Jellinger, K. A., Kovacs, G. G., Engelborghs, S., Lafosse, C., Bertolucci, P. H., Brucki, S., Caramelli, P., de Toledo Ferraz Alves, T. C., Bocti, C., Fulop, T., Hogan, D. B., Hsiung, G. R., Kirk, A., Leach, L., Robillard, A., Sahlas, D. J., Guo, Q., Tian, J., Hokkanen, L., Jokinen, H., Benisty, S., Deramecourt, V., Hauw, J., Lenoir, H., Tsatali, M., Tsolaki, M., Sundar, U., Coen, R. F., Korczyn, A. D., Altieri, M., Baldereschi, M., Caltagirone, C., Caravaglios, G., Di Carlo, A., Di Piero, V., Gainotti, Guido, Galluzzi, S., Logroscino, G., Mecocci, P., Moretti, D. V., Padovani, A., Fukui, T., Ihara, M., Mizuno, T., Kim, S. Y., Akinyemi, R., Baiyewu, O., Ogunniyi, A., Szczudlik, A., Bastos-Leite, A. J., Firmino, H., Massano, J., Verdelho, A., Kruglov, L. S., Ikram, M. K., Kandiah, N., Arana, E., Barroso-Ribal, J., Calatayud, T., Cruz-Jentoft, A. J., Lopez-Pousa, S., Martinez-Lage, P., Mataro, M., Borjesson-Hanson, A., Englund, E., Laukka, E. J., Qiu, C., Viitanen, M., Biessels, G. J., de Leeuw, F. -E., den Heijer, T., Exalto, L. G., Kappelle, L. J., Prins, N. D., Richard, E., Schmand, B., van den Berg, E., van der Flier, W. M., Bilgic, B., Allan, L. M., Archer, J., Attems, J., Bayer, A., Blackburn, D., Brayne, C., Bullock, R., Connelly, P. J., Farrant, A., Fish, M., Harkness, K., Ince, P. G., Langhorne, P., Mann, J., Matthews, F. E., Mayer, P., Pendlebury, S. T., Perneczky, R., Peters, R., Smithard, D., Stephan, B. C., Swartz, J. E., Todd, S., Werring, D. J., Wijayasiri, S. N., Wilcock, G., Zamboni, G., Au, R., Borson, S., Bozoki, A., Browndyke, J. N., Corrada, M. M., Crane, P. K., Diniz, B. S., Etcher, L., Fillit, H., Greenberg, S. M., Grinberg, L. T., Hurt, S. W., Lamar, M., Mielke, M., Ott, B. R., Perry, G., Powers, W. J., Ramos-Estebanez, C., Reed, B., Roberts, R. O., Romero, J. R., Saykin, A. J., Seshadri, S., Silbert, L., Stern, Y., Zarow, C., Ben-Shlomo, Y., Passmore, A. P., Love, S., Kehoe, P. G., Gainotti G., Skrobot, O. A., Black, S. E., Chen, C., Decarli, C., Erkinjuntti, T., Ford, G. A., Kalaria, R. N., O'Brien, J., Pantoni, L., Pasquier, F., Roman, G. C., Wallin, A., Sachdev, P., Skoog, I., Taragano, F. E., Kril, J., Cavalieri, M., Jellinger, K. A., Kovacs, G. G., Engelborghs, S., Lafosse, C., Bertolucci, P. H., Brucki, S., Caramelli, P., de Toledo Ferraz Alves, T. C., Bocti, C., Fulop, T., Hogan, D. B., Hsiung, G. R., Kirk, A., Leach, L., Robillard, A., Sahlas, D. J., Guo, Q., Tian, J., Hokkanen, L., Jokinen, H., Benisty, S., Deramecourt, V., Hauw, J., Lenoir, H., Tsatali, M., Tsolaki, M., Sundar, U., Coen, R. F., Korczyn, A. D., Altieri, M., Baldereschi, M., Caltagirone, C., Caravaglios, G., Di Carlo, A., Di Piero, V., Gainotti, Guido, Galluzzi, S., Logroscino, G., Mecocci, P., Moretti, D. V., Padovani, A., Fukui, T., Ihara, M., Mizuno, T., Kim, S. Y., Akinyemi, R., Baiyewu, O., Ogunniyi, A., Szczudlik, A., Bastos-Leite, A. J., Firmino, H., Massano, J., Verdelho, A., Kruglov, L. S., Ikram, M. K., Kandiah, N., Arana, E., Barroso-Ribal, J., Calatayud, T., Cruz-Jentoft, A. J., Lopez-Pousa, S., Martinez-Lage, P., Mataro, M., Borjesson-Hanson, A., Englund, E., Laukka, E. J., Qiu, C., Viitanen, M., Biessels, G. J., de Leeuw, F. -E., den Heijer, T., Exalto, L. G., Kappelle, L. J., Prins, N. D., Richard, E., Schmand, B., van den Berg, E., van der Flier, W. M., Bilgic, B., Allan, L. M., Archer, J., Attems, J., Bayer, A., Blackburn, D., Brayne, C., Bullock, R., Connelly, P. J., Farrant, A., Fish, M., Harkness, K., Ince, P. G., Langhorne, P., Mann, J., Matthews, F. E., Mayer, P., Pendlebury, S. T., Perneczky, R., Peters, R., Smithard, D., Stephan, B. C., Swartz, J. E., Todd, S., Werring, D. J., Wijayasiri, S. N., Wilcock, G., Zamboni, G., Au, R., Borson, S., Bozoki, A., Browndyke, J. N., Corrada, M. M., Crane, P. K., Diniz, B. S., Etcher, L., Fillit, H., Greenberg, S. M., Grinberg, L. T., Hurt, S. W., Lamar, M., Mielke, M., Ott, B. R., Perry, G., Powers, W. J., Ramos-Estebanez, C., Reed, B., Roberts, R. O., Romero, J. R., Saykin, A. J., Seshadri, S., Silbert, L., Stern, Y., Zarow, C., Ben-Shlomo, Y., Passmore, A. P., Love, S., Kehoe, P. G., and Gainotti G.

Abstract

Introduction: Progress in understanding and management of vascular cognitive impairment (VCI) has been hampered by lack of consensus on diagnosis, reflecting the use of multiple different assessment protocols. A large multinational group of clinicians and researchers participated in a two-phase Vascular Impairment of Cognition Classification Consensus Study (VICCCS) to agree on principles (VICCCS-1) and protocols (VICCCS-2) for diagnosis of VCI. We present VICCCS-2. Methods: We used VICCCS-1 principles and published diagnostic guidelines as points of reference for an online Delphi survey aimed at achieving consensus on clinical diagnosis of VCI. Results: Six survey rounds comprising 65–79 participants agreed guidelines for diagnosis of VICCCS-revised mild and major forms of VCI and endorsed the National Institute of Neurological Disorders–Canadian Stroke Network neuropsychological assessment protocols and recommendations for imaging. Discussion: The VICCCS-2 suggests standardized use of the National Institute of Neurological Disorders–Canadian Stroke Network recommendations on neuropsychological and imaging assessment for diagnosis of VCI so as to promote research collaboration.

Published
2018

16. The Vascular Impairment of Cognition Classification Consensus Study

Author

Skrobot, O. A., Love, S., Kehoe, P. G., O'Brien, J., Black, S., Chen, C., DeCarli, C., Erkinjuntti, T., Ford, G. A., Kalaria, R. N., Pantoni, L., Pasquier, F., Roman, G. C., Wallin, A., Sachdev, P., Kril, J., Skoog, I., Ben-Shlomo, Y., Passmore, A. P., Engelborghs, S., Lafosse, C., Bertolucci, P. H., Brucki, S., Caramelli, P., de Toledo Ferraz Alves, T. C., Bocti, C., Fulop, T., Hogan, D. B., Hsiung, G. R., Kirk, A., Leach, L., Robillard, A., Sahlas, D. J., Guo, Q., Tian, J., Hokkanen, L., Jokinen, H., Benisty, S., Deramecourt, V., Hauw, J., Lenoir, H., Tsatali, M., Tsolaki, M., Sundar, U., Coen, R. F., Korczyn, A. D., Altieri, M., Baldereschi, M., Caltagirone, C., Caravaglios, G., Di Carlo, A., DI Piero, V., Gainotti, G., Galluzzi, S., Logroscino, G., Mecocci, P., Moretti, D. V., Padovani, A., Fukui, T., Ihara, M., Mizuno, T., Kim, S. Y., Akinyemi, R., Baiyewu, O., Ogunniyi, A., Szczudlik, A., Bastos-Leite, A. J., Firmino, H., Massano, J., Verdelho, A., Kruglov, L. S., Ikram, M. K., Kandiah, N., Arana, E., Barroso-Ribal, J., Calatayud, T., Cruz-Jentoft, A. J., Lopez-Pousa, S., Martinez-Lage, P., Mataro, M., Borjesson-Hanson, A., Englund, E., Laukka, E. J., Qiu, C., Viitanen, M., Biessels, G. J., de Leeuw, F. -E., den Heijer, T., Exalto, L. G., Kappelle, L. J., Prins, N. D., Richard, E., Schmand, B., van den Berg, E., van der Flier, W. M., Bilgic, B., Allan, L. M., Archer, J., Attems, J., Bayer, A., Blackburn, D., Brayne, C., Bullock, R., Connelly, P. J., Farrant, A., Fish, M., Harkness, K., Ince, P. G., Langhorne, P., Mann, J., Matthews, F. E., Mayer, P., Pendlebury, S. T., Perneczky, R., Peters, R., Smithard, D., Stephan, B. C., Swartz, J. E., Todd, S., Werring, D. J., Wijayasiri, S. N., Wilcock, G., Zamboni, G., Au, R., Borson, S., Bozoki, A., Browndyke, J. N., Corrada, M. M., Crane, P. K., Diniz, B. S., Etcher, L., Fillit, H., Greenberg, S. M., Grinberg, L. T., Hurt, S. W., Lamar, M., Mielke, M., Ott, B. R., Perry, G., Powers, W. J., Ramos-Estebanez, C., Reed, B., Roberts, R. O., Romero, J. R., Saykin, A. J., Seshadri, S., Silbert, L., Stern, Y., Zarow, C., Gainotti G., Logroscino G. (ORCID:0000-0003-1301-5343), Skrobot, O. A., Love, S., Kehoe, P. G., O'Brien, J., Black, S., Chen, C., DeCarli, C., Erkinjuntti, T., Ford, G. A., Kalaria, R. N., Pantoni, L., Pasquier, F., Roman, G. C., Wallin, A., Sachdev, P., Kril, J., Skoog, I., Ben-Shlomo, Y., Passmore, A. P., Engelborghs, S., Lafosse, C., Bertolucci, P. H., Brucki, S., Caramelli, P., de Toledo Ferraz Alves, T. C., Bocti, C., Fulop, T., Hogan, D. B., Hsiung, G. R., Kirk, A., Leach, L., Robillard, A., Sahlas, D. J., Guo, Q., Tian, J., Hokkanen, L., Jokinen, H., Benisty, S., Deramecourt, V., Hauw, J., Lenoir, H., Tsatali, M., Tsolaki, M., Sundar, U., Coen, R. F., Korczyn, A. D., Altieri, M., Baldereschi, M., Caltagirone, C., Caravaglios, G., Di Carlo, A., DI Piero, V., Gainotti, G., Galluzzi, S., Logroscino, G., Mecocci, P., Moretti, D. V., Padovani, A., Fukui, T., Ihara, M., Mizuno, T., Kim, S. Y., Akinyemi, R., Baiyewu, O., Ogunniyi, A., Szczudlik, A., Bastos-Leite, A. J., Firmino, H., Massano, J., Verdelho, A., Kruglov, L. S., Ikram, M. K., Kandiah, N., Arana, E., Barroso-Ribal, J., Calatayud, T., Cruz-Jentoft, A. J., Lopez-Pousa, S., Martinez-Lage, P., Mataro, M., Borjesson-Hanson, A., Englund, E., Laukka, E. J., Qiu, C., Viitanen, M., Biessels, G. J., de Leeuw, F. -E., den Heijer, T., Exalto, L. G., Kappelle, L. J., Prins, N. D., Richard, E., Schmand, B., van den Berg, E., van der Flier, W. M., Bilgic, B., Allan, L. M., Archer, J., Attems, J., Bayer, A., Blackburn, D., Brayne, C., Bullock, R., Connelly, P. J., Farrant, A., Fish, M., Harkness, K., Ince, P. G., Langhorne, P., Mann, J., Matthews, F. E., Mayer, P., Pendlebury, S. T., Perneczky, R., Peters, R., Smithard, D., Stephan, B. C., Swartz, J. E., Todd, S., Werring, D. J., Wijayasiri, S. N., Wilcock, G., Zamboni, G., Au, R., Borson, S., Bozoki, A., Browndyke, J. N., Corrada, M. M., Crane, P. K., Diniz, B. S., Etcher, L., Fillit, H., Greenberg, S. M., Grinberg, L. T., Hurt, S. W., Lamar, M., Mielke, M., Ott, B. R., Perry, G., Powers, W. J., Ramos-Estebanez, C., Reed, B., Roberts, R. O., Romero, J. R., Saykin, A. J., Seshadri, S., Silbert, L., Stern, Y., Zarow, C., Gainotti G., and Logroscino G. (ORCID:0000-0003-1301-5343)

Abstract

Introduction Numerous diagnostic criteria have tried to tackle the variability in clinical manifestations and problematic diagnosis of vascular cognitive impairment (VCI) but none have been universally accepted. These criteria have not been readily comparable, impacting on clinical diagnosis rates and in turn prevalence estimates, research, and treatment. Methods The Vascular Impairment of Cognition Classification Consensus Study (VICCCS) involved participants (81% academic researchers) from 27 countries in an online Delphi consensus study. Participants reviewed previously proposed concepts to develop new guidelines. Results VICCCS had a mean of 122 (98–153) respondents across the study and a 67% threshold to represent consensus. VICCCS redefined VCI including classification of mild and major forms of VCI and subtypes. It proposes new standardized VCI-associated terminology and future research priorities to address gaps in current knowledge. Discussion VICCCS proposes a consensus-based updated conceptualization of VCI intended to facilitate standardization in research.

Published
2017

19. Structural and functional brain connectivity in presymptomatic familial frontotemporal dementia

Author

Dopper, E. G. P., primary, Rombouts, S. A. R. B., additional, Jiskoot, L. C., additional, den Heijer, T., additional, de Graaf, J. R. A., additional, de Koning, I., additional, Hammerschlag, A. R., additional, Seelaar, H., additional, Seeley, W. W., additional, Veer, I. M., additional, van Buchem, M. A., additional, Rizzu, P., additional, and van Swieten, J. C., additional

Published
2014
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20. Brain changes with aging: MR spectroscopy at supraventricular plane shows differences between women and women: MR spectroscopy at supraventricular plane shows differences between women and women

Author

Sijens, P.E., den Heijer, T., Origgi, D., Vermeer, S.E., Breteler, M.M.B., Hofman, A., Oudkerk, M., and Rijksuniversiteit Groningen

Subjects
PROTON MRS, AGE, aging, MAGNETIC-RESONANCE SPECTROSCOPY, CONTRAST, SEX, WHITE-MATTER LESIONS, QUANTIFICATION, GENDER DIFFERENCES, magnetic resonance (MR), spectroscopy, METABOLITE CONCENTRATIONS, brain, metabolism, SIGNAL HYPERINTENSITIES
Published
2003

21. Association between blood pressure levels over time and brain atrophy in the elderly

Author

den Heijer, T, Skoog, [No Value], Oudkerk, M, de Leeuw, FE, de Groot, JC, Hofman, A, and Breteler, MMB

Subjects
ALZHEIMERS-DISEASE, atrophy, HYPERTENSION, ABNORMALITIES, brain, DEMENTIA, blood pressure, epidemiology, WHITE-MATTER LESIONS, ROTTERDAM SCAN, NEUROFIBRILLARY TANGLES, HYPOPERFUSION
Abstract

The relation between blood pressure level and degree of global brain atrophy is equivocal. We evaluated past and present blood pressure levels and change in blood pressure over 20 years in relation to the degree of cortical atrophy on magnetic resonance imaging (MRI). In 1995-1996, we measured blood pressure and performed MRI in 1077 nondemented elderly (age 60-90 years). For 513 of these, we had information on a blood pressure level 20 years before. The degree of cortical atrophy was semi-quantitatively scored (range 0-15). In late life, a high (greater than or equal to 90 mmHg) and low (

Published
2003

22. Homocysteine and cognitive function in the elderly: the Rotterdam Scan Study. 10901, 11220, 20611

Author

Prins, N.D., den Heijer, T., Clarke, R., Jolles, J., Koudstaal, P.J., Hofman, A., Breteler, M.M.B., Neuropsychology & Psychopharmacology, Dep.Medische en Klin. Experimentele Psy., and RS: FPN NPPP I

Abstract

Background: Elevated plasma total homocysteine (tHcy) concentrations are associated with AD and vascular dementia, but the relation with cognitive performance in nondemented elderly people is not known. Objective: To examine the association of tHcy and cognitive function in the elderly, and assess whether this may be mediated by structural brain changes on MRI. Methods: The Rotterdam Scan Study is a population-based study of 1,077 nondemented elderly. Cognitive performance was assessed, and compound scores were constructed for psychomotor speed, memory function, and global cognitive function. Cerebral infarcts, white matter lesions, and generalized brain atrophy were measured on MRI. The cross-sectional relationship between tHcy levels and neuropsychological test scores was assessed by multiple regression. Results: Mean tHcy level was 11.5 mumol/L (SD 4.1). Increasing tHcy levels were associated with lower scores for psychomotor speed, memory function, and global cognitive function, and this was largely due to the association with tHcy levels in the upper quintile (>14 mumol/L). Adjusted differences between test scores of participants in the upper quintile as compared with the lower four quintiles of tHcy were -0.26 (95% CI: -0.37; -0.14) for psychomotor speed, -0.13 (95% CI: -0.27; 0.01) for memory function, and -0.20 (95% CL -0.30; -0.11) for global cognitive function. These associations were not mediated by structural brain changes on MRI. Conclusion: Elevated tHcy levels are associated with decreased cognitive performance in nondemented elderly people, and the relation was most marked for psychomotor speed. This association was independent of structural brain changes on MRI.

Published
2002

23. The Thyroid Hormone Receptor Alpha Locus and White Matter Lesions: A Role for the Clock Gene REV-ERB?

Author

Medici, M. (author), Arfan Ikram, M. (author), Van der Lijn, F. (author), Den Heijer, T. (author), Vernooij, M.W. (author), Hofman, A. (author), Niessen, W.J. (author), Visser, T.J. (author), Breteler, M.M.B. (author), Peeters, R.P. (author), Medici, M. (author), Arfan Ikram, M. (author), Van der Lijn, F. (author), Den Heijer, T. (author), Vernooij, M.W. (author), Hofman, A. (author), Niessen, W.J. (author), Visser, T.J. (author), Breteler, M.M.B. (author), and Peeters, R.P. (author)

Abstract

Background: Thyroid disorders are associated with an increased risk of cognitive impairment and Alzheimer's disease. Both small vessel disease and neurodegeneration have a role in the pathogenesis of cognitive impairment and Alzheimer's disease. Thyroid hormone receptor alpha (TR?) is the predominant TR in brain. The circadian clock gene REV-ERB? overlaps with the TR? gene and interferes with TR? expression. Limited data are available on the role of the TR?/REV-ERB? locus in small vessel disease and neurodegeneration. We therefore studied genetic variation in the TR?/REV-ERB? locus in relation to brain imaging data, as early markers for small vessel disease and neurodegeneration. Methods: Fifteen polymorphisms, covering the TR?/REV-ERB? locus, were studied in relation to white matter lesion (WML), total brain, and hippocampal volumes in the Rotterdam Study I (RS-I, n=454). Associations that remained significant after multiple testing correction were subsequently studied in an independent population for replication (RS-II, n=607). Results: No associations with total brain or hippocampal volumes were detected. A haplotype block in REV-ERB? was associated with WML volumes in RS-I. Absence of this haplotype was associated with larger WML volumes in women (0.38%±0.18% [?±SE], p=0.007), but not in men (0.04%±0.11%, p=0.24), which was replicated in RS-II (women: 0.15%±0.05%, p=0.04; men: 0.05%±0.07%, p=0.80). Meta-analysis of the two populations showed that women lacking this haplotype have a 1.9 times larger WML volume (p=0.001). Conclusion: Our results suggest a role for REV-ERB? in the pathogenesis of WMLs., IST/Imaging Science and Technology, Applied Sciences

Published
2012
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32. Homocysteine and cerebral white matter lesions: the Rotterdam Scan Study

Author

van Dijk, E, Vermeer, SE, den Heijer, T, Oudkerk, M, Hofman, A, Koudstaal, P, Clarke, R, and Breteler, M

Subjects
Advanced and Specialized Nursing, Neurology (clinical), Cardiology and Cardiovascular Medicine
Abstract

31 Background White matter lesions are frequently observed on cerebral MRI scans. There is evidence that white matter lesions are involved in the pathophysiology of cognitive decline, dementia and late-onset depression. Cardiovascular risk factors are associated with these lesions. A high homocysteine level is associated with an increased risk of cardiovascular disease. Therefore, we studied the association between homocysteine and white matter lesions. Method This study forms part of the Rotterdam Scan Study, a prospective population-based cohort study among 1077 subjects, aged 60 to 90 years. All participants underwent MRI scanning of the brain. White matter lesions were defined as hyperintense lesions on both proton-density and T2-weighted images, without prominent hypointensity on T1-weighted images. Periventricular white matter lesions were rated on a nine-point scale. For subcortical white matter lesions an approximated total lesion volume was calculated. Homocysteine levels were determined in plasma samples, obtained within 3 weeks before scanning. The association between total plasma homocysteine and white matter lesions was assessed through multiple linear regression analysis, adjusted for age and gender. Results The total plasma homocysteine levels ranged from 3.4 to 70.7 μmol/l with a mean of 11.7 μmol/l [95%CI 11.4–12.0]. We found a mean value of 2.4 [95%CI 2.3–2.5] for periventricular white matter lesion severity and of 1.4 ml [95%CI 1.2–1.6] for subcortical white matter lesion volume. Periventricular white matter lesions increased with 0.4 [95%CI 0.1–0.6] and subcortical white matter lesions with 0.5 ml [95%CI 0.1–0.8] per 10 μmol/l increase in homocysteine level. Conclusion Higher homocysteine levels are associated with an increased severity of both periventricular and subcortical white matter lesions.

Published
2001
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33. Variations in estrogen receptoragene and risk of dementia, and brain volumes on MRI.

Author

den Heijer, T., Schuit, S. C. E., Pols, H. A. P., van Meurs, J. B. J., Hofman, A., Koudstaal, P. J., van Duijn, C. M., Uitterlinden, A. G., and Breteler, M. M. B.

Subjects
ESTROGEN, SEX hormones, ALZHEIMER'S disease, SENILE dementia, GENETIC polymorphisms, BIOLOGICAL psychiatry
Abstract

The role of estrogens in Alzheimer's disease (AD) is controversial. We investigated the association between well-recognized, and potentially functional, polymorphisms in the estrogen receptor (ER)agene and the risk of AD in a prospective study of 6056 Caucasian older men and women aged 55 years and over. In a subset of 468 participants, we assessed volumes of the hippocampus and amygdala, which have a high density of ERa, with brain magnetic resonance imaging (MRI) (1.5?T MR unit). During a total of 35?405 person-years of follow-up (mean per persons 5.8 years), 312 new cases of dementia were detected, of whom 230 were diagnosed with AD. Neither the PvuII nor the XbaI polymorphism or haplotypes thereof were associated with the risk of all-cause dementia or AD. In contrast, we found that nondemented women who carried the PvuII p allele or haplotype‘px’had smaller amygdalar volumes on MRI in an allele-dose-dependent fashion. Total amygdalar volume was 4.50 (SE 0.10) in PP genotype, 4.45 (SE 0.06) in Pp genotype, and 4.18?ml (SE 0.08) in pp genotype (P trend=0.008). Further studies are required to investigate whether this smaller amygdalar volume has functional significance.Molecular Psychiatry (2004) 9, 1129-1135. doi:10.1038/sj.mp.4001553 Published online 20 July 2004 [ABSTRACT FROM AUTHOR]

Published
2004
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38. Trigger factors in patients with a patent foramen ovale-associated stroke: A case-crossover study.

Author

Immens MH, Ekker MS, Verburgt E, Verhoeven JI, Schellekens MM, Hilkens NA, Boot EM, Van Alebeek ME, Brouwers PJ, Arntz RM, Van Dijk GW, Gons RA, Van Uden IW, den Heijer T, de Kort PL, de Laat KF, Van Norden AG, Vermeer SE, Van Zagten MS, Van Oostenbrugge RJ, Wermer MJ, Nederkoorn PJ, Kerkhoff H, Rooyer FA, Van Rooij FG, Van den Wijngaard IR, Klijn CJ, Tuladhar AM, Ten Cate TJ, and de Leeuw FE

Subjects
Humans, Male, Adult, Female, Middle Aged, Prospective Studies, Risk Factors, Young Adult, Adolescent, Stroke epidemiology, Stroke etiology, Ischemic Stroke epidemiology, Ischemic Stroke etiology, Surveys and Questionnaires, Foramen Ovale, Patent complications, Foramen Ovale, Patent epidemiology, Cross-Over Studies
Abstract

Background: Patent foramen ovale (PFO) is a congenital anatomical variant which is associated with strokes in young adults. Contrary to vascular risk factors and atherosclerosis, a PFO is present from birth. However, it is completely unknown how an anatomical structure that is already present at birth in a large proportion of the population can convert into a PFO that causes stroke in a few. Recent studies reported a significant association between certain trigger factors and ischemic stroke in young adults. This study aims to investigate these triggers in PFO-associated stroke., Methods: The ODYSSEY study, a multicenter prospective cohort study between 2013 and 2021, included patients aged 18-49 years experiencing their first-ever ischemic event. Participants completed a questionnaire about exposure to potential trigger factors. A case-crossover design was used to assess the relative risks (RR) with 95% confidence intervals (95% CI). The primary outcome was the RR of potential trigger factors for PFO-associated stroke., Results: Overall, 1043 patients completed the questionnaire and had an ischemic stroke, of which 124 patients had a PFO-associated stroke (median age 42.1 years, 45.2% men). For patients with PFO-associated stroke, the RR was 26.0 (95% CI 8.0-128.2) for fever, 24.2 (95% CI 8.5-68.7) for flu-like disease, and 3.31 (95% CI 2.2-5.1) for vigorous exercise., Conclusion: In conclusion, flu-like disease, fever, and vigorous exercise may convert an asymptomatic PFO into a stroke-causing PFO in young adults., Data Access Statement: The raw and anonymized data used in this study can be made available to other researchers on request. Written proposals can be addressed to the corresponding author and will be assessed by the ODYSSEY investigators for appropriateness of use, and a data sharing agreement in accordance with Dutch regulations will be put in place before data are shared., Competing Interests: Declaration of conflicting interestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Published
2024
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39. Cognitive trajectory in the first year after first-ever ischaemic stroke in young adults: the ODYSSEY study.

Author

Schellekens MMI, Springer RCS, Boot EM, Verhoeven JI, Ekker MS, van Alebeek ME, Brouwers PJAM, Arntz RM, van Dijk GW, Gons RAR, van Uden IWM, den Heijer T, van Tuijl JH, de Laat KF, van Norden AGW, Vermeer SE, van Zagten MSG, Van Oostenbrugge RJ, Wermer MJH, Nederkoorn PJ, van Rooij FG, van den Wijngaard IR, de Kort PLM, De Leeuw FE, Kessels RPC, and Tuladhar AM

Subjects
Humans, Adult, Male, Female, Middle Aged, Prospective Studies, Young Adult, Neuropsychological Tests, Cognition physiology, Adolescent, Recovery of Function, Executive Function physiology, Age Factors, Ischemic Stroke complications, Ischemic Stroke psychology, Cognitive Dysfunction
Abstract

Background: Limited data exists on cognitive recovery in young stroke patients. We aimed to investigate the longitudinal course of cognitive performance during the first year after stroke at young age and identify predictors for cognitive recovery., Methods: We conducted a multicentre prospective cohort study between 2013 and 2021, enrolling patients aged 18-49 years with first-ever ischaemic stroke. Cognitive assessments were performed within 6 months and after 1 year following the index event, covering seven cognitive domains. Composite Z-scores using normative data determined cognitive impairment (Z-score<-1.5). A Reliable Change Index (RCI) assessed cognitive recovery (RCI>1.96) or decline (RCI<-1.96)., Results: 393 patients (median age 44.3 years, IQR 38.4-47.2) completed cognitive assessments with a median time interval of 403 days (IQR 364-474) between assessments. Based on RCI, a similar proportion of patients showed improvement and decline in each cognitive domain, while the majority exhibited no cognitive change. Among cognitively impaired patients at baseline, improvements were observed in processing speed (23.1%), visuoconstruction (40.1%) and executive functioning (20.0%). Younger age was associated with better cognitive recovery in visuoconstruction, and larger lesion volume was related to cognitive recovery in processing speed. No other predictors for cognitive recovery were identified., Conclusions: Cognitive impairment remains prevalent in young stroke even 1 year after the event. Most patients showed no cognitive change, however, recovery may have occurred in the early weeks after stroke, which was not assessed in our study. Among initially cognitively impaired patients, cognitive recovery is observed in processing speed, visuoconstruction and executive functioning. It is still not possible to predict cognitive recovery in individual patients., Competing Interests: Competing interests: AMT is a junior staff member of the Dutch Heart Foundation (grant number 2016T044). F-EDL is a clinical established investigator of the Dutch Heart Foundation (2014 T060). MJHW has received a VIDI grant (9171337) of the ZonMw/NWO and the clinical established investigator Dutch Heart Foundation grant (2016T86)., (© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Published
2024
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40. Short-Term and Long-Term Risk of Recurrent Vascular Event by Cause After Ischemic Stroke in Young Adults.

Author

Verburgt E, Hilkens NA, Ekker MS, Schellekens MMI, Boot EM, Immens MHM, van Alebeek ME, Brouwers PJAM, Arntz RM, van Dijk GW, Gons RAR, van Uden IWM, den Heijer T, van Tuijl JH, de Laat KF, van Norden AGW, Vermeer SE, van Zagten MSG, van Oostenbrugge RJ, Wermer MJH, Nederkoorn PJ, Kerkhoff H, Rooyer FA, van Rooij FG, van den Wijngaard IR, Ten Cate TJF, Tuladhar AM, de Leeuw FE, and Verhoeven JI

Subjects
Humans, Female, Male, Young Adult, Adolescent, Adult, Cohort Studies, Prospective Studies, Ischemic Stroke epidemiology, Ischemic Stroke etiology, Stroke epidemiology, Stroke etiology, Ischemic Attack, Transient epidemiology, Ischemic Attack, Transient etiology
Abstract

Importance: Cause of ischemic stroke in young people is highly variable; however, the risk of recurrence is often presented with all subtypes of stroke grouped together in classification systems such as the Trial of ORG (danaparoid sodium [Orgaran]) 10172 in Acute Stroke Treatment (TOAST) criteria, which limits the ability to individually inform young patients with stroke about their risk of recurrence., Objective: To determine the short-term and long-term risk of recurrent vascular events after ischemic stroke at a young age by stroke cause and to identify factors associated with recurrence., Design, Setting, and Participants: This cohort study used data from the Observational Dutch Young Symptomatic Stroke Study, a prospective, multicenter, hospital-based cohort study, conducted at 17 hospitals in the Netherlands between 2013 and 2021. Eligible participants included 30-day survivors of an initial, neuroimaging-proven ischemic stroke (aged 18-49 years). Data analysis was conducted from June to July 2023., Exposure: Diagnosis of a first-ever, ischemic stroke via neuroimaging., Main Outcome and Measures: The primary outcome was short-term (within 6 months) and long-term (within 5 years) recurrence risk of any vascular event, defined as fatal or nonfatal recurrent ischemic stroke, transient ischemic attack, myocardial infarction, and revascularization procedure. Predefined characteristics were chosen to identify factors associated with risk of recurrence (cause of stroke, age, sex, stroke severity, and cardiovascular health factors)., Results: A total of 1216 patients (median [IQR] age, 44.2 [38.4-47.7] years; 632 male [52.0%]; 584 female [48.0%]) were included, with a median (IQR) follow-up of 4.3 (2.6-6.0) years. The 6-month risk of any recurrent ischemic event was 6.7% (95% CI, 5.3%-8.1%), and the 5-year risk was 12.2% (95% CI, 10.2%-14.2%)The short-term risk was highest for patients with cervical artery dissections (13.2%; 95% CI, 7.6%-18.7%). Other factors associated with a recurrent short-term event were atherothrombotic stroke, rare causes of stroke, and hypertension. The long-term cumulative risk was highest for patients with atherothrombotic stroke (22.7%; 95% CI, 10.6%-34.7%) and lowest for patients with cryptogenic stroke (5.8%; 95% CI, 3.0%-8.5%). Cardioembolic stroke was associated with a recurrent long-term event, as were diabetes and alcohol abuse., Conclusions and Relevance: The findings of this cohort study of 1216 patients with an ischemic stroke at a young age suggest that the risk of recurrent vascular events was high and varied by cause of stroke both for short-term and long-term follow-up, including causes that remained concealed when combined into 1 category in the routinely used TOAST criteria. This knowledge will allow for more personalized counseling of young patients with stroke.

Published
2024
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41. Subacute cognitive impairment after first-ever transient ischemic attack or ischemic stroke in young adults: The ODYSSEY study.

Author

Schellekens MM, Boot EM, Verhoeven JI, Ekker MS, van Alebeek ME, Brouwers PJ, Arntz RM, van Dijk GW, Gons RA, van Uden IW, den Heijer T, de Kort PL, de Laat KF, van Norden A, Vermeer SE, van Zagten MS, van Oostenbrugge RJ, Wermer MJ, Nederkoorn PJ, van Rooij FG, van den Wijngaard IR, de Leeuw FE, Kessels RP, and Tuladhar AM

Subjects
Humans, Young Adult, Prospective Studies, Ischemic Attack, Transient complications, Ischemic Stroke complications, Cognitive Dysfunction epidemiology, Stroke complications
Abstract

Introduction: We aimed to investigate the prevalence of cognitive impairment in the subacute phase after transient ischemic attack (TIA) and ischemic stroke (IS), factors associated with a vascular cognitive disorder, and the prevalence of subjective cognitive complaints and their relation with objective cognitive performance., Patients and Methods: In this multicenter prospective cohort study, we recruited patients with first-ever TIA and IS, aged 18-49 years, between 2013 and 2021 for cognitive assessment up to 6 months after index event. We calculated composite Z-scores for seven cognitive domains. We defined cognitive impairment as a composite Z-score < -1.5. We defined major vascular cognitive disorder as a Z-score < -2.0 in one or more cognitive domains., Results: Fifty three TIA and 545 IS patients completed cognitive assessment with mean time to assessment of 89.7 (SD 40.7) days. The median NIHSS at admission was 3 (interquartile range, 1-5). Cognitive impairment was common in five domains (up to 37%), with similar proportion in TIA and IS patients. Patients with major vascular cognitive disorder had a lower education level, higher NIHSS scores and more frequent lesions in the left frontotemporal lobe than without vascular cognitive disorder ( p  < 0.05 FDR-corrected). Subjective memory and executive cognitive complaints were present in about two-thirds of the patients, but were weakly associated with objective cognitive performance (β: -0.32 and -0.21, respectively)., Discussion and Conclusion: In the subacute phase after TIA or stroke in young adults, cognitive impairment and subjective cognitive complaints are prevalent, but they are weakly associated with each other., Competing Interests: The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: AT is a junior staff member of the Dutch Heart Foundation (grant number 2016T044). FEL has received a VIDI grant (016-126-351); and the Clinical established investigator Dutch Heart Foundation grant (2014 T060). MW has received a VIDI grant (9171337) of the ZonMw/NWO and the Clinical established investigator Dutch Heart Foundation grant (2016T86)., (© European Stroke Organisation 2022.)

Published
2023
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42. Risk Factors and Causes of Ischemic Stroke in 1322 Young Adults.

Author

Ekker MS, Verhoeven JI, Schellekens MMI, Boot EM, van Alebeek ME, Brouwers PJAM, Arntz RM, van Dijk GW, Gons RAR, van Uden IWM, den Heijer T, de Kort PLM, de Laat KF, van Norden AGW, Vermeer SE, van Zagten MSG, van Oostenbrugge RJ, Wermer MJH, Nederkoorn PJ, Zonneveld TP, Kerkhoff H, Rooyer FA, van Rooij FG, van den Wijngaard IR, Klijn CJM, Tuladhar AM, and de Leeuw FE

Subjects
Male, Humans, Young Adult, Child, Adult, Female, Prospective Studies, Risk Factors, Ischemic Stroke complications, Stroke therapy, Atherosclerosis complications
Abstract

Background: Identification of risk factors and causes of stroke is key to optimize treatment and prevent recurrence. Up to one-third of young patients with stroke have a cryptogenic stroke according to current classification systems (Trial of ORG 10172 in Acute Stroke Treatment [TOAST] and atherosclerosis, small vessel disease, cardiac pathology, other causes, dissection [ASCOD]). The aim was to identify risk factors and leads for (new) causes of cryptogenic ischemic stroke in young adults, using the pediatric classification system from the IPSS study (International Pediatric Stroke Study)., Methods: This is a multicenter prospective cohort study conducted in 17 hospitals in the Netherlands, consisting of 1322 patients aged 18 to 49 years with first-ever, imaging confirmed, ischemic stroke between 2013 and 2021. The main outcome was distribution of risk factors according to IPSS classification in patients with cryptogenic and noncryptogenic stroke according to the TOAST and ASCOD classification., Results: The median age was 44.2 years, and 697 (52.7%) were men. Of these 1322 patients, 333 (25.2%) had a cryptogenic stroke according to the TOAST classification. Additional classification using the ASCOD criteria reduced the number patients with cryptogenic stroke from 333 to 260 (19.7%). When risk factors according to the IPSS were taken into account, the number of patients with no potential cause or risk factor for stroke reduced to 10 (0.8%)., Conclusions: Among young adults aged 18 to 49 years with a cryptogenic ischemic stroke according to the TOAST classification, risk factors for stroke are highly prevalent. Using a pediatric classification system provides new leads for the possible causes in cryptogenic stroke, and could potentially lead to more tailored treatment for young individuals with stroke.

Published
2023
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43. Trigger Factors for Stroke in Young Adults: A Case-Crossover Study.

Author

Ekker MS, Verhoeven JI, Rensink KML, Schellekens MMI, Boot EM, van Alebeek ME, Brouwers PJAM, Arntz RM, van Dijk GW, Gons RAR, van Uden IWM, den Heijer T, de Kort PLM, de Laat KF, van Norden AGW, Vermeer SE, van Zagten M, van Oostenbrugge RJ, Wermer MJH, Nederkoorn PJ, Kerkhoff H, Rooyer F, van Rooij FG, van den Wijngaard IR, Klijn CJM, Tuladhar AM, and de Leeuw FE

Subjects
Aged, Male, Humans, Young Adult, Adult, Female, Cross-Over Studies, Risk Factors, Cerebral Hemorrhage etiology, Cerebral Hemorrhage complications, Stroke epidemiology, Stroke etiology, Ischemic Stroke complications, Illicit Drugs
Abstract

Background and Objectives: Causes of stroke in young adults differ from those in the elderly individuals, and in a larger percentage, no cause can be determined. To gain more insight into the etiology of (cryptogenic) stroke in the young population, we investigated whether trigger factors, such as short-lasting exposure to toxins or infection, may play a role., Methods: Patients aged 18-49 years with a first-ever ischemic stroke or intracerebral hemorrhage (ICH) in 17 participating centers in the Netherlands completed a questionnaire about exposure to 9 potential trigger factors in hazard periods and on a regular yearly basis. A case-crossover design was used to assess relative risks (RRs) with 95% confidence intervals (95% CIs) by the Mantel-Haenszel case-crossover method, for any stroke (ischemic stroke and ICH combined) and for different etiologic subgroups of ischemic stroke., Results: One thousand one hundred forty-six patients completed the questionnaire (1,043 patients with an ischemic stroke and 103 with an ICH, median age 44.0 years, 52.6% men). For any stroke, an increased risk emerged within 1 hour of cola consumption (RR 2.0, 95% CI 1.5-2.8) and vigorous physical exercise (RR 2.6, 95% CI 2.2-3.0), within 2 hours after sexual activity (RR 2.4, 95% CI 1.6-3.5), within 4 hours after illicit drug use (RR 2.8, 95% CI 1.7-4.9), and within 24 hours after fever or flu-like disease (RR 14.1, 95% CI 10.5-31.2; RR 13.9, 95% CI 8.9-21.9). Four trigger factors increased the risk of other determined and cryptogenic ischemic stroke, 3 that of cardioembolic stroke, 2 that of large vessel atherosclerosis and likely atherothrombotic stroke combined and stroke with multiple causes, and none that of stroke due to small vessel disease., Discussion: We identified cola consumption, vigorous physical exercise, sexual activity, illicit drug use, fever, and flu-like disease as potential trigger factors for stroke in the young population and found differences in the type and number of trigger factors associated with different etiologic subgroups of ischemic stroke. These findings might help in better understanding the pathophysiologic mechanisms of (cryptogenic) stroke in the young population., (© 2022 American Academy of Neurology.)

Published
2023
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44. Effects of the DICE Method to Improve Timely Recognition and Treatment of Neuropsychiatric Symptoms in Early Alzheimer's Disease at the Memory Clinic: The BEAT-IT Study.

Author

Eikelboom WS, van den Berg E, Coesmans M, Goudzwaard JA, Koopmanschap M, Lazaar N, van Bruchem-Visser RL, Driesen JJM, den Heijer T, Hoogers S, de Jong FJ, Mattace-Raso F, Thomeer EC, Vrenken S, Vroegindeweij LJHM, Zuidema SU, Singleton EH, van Swieten JC, Ossenkoppele R, and Papma JM

Subjects
Humans, Quality of Life psychology, Caregivers psychology, Independent Living, Alzheimer Disease diagnosis, Alzheimer Disease therapy, Alzheimer Disease complications, Cognitive Dysfunction diagnosis
Abstract

Background: Neuropsychiatric symptoms (NPS) are highly prevalent in Alzheimer's disease (AD) and are associated with negative outcomes. However, NPS are currently underrecognized at the memory clinic and non-pharmacological interventions are scarcely implemented., Objective: To evaluate the effectiveness of the Describe, Investigate, Create, Evaluate (DICE) method™ to improve the care for NPS in AD at the memory clinic., Methods: We enrolled sixty community-dwelling people with mild cognitive impairment or AD dementia and NPS across six Dutch memory clinics with their caregivers. The first wave underwent care as usual (n = 36) and the second wave underwent the DICE method (n = 24). Outcomes were quality of life (QoL), caregiver burden, NPS severity, NPS-related distress, competence managing NPS, and psychotropic drug use. Reliable change index was calculated to identify responders to the intervention. A cost-effectiveness analysis was performed and semi-structured interviews with a subsample of the intervention group (n = 12)., Results: The DICE method did not improve any outcomes over time compared to care as usual. Half of the participants of the intervention group (52%) were identified as responders and showed more NPS and NPS-related distress at baseline compared to non-responders. Interviews revealed substantial heterogeneity among participants regarding NPS-related distress, caregiver burden, and availability of social support. The intervention did not lead to significant gains in quality-adjusted life years and well-being years nor clear savings in health care and societal costs., Conclusion: The DICE method showed no benefits at group-level, but individuals with high levels of NPS and NPS-related distress may benefit from this intervention.

Published
2023
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45. Spinal cord ischaemia due to fibrocartilaginous embolism…?

Author

den Heijer T

Subjects
Humans, Infarction diagnostic imaging, Infarction etiology, Spinal Cord diagnostic imaging, Cartilage Diseases, Embolism complications, Embolism diagnostic imaging, Spinal Cord Ischemia diagnostic imaging, Spinal Cord Ischemia etiology
Abstract

Competing Interests: Competing interests: None declared.

Published
2022
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46. Sjögren-Larsson syndrome: The mild end of the phenotypic spectrum.

Author

Staps P, van Gaalen J, van Domburg P, Steijlen PM, Ferdinandusse S, den Heijer T, Seyger MMB, Theelen T, and Willemsen MAAP

Abstract

Sjögren-Larsson syndrome (SLS) is a rare inborn error of lipid metabolism. The syndrome is caused by mutations in the ALDH3A2 gene, resulting in a deficiency of fatty aldehyde dehydrogenase. Most patients have a clearly recognizable severe phenotype, with congenital ichthyosis, intellectual disability, and spastic diplegia. In this study, we describe two patients with a remarkably mild phenotype. In both patients, males with actual ages of 45 and 61 years, the diagnosis was only established at an adult age. Their skin had been moderately affected from childhood onward, and both men remained ambulant with mild spasticity of their legs. Cognitive development, as reflected by school performance and professional career, had been unremarkable. Magnetic resonance spectroscopy of the first patient was lacking the characteristic lipid peak. We performed a literature search to identify additional SLS patients with a mild phenotype. We compared the clinical, radiologic, and molecular features of the mildly affected patients with the classical phenotype. We found 10 cases in the literature with a molecular proven diagnosis and a mild phenotype. Neither a genotype-phenotype correlation nor an alternative explanation for the strikingly mild phenotypes was found. New biochemical techniques to study the underlying metabolic defect in SLS, like lipidomics, may in the future help to unravel the reasons for the exceptionally mild phenotypes. In the meantime, it is important to recognize these mildly affected patients to provide them with appropriate care and genetic counseling, and to increase our insights in the true disease spectrum of SLS., Competing Interests: The authors declare no potential conflict of interest., (© 2020 The Authors. Journal of Inherited Metabolic Disease published by John Wiley & Sons Ltd on behalf of SSIEM.)

Published
2020
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47. Viral encephalitis associated with rituximab maintenance therapy: two cases and a review of literature.

Author

Noij DP, den Heijer T, and van Zaanen HCT

Subjects
Aged, Antigens, CD, Antineoplastic Agents, Immunological therapeutic use, Fatal Outcome, Female, Humans, Lymphoma, Mantle-Cell drug therapy, Lymphoma, Non-Hodgkin drug therapy, Male, Rituximab therapeutic use, Treatment Outcome, Antineoplastic Agents, Immunological adverse effects, Encephalitis, Viral chemically induced, Rituximab adverse effects
Abstract

Rituximab is increasingly used in the treatment of CD20-positive B-cell-mediated disease. Prolonged use may cause B-cell dysfunction, dose-dependent T-cell dysfunction, and hypogammaglobulinaemia and result in severe non-neutropenic infections. We present two cases of viral encephalitis in patients treated with rituximab maintenance therapy: one patient presented with deafness; the other patient with paroxysmal light flashes, apraxia, and weakness.

Published
2020

48. Early recognition and treatment of neuropsychiatric symptoms to improve quality of life in early Alzheimer's disease: protocol of the BEAT-IT study.

Author

Eikelboom WS, Singleton E, van den Berg E, Coesmans M, Mattace Raso F, van Bruchem RL, Goudzwaard JA, de Jong FJ, Koopmanschap M, den Heijer T, Driesen JJM, Vroegindeweij LJHM, Thomeer EC, Hoogers SE, Dijkstra AA, Zuidema SU, Pijnenburg YAL, Scheltens P, van Swieten JC, Ossenkoppele R, and Papma JM

Subjects
Humans, Cost-Benefit Analysis, Follow-Up Studies, Neuropsychological Tests, Outcome Assessment, Health Care, Psychiatric Status Rating Scales, Research Design, Controlled Clinical Trials as Topic, Multicenter Studies as Topic, Alzheimer Disease complications, Alzheimer Disease diagnosis, Behavioral Symptoms diagnosis, Behavioral Symptoms etiology, Behavioral Symptoms therapy, Cognitive Dysfunction complications, Cognitive Dysfunction diagnosis, Psychological Distress, Quality of Life
Abstract

Background: Neuropsychiatric symptoms (NPS) are very common in patients with mild cognitive impairment (MCI) and Alzheimer's disease (AD) dementia and are associated with various disadvantageous clinical outcomes including a negative impact on quality of life, caregiver burden, and accelerated disease progression. Despite growing evidence of the efficacy of (non)pharmacological interventions to reduce these symptoms, NPS remain underrecognized and undertreated in memory clinics. The BEhavioural symptoms in Alzheimer's disease Towards early Identification and Treatment (BEAT-IT) study is developed to (1) investigate the neurobiological etiology of NPS in AD and (2) study the effectiveness of the Describe, Investigate, Create, Evaluate (DICE) approach to structure and standardize the current care of NPS in AD. By means of the DICE method, we aim to improve the quality of life of AD patients with NPS and their caregivers who visit the memory clinic. This paper describes the protocol for the intervention study that incorporates the latter aim., Methods: We aim to enroll a total of 150 community-dwelling patients with MCI or AD and their caregivers in two waves. First, we will recruit a control group who will receive care as usual. Next, the second wave of participants will undergo the DICE method. This approach consists of the following steps: (1) describe the context in which NPS occur, (2) investigate the possible causes, (3) create and implement a treatment plan, and (4) evaluate whether these interventions are effective. Primary outcomes are the quality of life of patients and their caregivers. Secondary outcomes include NPS change, caregiver burden, caregivers' confidence managing NPS, psychotropic medication use, the experiences of patients and caregivers who underwent the DICE method, and the cost-effectiveness of the intervention., Conclusions: This paper describes the protocol of an intervention study that is part of the BEAT-IT study and aims to improve current recognition and treatment of NPS in AD by structuring and standardizing the detection and treatment of NPS in AD using the DICE approach., Trial Registration: The trial was registered on the Netherlands Trial Registry ( NTR7459 ); registered 6 September 2018.

Published
2019
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49. [Vitamin B6 deficiency caused by the use of levodopa].

Author

van der Steen W, den Heijer T, and Groen J

Subjects
Administration, Oral, Aged, Antiparkinson Agents administration & dosage, Carbidopa administration & dosage, Drug Combinations, Humans, Levodopa administration & dosage, Middle Aged, Tablets, Antiparkinson Agents adverse effects, Carbidopa adverse effects, Levodopa adverse effects, Vitamin B 6 Deficiency chemically induced
Abstract

Background: There are indications that the use of levodopa/carbidopa can cause symptomatic vitamin B6 deficiency. However, this has only been described for patients who used the product in the form of an intestinal gel., Case Description: We are describing 3 patients who developed vitamin B6 deficiency while using levodopa/carbidopa in tablet form. All 3 patients developed symptoms consistent with peripheral axonal polyneuropathy., Conclusion: The cases of our patients are providing support for the idea that oral use of levodopa/carbidopa can cause symptomatic vitamin B6 deficiency.

Published
2018

50. Cognition and gray and white matter characteristics of presymptomatic C9orf72 repeat expansion.

Author

Papma JM, Jiskoot LC, Panman JL, Dopper EG, den Heijer T, Donker Kaat L, Pijnenburg YAL, Meeter LH, van Minkelen R, Rombouts SARB, and van Swieten JC

Subjects
Adult, C9orf72 Protein, Cognitive Dysfunction diagnostic imaging, Diffusion Tensor Imaging, Female, Gray Matter diagnostic imaging, Heterozygote, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Neuropsychological Tests, White Matter diagnostic imaging, Cognitive Dysfunction pathology, Cognitive Dysfunction physiopathology, DNA Repeat Expansion genetics, Frontotemporal Dementia diagnostic imaging, Frontotemporal Dementia genetics, Frontotemporal Dementia pathology, Frontotemporal Dementia physiopathology, Gray Matter pathology, Proteins genetics, White Matter pathology
Abstract

Objective: To investigate cognitive function, gray matter volume, and white matter integrity in the presymptomatic stage of chromosome 9 open reading frame 72 repeat expansion ( C9orf72RE )., Methods: Presymptomatic C9orf72RE carriers (n = 18) and first-degree family members without a pathogenic expansion (healthy controls [HC], n = 15) underwent a standardized protocol of neuropsychological tests, T1-weighted MRI, and diffusion tensor imaging within our cohort study of autosomal dominant frontotemporal dementia (FTD). We investigated group differences in cognitive function, gray matter volume through voxel-based morphometry, and white matter integrity by means of tract-based spatial statistics. We correlated cognitive change with underlying gray or white matter., Results: Our data demonstrate lower scores on letter fluency, Stroop card I, and Stroop card III, accompanied by white matter integrity loss in tracts connecting the frontal lobe, the thalamic radiation, and tracts associated with motor functioning in presymptomatic C9orf72RE compared with HC. In a subgroup of C9orf72RE carriers above 40 years of age, we found gray matter volume loss in the thalamus, cerebellum, and parietal and temporal cortex. We found no significant relationship between subtle cognitive decline and underlying gray or white matter., Conclusions: This study demonstrates that a decline in cognitive functioning, white matter integrity, and gray matter volumes are present in presymptomatic C9orf72RE carriers. These findings suggest that neuropsychological assessment, T1-weighted MRI, and diffusion tensor imaging might be useful to identify early biomarkers in the presymptomatic stage of FTD or amyotrophic lateral sclerosis., (© 2017 American Academy of Neurology.)

Published
2017
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