137 results on '"Hu, Shu-Ching"'
Search Results
2. Cognition as a mediator for gait and balance impairments in GBA-related Parkinson’s disease
- Author
-
Morris, Rosie, Martini, Douglas N., Ramsey, Katrina, Kelly, Valerie E., Smulders, Katrijn, Hiller, Amie, Chung, Kathryn A., Hu, Shu-Ching, Zabetian, Cyrus P., Poston, Kathleen L., Mata, Ignacio F., Edwards, Karen L., Lapidus, Jodi, Cholerton, Brenna, Montine, Thomas J., Quinn, Joseph F., and Horak, Fay
- Published
- 2022
- Full Text
- View/download PDF
3. Clinical and dopamine transporter imaging characteristics of non-manifest LRRK2 and GBA mutation carriers in the Parkinson's Progression Markers Initiative (PPMI): a cross-sectional study
- Author
-
Arnedo, Vanessa, Clark, Adrienne, Fraiser, Mark, Kopil, Catherine, Chowdhury, Sohini, Sherer, Todd, Daegele, Nichole, Casaceli, Cynthia, Dorsey, Ray, Wilson, Renee, Mahes, Sugi, Salerno, Christina, Crawford, Karen, Casalin, Paola, Malferrari, Giulia, Weisz, Mali Gani, Orr-Urtreger, Avi, Montine, Thomas, Baglieri, Chris, Christini, Amanda, Russell, David, Dahodwala, Nabila, Giladi, Nir, Factor, Stewart, Hogarth, Penelope, Standaert, David, Hauser, Robert, Jankovic, Joseph, Saint-Hilaire, Marie, Richard, Irene, Shprecher, David, Fernandez, Hubert, Brockmann, Katrina, Rosenthal, Liana, Barone, Paolo, Espay, Alberto, Rowe, Dominic, Marder, Karen, Santiago, Anthony, Hu, Shu-Ching, Isaacson, Stuart, Corvol, Jean-Christophe, Ruiz Martinez, Javiar, Tolosa, Eduardo, Tai, Yen, Politis, Marios, Smejdir, Debra, Rees, Linda, Williams, Karen, Kausar, Farah, Richardson, Whitney, Willeke, Diana, Peacock, Shawnees, Sommerfeld, Barbara, Freed, Alison, Wakeman, Katrina, Blair, Courtney, Guthrie, Stephanie, Harrell, Leigh, Hunter, Christine, Thomas, Cathi-Ann, James, Raymond, Zimmerman, Grace, Brown, Victoria, Mule, Jennifer, Hilt, Ella, Ribb, Kori, Ainscough, Susan, Wethington, Misty, Ranola, Madelaine, Mejia Santana, Helen, Moreno, Juliana, Raymond, Deborah, Speketer, Krista, Carvajal, Lisbeth, Carvalo, Stephanie, Croitoru, Ioana, Garrido, Alicia, Payne, Laura Marie, Viswanth, Veena, Severt, Lawrence, Facheris, Maurizio, Soares, Holly, Mintun, Mark A., Cedarbaum, Jesse, Taylor, Peggy, Biglan, Kevin, Vandenbroucke, Emily, Haider Sheikh, Zulfiqar, Bingol, Baris, Fischer, Tanya, Sardi, Pablo, Forrat, Remi, Reith, Alastair, Egebjerg, Jan, Ahlberg Hillert, Gabrielle, Saba, Barbara, Min, Chris, Umek, Robert, Mather, Joe, De Santi, Susan, Post, Anke, Boess, Frank, Taylor, Kirsten, Grachev, Igor, Avbersek, Andreja, Muglia, Pierandrea, Merchant, Kaplana, Tauscher, Johannes, Simuni, Tanya, Uribe, Liz, Cho, Hyunkeun Ryan, Caspell-Garcia, Chelsea, Coffey, Christopher S, Siderowf, Andrew, Trojanowski, John Q, Shaw, Leslie M, Seibyl, John, Singleton, Andrew, Toga, Arthur W, Galasko, Doug, Foroud, Tatiana, Tosun, Duygu, Poston, Kathleen, Weintraub, Daniel, Mollenhauer, Brit, Tanner, Caroline M, Kieburtz, Karl, Chahine, Lana M, Reimer, Alyssa, Hutten, Samantha J, Bressman, Susan, and Marek, Kenneth
- Published
- 2020
- Full Text
- View/download PDF
4. Cognitive associations with comprehensive gait and static balance measures in Parkinson's disease
- Author
-
Morris, Rosie, Martini, Douglas N., Smulders, Katrijn, Kelly, Valerie E., Zabetian, Cyrus P., Poston, Kathleen, Hiller, Amie, Chung, Kathryn A., Yang, Laurice, Hu, Shu-Ching, Edwards, Karen L., Cholerton, Brenna, Grabowski, Thomas J., Montine, Thomas J., Quinn, Joseph F., and Horak, Fay
- Published
- 2019
- Full Text
- View/download PDF
5. Prediction of cognitive progression in Parkinson's disease using three cognitive screening measures
- Author
-
Kim, Hojoong M., Nazor, Carter, Zabetian, Cyrus P., Quinn, Joseph F., Chung, Kathryn A., Hiller, Amie L., Hu, Shu-Ching, Leverenz, James B., Montine, Thomas J., Edwards, Karen L., and Cholerton, Brenna
- Published
- 2019
- Full Text
- View/download PDF
6. Sex differences in progression to mild cognitive impairment and dementia in Parkinson's disease
- Author
-
Cholerton, Brenna, Johnson, Catherine O., Fish, Brian, Quinn, Joseph F., Chung, Kathryn A., Peterson-Hiller, Amie L., Rosenthal, Liana S., Dawson, Ted M., Albert, Marilyn S., Hu, Shu-Ching, Mata, Ignacio F., Leverenz, James B., Poston, Kathleen L., Montine, Thomas J., Zabetian, Cyrus P., and Edwards, Karen L.
- Published
- 2018
- Full Text
- View/download PDF
7. Homocysteine and cognitive function in Parkinson's disease
- Author
-
Licking, Nicole, Murchison, Charles, Cholerton, Brenna, Zabetian, Cyrus P., Hu, Shu-Ching, Montine, Thomas J., Peterson-Hiller, Amie L., Chung, Kathryn A., Edwards, Karen, Leverenz, James B., and Quinn, Joseph F.
- Published
- 2017
- Full Text
- View/download PDF
8. Dendrite Development Regulated by CREST, a Calcium-Regulated Transcriptional Activator
- Author
-
Aizawa, Hiroyuki, Hu, Shu-Ching, Bobb, Kathryn, Balakrishnan, Karthik, Ince, Gulayse, Gurevich, Inga, Cowan, Mitra, and Ghosh, Anirvan
- Published
- 2004
9. Multivariate prediction of dementia in Parkinson’s disease
- Author
-
Phongpreecha, Thanaphong, Cholerton, Brenna, Mata, Ignacio F., Zabetian, Cyrus P., Poston, Kathleen L., Aghaeepour, Nima, Tian, Lu, Quinn, Joseph F., Chung, Kathryn A., Hiller, Amie L., Hu, Shu-Ching, Edwards, Karen L., and Montine, Thomas J.
- Published
- 2020
- Full Text
- View/download PDF
10. Haptoglobin phenotype modifies serum iron levels and the effect of smoking on Parkinson disease risk
- Author
-
Costa-Mallen, Paola, Zabetian, Cyrus P., Agarwal, Pinky, Hu, Shu-Ching, Yearout, Dora, Samii, Ali, Leverenz, James B., Roberts, John W., and Checkoway, Harvey
- Published
- 2015
- Full Text
- View/download PDF
11. Smoking and haptoglobin phenotype modulate serum ferritin and haptoglobin levels in Parkinson disease
- Author
-
Costa-Mallen, Paola, Zabetian, Cyrus P., Hu, Shu-Ching, Agarwal, Pinky, Yearout, Dora, and Checkoway, Harvey
- Published
- 2016
- Full Text
- View/download PDF
12. Plasma exosomal α-synuclein is likely CNS-derived and increased in Parkinson’s disease
- Author
-
Shi, Min, Liu, Changqin, Cook, Travis J., Bullock, Kristin M., Zhao, Yanchun, Ginghina, Carmen, Li, Yanfei, Aro, Patrick, Dator, Romel, He, Chunmei, Hipp, Michael J., Zabetian, Cyrus P., Peskind, Elaine R., Hu, Shu-Ching, Quinn, Joseph F., Galasko, Douglas R., Banks, William A., and Zhang, Jing
- Published
- 2014
- Full Text
- View/download PDF
13. Large-scale exploratory genetic analysis of cognitive impairment in Parkinson's disease
- Author
-
Mata, Ignacio F., Johnson, Catherine O., Leverenz, James B., Weintraub, Daniel, Trojanowski, John Q., Van Deerlin, Vivianna M., Ritz, Beate, Rausch, Rebecca, Factor, Stewart A., Wood-Siverio, Cathy, Quinn, Joseph F., Chung, Kathryn A., Peterson-Hiller, Amie L., Espay, Alberto J., Revilla, Fredy J., Devoto, Johnna, Yearout, Dora, Hu, Shu-Ching, Cholerton, Brenna A., Montine, Thomas J., Edwards, Karen L., and Zabetian, Cyrus P.
- Published
- 2017
- Full Text
- View/download PDF
14. GBA Variants Are Associated With a Distinct Pattern of Cognitive Deficits in Parkinsonʼs Disease
- Author
-
Mata, Ignacio F., Leverenz, James B., Weintraub, Daniel, Trojanowski, John Q., Chen-Plotkin, Alice, Van Deerlin, Vivianna M., Ritz, Beate, Rausch, Rebecca, Factor, Stewart A., Wood-Siverio, Cathy, Quinn, Joseph F., Chung, Kathryn A., Peterson-Hiller, Amie L., Goldman, Jennifer G., Stebbins, Glenn T., Bernard, Bryan, Espay, Alberto J., Revilla, Fredy J., Devoto, Johnna, Rosenthal, Liana S., Dawson, Ted M., Albert, Marilyn S., Tsuang, Debby, Huston, Haley, Yearout, Dora, Hu, Shu-Ching, Cholerton, Brenna A., Montine, Thomas J., Edwards, Karen L., and Zabetian, Cyrus P.
- Published
- 2016
- Full Text
- View/download PDF
15. Cerebrospinal Fluid Particles in Alzheimer Disease and Parkinson Disease
- Author
-
Yang, Yue, Keene, C. Dirk, Peskind, Elaine R., Galasko, Douglas R., Hu, Shu-Ching, Cudaback, Eiron, Wilson, Angela M., Li, Ge, Yu, Chang-En, Montine, Kathleen S., Zhang, Jing, Baird, Geoffrey S., Hyman, Bradley T., and Montine, Thomas J.
- Published
- 2015
- Full Text
- View/download PDF
16. Cognitive Profile of LRRK2-Related Parkinsonʼs Disease
- Author
-
Srivatsal, Sindhu, Cholerton, Brenna, Leverenz, James B., Wszolek, Zbigniew K., Uitti, Ryan J., Dickson, Dennis W., Weintraub, Daniel, Trojanowski, John Q., Van Deerlin, Vivianna M., Quinn, Joseph F., Chung, Kathryn A., Peterson, Amie L., Factor, Stewart A., Wood-Siverio, Cathy, Goldman, Jennifer G., Stebbins, Glenn T., Bernard, Bryan, Ritz, Beate, Rausch, Rebecca, Espay, Alberto J., Revilla, Fredy J., Devoto, Johnna, Rosenthal, Liana S., Dawson, Ted M., Albert, Marilyn S., Mata, Ignacio F., Hu, Shu-Ching, Montine, Kathleen S., Johnson, Catherine, Montine, Thomas J., Edwards, Karen L., Zhang, Jing, and Zabetian, Cyrus P.
- Published
- 2015
- Full Text
- View/download PDF
17. APOE, MAPT, and SNCA Genes and Cognitive Performance in Parkinson Disease
- Author
-
Mata, Ignacio F., Leverenz, James B., Weintraub, Daniel, Trojanowski, John Q., Hurtig, Howard I., Van Deerlin, Vivianna M., Ritz, Beate, Rausch, Rebecca, Rhodes, Shannon L., Factor, Stewart A., Wood-Siverio, Cathy, Quinn, Joseph F., Chung, Kathryn A., Peterson, Amie L., Espay, Alberto J., Revilla, Fredy J., Devoto, Johnna, Hu, Shu-Ching, Cholerton, Brenna A., Wan, Jia Y., Montine, Thomas J., Edwards, Karen L., and Zabetian, Cyrus P.
- Published
- 2014
- Full Text
- View/download PDF
18. Evaluation of mild cognitive impairment subtypes in Parkinsonʼs disease
- Author
-
Cholerton, Brenna A., Zabetian, Cyrus P., Wan, Jia Y., Montine, Thomas J., Quinn, Joseph F., Mata, Ignacio F., Chung, Kathryn A., Peterson, Amie, Espay, Alberto J., Revilla, Fredy J., Devoto, Johnna, Watson, Stennis G., Hu, Shu-Ching, Leverenz, James B., and Edwards, Karen L.
- Published
- 2014
- Full Text
- View/download PDF
19. Enhancing case ascertainment of Parkinsonʼs disease using Medicare claims data in a population-based cohort: the Cardiovascular Health Study
- Author
-
Ton, Thanh G. N., Biggs, Mary Lou, Comer, Diane, Curtis, Lesley, Hu, Shu-Ching, Thacker, Evan L., Searles Nielsen, Susan, Delaney, Joseph A., Landsittel, Douglas, Longstreth, William T., Jr., Checkoway, Harvey, and Jain, Samay
- Published
- 2014
- Full Text
- View/download PDF
20. Emergency treatment of movement disorders
- Author
-
Hu, Shu-Ching and Frucht, Steven J.
- Published
- 2007
- Full Text
- View/download PDF
21. The genetic architecture of the human cerebral cortex
- Author
-
Grasby, Katrina L, Jahanshad, Neda, Shatokhina, Natalia, Mirza-Schreiber, Nazanin, Moreira, Jose C V, Mühleisen, Thomas W, Müller-Myhsok, Bertram, Najt, Pablo, Nakahara, Soichiro, Nho, Kwangsik, Olde Loohuis, Loes M, Orfanos, Dimitri Papadopoulos, Pearson, John F, Zsembik, Leo C P, Pitcher, Toni L, Pütz, Benno, Quidé, Yann, Ragothaman, Anjanibhargavi, Rashid, Faisal M, Reay, William R, Redlich, Ronny, Reinbold, Céline S, Repple, Jonathan, Richard, Geneviève, Thomopoulos, Sophia I, Riedel, Brandalyn C, Risacher, Shannon L, Rocha, Cristiane S, Mota, Nina Roth, Salminen, Lauren, Saremi, Arvin, Saykin, Andrew J, Schlag, Fenja, Schmaal, Lianne, Schofield, Peter R, Zhu, Alyssa H, Secolin, Rodrigo, Shapland, Chin Yang, Shen, Li, Shin, Jean, Shumskaya, Elena, Sønderby, Ida E, Sprooten, Emma, Tansey, Katherine E, Teumer, Alexander, Thalamuthu, Anbupalam, Strike, Lachlan T, Tordesillas-Gutiérrez, Diana, Turner, Jessica A, Uhlmann, Anne, Vallerga, Costanza Ludovica, van der Meer, Dennis, van Donkelaar, Marjolein M J, van Eijk, Liza, van Erp, Theo G M, van Haren, Neeltje E M, van Rooij, Daan, Agartz, Ingrid, van Tol, Marie-José, Veldink, Jan H, Verhoef, Ellen, Walton, Esther, Wang, Mingyuan, Wang, Yunpeng, Wardlaw, Joanna M, Wen, Wei, Westlye, Lars T, Whelan, Christopher D, Alhusaini, Saud, Witt, Stephanie H, Wittfeld, Katharina, Wolf, Christiane, Wolfers, Thomas, Wu, Jing Qin, Yasuda, Clarissa L, Zaremba, Dario, Zhang, Zuo, Zwiers, Marcel P, Artiges, Eric, Almeida, Marcio A A, Assareh, Amelia A, Ayesa-Arriola, Rosa, Belger, Aysenil, Brandt, Christine L, Brown, Gregory G, Cichon, Sven, Curran, Joanne E, Davies, Gareth E, Degenhardt, Franziska, Dennis, Michelle F, Alnæs, Dag, Dietsche, Bruno, Djurovic, Srdjan, Doherty, Colin P, Espiritu, Ryan, Garijo, Daniel, Gil, Yolanda, Gowland, Penny A, Green, Robert C, Häusler, Alexander N, Heindel, Walter, Amlien, Inge K, Ho, Beng-Choon, Hoffmann, Wolfgang U, Holsboer, Florian, Homuth, Georg, Hosten, Norbert, Jack, Clifford R, Jang, MiHyun, Jansen, Andreas, Kimbrel, Nathan A, Kolskår, Knut, Painter, Jodie N, Andersson, Micael, Koops, Sanne, Krug, Axel, Lim, Kelvin O, Luykx, Jurjen J, Mathalon, Daniel H, Mather, Karen A, Mattay, Venkata S, Matthews, Sarah, Mayoral Van Son, Jaqueline, McEwen, Sarah C, Ard, Tyler, Melle, Ingrid, Morris, Derek W, Mueller, Bryon A, Nauck, Matthias, Nordvik, Jan E, Nöthen, Markus M, O'Leary, Daniel S, Opel, Nils, Martinot, Marie-Laure Paillère, Pike, G Bruce, Armstrong, Nicola J, Preda, Adrian, Quinlan, Erin B, Rasser, Paul E, Ratnakar, Varun, Reppermund, Simone, Steen, Vidar M, Tooney, Paul A, Torres, Fábio R, Veltman, Dick J, Voyvodic, James T, Ashley-Koch, Allison, Whelan, Robert, White, Tonya, Yamamori, Hidenaga, Adams, Hieab H H, Bis, Joshua C, Debette, Stephanie, Decarli, Charles, Fornage, Myriam, Gudnason, Vilmundur, Hofer, Edith, Atkins, Joshua R, Ikram, M Arfan, Launer, Lenore, Longstreth, W. T., Lopez, Oscar L, Mazoyer, Bernard, Mosley, Thomas H, Roshchupkin, Gennady V, Satizabal, Claudia L, Schmidt, Reinhold, Seshadri, Sudha, Bernard, Manon, Yang, Qiong, Initiative, Alzheimer’s Disease Neuroimaging, Consortium, CHARGE, Consortium, EPIGEN, Consortium, IMAGEN, Consortium, SYS, Initiative, Parkinson’s Progression Markers, Alvim, Marina K M, Ames, David, Anderson, Tim J, Brouwer, Rachel M, Andreassen, Ole A, Arias-Vasquez, Alejandro, Bastin, Mark E, Baune, Bernhard T, Beckham, Jean C, Blangero, John, Boomsma, Dorret I, Brodaty, Henry, Brunner, Han G, Buckner, Randy L, Buimer, Elizabeth E L, Buitelaar, Jan K, Bustillo, Juan R, Cahn, Wiepke, Cairns, Murray J, Calhoun, Vince, Carr, Vaughan J, Caseras, Xavier, Caspers, Svenja, Cavalleri, Gianpiero L, Cendes, Fernando, Bülow, Robin, Corvin, Aiden, Crespo-Facorro, Benedicto, Dalrymple-Alford, John C, Dannlowski, Udo, de Geus, Eco J C, Deary, Ian J, Delanty, Norman, Depondt, Chantal, Desrivières, Sylvane, Donohoe, Gary, Bürger, Christian, Espeseth, Thomas, Fernández, Guillén, Fisher, Simon E, Flor, Herta, Forstner, Andreas J, Francks, Clyde, Franke, Barbara, Glahn, David C, Gollub, Randy L, Grabe, Hans J, Colodro-Conde, Lucía, Cannon, Dara M, Gruber, Oliver, Håberg, Asta K, Hariri, Ahmad R, Hartman, Catharina A, Hashimoto, Ryota, Heinz, Andreas, Henskens, Frans A, Hillegers, Manon H J, Hoekstra, Pieter J, Holmes, Avram J, Chakravarty, Mallar, Hong, L Elliot, Hopkins, William D, Hulshoff Pol, Hilleke E, Jernigan, Terry L, Jönsson, Erik G, Kahn, René S, Kennedy, Martin A, Kircher, Tilo T J, Kochunov, Peter, Kwok, John B J, Chen, Qiang, Le Hellard, Stephanie, Loughland, Carmel M, Martin, Nicholas G, Martinot, Jean-Luc, McDonald, Colm, McMahon, Katie L, Meyer-Lindenberg, Andreas, Michie, Patricia T, Morey, Rajendra A, Mowry, Bryan, Cheung, Joshua W, Nyberg, Lars, Oosterlaan, Jaap, Ophoff, Roel A, Pantelis, Christos, Paus, Tomas, Pausova, Zdenka, Penninx, Brenda W J H, Polderman, Tinca J C, Posthuma, Danielle, Rietschel, Marcella, Couvy-Duchesne, Baptiste, Roffman, Joshua L, Rowland, Laura M, Sachdev, Perminder S, Sämann, Philipp G, Schall, Ulrich, Schumann, Gunter, Scott, Rodney J, Sim, Kang, Sisodiya, Sanjay M, Smoller, Jordan W, Dale, Anders M, Sommer, Iris E, St Pourcain, Beate, Stein, Dan J, Toga, Arthur W, Trollor, Julian N, Van der Wee, Nic J A, van 't Ent, Dennis, Völzke, Henry, Walter, Henrik, Weber, Bernd, Dalvie, Shareefa, Weinberger, Daniel R, Wright, Margaret J, Zhou, Juan, Stein, Jason L, Thompson, Paul M, Medland, Sarah E, Consortium, Enhancing NeuroImaging Genetics through Meta-Analysis, Witte, A Veronica, Darin, Abigail, Fleisher, Adam, de Araujo, Tânia K, Pierce, Aimee, Mintz, Akiva, Lerner, Alan, Reith, Alastair D, Hofman, Albert, Espay, Alberto, Ihlenfeld, Albrecht, Ing, Alex, Iranzo, Alex, Beiser, Alexa S, de Zubicaray, Greig I, Norbash, Alexander, Barbot, Alexis, Rudolph, Alice, Portillo, Alicia, Chalker, Alison, Levey, Allan I, Rosen, Allyson, Smith, Amanda, Catafau, Ana, de Zwarte, Sonja M C, Ulysse, Anaztasia, Uitterlinden, André G, Becker, Andreas, Budson, Andrew E, Kertesz, Andrew, Siderowf, Andrew, Bralten, Janita, den Braber, Anouk, Singleton, Andrew, James, Angela, Oliver, Angela, Mishra, Aniket, Hake, Ann Marie, Burke, Anna, Sarrael, Antero, Porsteinsson, Anton P, Stringaris, Argyris, McCoy, Arita, Doan, Nhat Trung, Villringer, Arno, Lenahan, Art, Toga, Arthur, Bokde, Arun, Rawlins, Ashlee, Lamb, Ashley, Lee, Athena, Raj, Balebail Ashok, Tran, Baochan, Dohm, Katharina, Ruggeri, Barbara, Saba, Barbara, Lane, Barton, Yanez, Beatriz, Ances, Beau, Dunlop, Becky, Mudge, Benita, Ravina, Bernard, Ittermann, Bernd, Ehrlich, Stefan, van Noort, Betteke, Lind, Betty, Shah, Bina, Stefanovic, Bojana, Goldstein, Bonnie S, Bonakdarpour, Borna, Matthews, Brandy R, Borowski, Bret, Ott, Brian R, Reynolds, Brigid, Engelbrecht, Hannah-Ruth, Mollenhauer, Brit, Miller, Bruce L, Psaty, Bruce M, Spann, Bryan M, Sadowsky, Carl, Linder, Carly, Franz, Carol E, Tanner, Caroline, Kopil, Catherine, Thomas, Cathi-Ann, Erk, Susanne, Ward, Chad, Bernick, Charles, Smith, Charles D, DeCarli, Charles, Caspell, Chelsea, Deeley, Cheryl, Riordan, Cheryl, Mathis, Chet, Onyike, Chiadi, Heyn, Chris Chinthaka, Fan, Chun Chieh, Hosein, Chris, Leach, Christi, Bÿchel, Christian, Gigliotti, Christina, Hunter, Christine, Belden, Christine M, Tzourio, Christophe, Coffey, Christopher, van Dyck, Christopher H, Clark, Christopher M, Fedko, Iryna O, Wu, Chuang-Kuo, Albers, Colleen S, Chu, Congying, Brand, Connie, Isensee, Corinna, van Duijn, Cornelia M, Bishop, Courtney, Bodge, Courtney, Foley, Sonya F, Tatsuoka, Curtis, Casaceli, Cynthia, Carlsson, Cynthia M, Mathews, Dana, D'Agostino, Daniel, Silverman, Daniel H S, Marson, Daniel, Berg, Daniela, Harvey, Danielle, Jennings, Danna, Ford, Judith M, Wolk, David A, Goldstein, David B, Bachman, David, Brooks, David, Clark, David, Geldmacher, David, Hart, David, Holtzman, David, Jones, David, Hibar, Derrek P, Fukunaga, Masaki, Knopman, David, Hewitt, David L, Perry, David, Russell, David, Standaert, David, Winkfield, David, Green, Davis Robert C, Fontaine, Deborah, Miller, Delwyn D, Gessert, Devon, Garrett, Melanie E, Kerwin, Diana, Willeke, Diana, Drost, Dick, Papadopoulos, Dimitri, Rowe, Dominic, Simpson, Donna M, Muni, Donna, Galasko, Douglas, Scharre, Douglas W, Fillmer, Ariane, Ge, Tian, Bartha, Rob, Celmins, Dzintra, Zimmerman, Earl A, Teng, Edmond, Tolosa, Eduardo, Coleman, Edward, Zamrini, Edward, Mitsis, Effie, Finger, Elizabeth, Giddaluru, Sudheer, Oates, Elizabeth, Sosa, Elizabeth, Woo, Ellen, Rogalski, Emily, Lethbridge, Emma, Dooley, Eoin, Foster, Eric, Reiman, Eric M, Quinlan, Erin Burke, Goldman, Aaron L, Franklin, Erin, Heinzen, Erin L, Fletcher, Evan, Sprenger, Fabienne, Crivello, Fabrice, Biondo, Francesca, Parfitt, Francine, Hefti, Franz, Beyer, Frauke, Nees, Frauke, Green, Melissa J, Leonard, Gabriel, Robert, Gabriel, Thai, Gaby, Marshall, Gad A, Barker, Gareth, Conrad, Gary, Tremont, Geoffrey, Bartzokis, George, Groenewold, Nynke A, Hsiung, Ging-Yuek Robin, Malferrari, Giulia, Chiang, Gloria, Pearlson, Godfrey D, Liang, Grace, Jicha, Greg, Sorensen, Greg, Todd, Gretchen, Jimenez, Gustavo, Grotegerd, Dominik, Zare, Habil, Grabe, Hans Jörgen, Vanderswag, Helen, Schmidt, Helena, Venkov, Heli, Lemaitre, Hervé, Gurholt, Tiril P, Grossman, Hillel, Shill, Holly, Soares, Holly, Lin, Honghuang, Capote, Horacio, Bergman, Howard, Chertkow, Howard, Feldman, Howard, Fillit, Howard, Rosen, Howard J, Gutman, Boris A, Koleva, Hristina, Fernandez, Hubert, Garavan, Hugh, Shim, Hyungsub, Grachev, Igor D, Richard, Irene, Filippi, Irina, Rachinsky, Irina, Wurster, Isabel, Lind, Penelope A, Hansell, Narelle K, Mintzer, Jacobo, Ziolkowski, Jaimie, Brewer, James, Lah, James J, Leverenz, James, Becker, James T, Tetrud, James, Singleton-Garvin, Jamika, Egebjerg, Jan, Cellar, Janet S, Harris, Mathew A, Pentilla, Jani, Brosch, Jared R, Tinklenberg, Jared, Karlawish, Jason H, Meyer, Javier Villanueva, Himali, Jayandra J, Poline, Jean-Baptiste, Gunter, Jeff, Kaye, Jeffrey A, Harrison, Marc B, Dalley, Jeffrey, Burns, Jeffrey M, Petrella, Jeffrey R, Mule, Jennifer, Salazar, Jennifer, Rotter, Jerome I, Yesavage, Jerome, Cedarbaum, Jesse, Jiang, Jiyang, Haswell, Courtney C, Allard, Joanne, Lord, Joanne L, Hetelle, Joel, Kwok, John B, Brockington, John, Morris, John C, Hsiao, John, Morris, John, Olichney, John, Trojanowki, John Q, Hauser, Michael, Rogers, John, Seibyl, John, Yankey, Jon, Dubow, Jordan S, Jankovic, Joseph, Quinn, Joseph, Kass, Joseph S, Taylor, Joy L, Heidebrink, Judith L, Herms, Stefan, Trollor, Julian, Fröhner, Juliane, Anderson, Karen, Blank, Karen, Crawford, Karen, Smith, Karen Ekstam, Bell, Karen L, Williams, Karen, Kieburtz, Karl, Heslenfeld, Dirk J, Gauss, Katharina, Gloer, Katherine, Johnson, Kathleen, Tingus, Kathleen, DeMarco, Kathryn, Sink, Kaycee M, Hawkins, Keith A, Johnson, Keith A, Kantarci, Kejal, Ho, New Fei, Faber, Kelley, Harless, Kelly, Makino, Kelly M, Marek, Kenneth, Spicer, Kenneth, Shianna, Kevin, Chen, Kewei, Nam, Ki Won, Martin, Kim, Poki-Walker, Kim, Hoehn, David, Seppi, Klaus, Johnson, Kris, Fargher, Kristin, Lipowski, Kristine, Espay, Kristy, Womack, Kyle, Chahine, Lama, Flashman, Laura A, Daedelow, Laura, Hoffmann, Per, Leary, Laura, Beckett, Laurel, Honig, Lawrence S, Thal, Leon, Shaw, Leslie M, Kuller, Lew, Apostolova, Liana, Teodoro, Liberty, Rees, Linda, Pizzagalli, Fabrizio, Holleran, Laurena, Lewis, Lindsay, Hergesheimer, Lindsey, Silbert, Lisa C, Ravdin, Lisa, Taylor-Reinwald, Lisa, Uribe, Liz, Schneider, Lon S, Daiello, Lori A, Richer, Louis, Poustka, Luise, Hoogman, Martine, Pirpamer, Lukas, Mesulam, M Marcel, Ismail, M Saleem, Ranola, Madelaine, Korecka, Magdalena, Raichle, Marc, Seltzer, Marc, van der Brug, Marcel, Hottenga, Jouke-Jan, Mesulam, Marek-Marsel, Carrillo, Maria, Carroll, Maria, Knol, Maria J, Kataki, Maria, Greig-Custo, Maria T, Paillere, Marie-Laure, Albert, Marilyn, Love, Marissa Natelson, Ikeda, Masashi, Mintun, Mark A, Frasier, Mark, Logue, Mark, Minton, Mark, Loeffler, Markus, Scholz, Markus, Baca, Marne, Farlow, Martin R, Sadowski, Martin, Janowitz, Deborah, Creech, Mary L, Hynes, Mary L, Quiceno, Mary, Oakley, MaryAnn, Harris, Mat, Senjem, Matt, Bernstein, Matthew, Panizzon, Matthew S, Stern, Matthew, Becerra, Mauricio, Jansen, Iris E, Witbracht, Megan, Vernooij, Meike W, Brandabur, Melanie, Keltz, Melanie, Lamar, Melissa, Yang, Mia, Ahlijanian, Michael, Borrie, Michael, Neale, Michael C, Donohue, Michael, Jia, Tianye, Lyons, Michael J, Lin, Michael, Rapp, Michael, Smolka, Michael, Weiner, Michael W, Weiner, Michael, Figurski, Michal, Perron, Michel, Assaly, Michele, Luciano, Michelle, Jockwitz, Christiane, Rainka, Michelle, Dang, Mimi, Sheikh, Mohammed O, Ghanbari, Mohsen, Gaikwad, Mrunalini, Chowdhury, Munir, Trncic, Nadira, Amin, Najaf, Johnson, Nancy, Kanai, Ryota, Kowalksi, Nancy, Monahan, Nancy, Gillespie, Nathan A, Pacini, Nathaniel, Buckholtz, Neil, Kowall, Neil, Graff-Radford, Neill R, Fox, Nick, Pavese, Nicola, Karama, Sherif, Cairns, Nigel J, Schuff, Norbert, Foster, Norm, Relkin, Norman, Oyonumo, Ntekim E, Pomara, Nunzio, James, Olga, Ogunlana, Olu, Ching, Christopher R K, Kasperaviciute, Dalia, Carmichael, Owen, Doraiswamy, P Murali, Casalin, Paola, Barone, Paolo, Fatica, Parianne, Conrod, Patricia, Johnson, Patricia Lynn, Samuels, Patricia, Aisen, Paul, Malloy, Paul, Kaufmann, Tobias, Thompson, Paul, Ogrocki, Paula, Bezivin-Frere, Pauline, Maillard, Pauline, Fontoura, Paulo, Taylor, Peggy, Hogarth, Penelope, Gowland, Penny, Davies, Peter, Kelly, Sinead, Hardy, Peter, Snyder, Peter J, Snyder, Peter, Amouyel, Philippe, Muglia, Pierandrea, Tariot, Pierre, Lu, Po H, Varma, Pradeep, Vemuri, Prashanthi, Kikuchi, Masataka, Doody, Rachelle S, Carter, Raina, Shah, Raj C, Griffith, Randall, Yeh, Randy, Duara, Ranjan, Tarawneh, Rawan, James, Raymond, Turner, Raymond Scott, Klein, Marieke, Hernando, Raymundo, Silverstein, Rebecca, Sperling, Reisa A, Wilson, Renee, Carson, Richard E, Frank, Richard, El Khouli, Riham, Koeppe, Robert A, Santulli, Robert B, Knapp, Michael, Hauser, Robert, Umek, Robert, Radtke, Rodney, Killiany, Ronald, Petersen, Ronald, Rodriguez, Rosemarie, Miranda, Ruben, Knodt, Annchen R, Bruehl, Ruediger, Xia, Rui, Swerdlow, Russell H, Ottmann, Ruth, Millenet, Sabina, Borges-Neto, Salvador, Frank, Samuel, Black, Sandra, Weintraub, Sandra, Obradov, Sanja, Krämer, Bernd, Asthana, Sanjay, Vaishnavi, Sanjeev, Dolen, Sara, Mason, Sara S, Hohmann, Sarah, Kremen, Sarah, Miller, Sarah, Walter, Sarah, Herring, Scott, Neu, Scott, Lam, Max, Aydin, Semiha, Ahmad, Shahzad, Harlan, Sherry, Sirrel, Sherye A, Lasch, Shirley, Hu, Shu-Ching, Li, Shuo, Kittur, Smita, Chowdhury, Sohini, Lancaster, Thomas M, Pawluczyk, Sonia, Maingault, Sophie, Schneider, Stacy, Seiler, Stephan, Guthrie, Stephanie, Kielb, Stephanie, Reeder, Stephanie, Correia, Stephen, Pasternak, Stephen, McMahon, Mary Agnes B, Lee, Phil H, Salloway, Stephen, Johnson, Sterling, Williams, Steve, Chao, Steven, Arnold, Steven E, Paul, Steven, Potkin, Steven, Factor, Stewart, Isaacson, Stuart, Lett, Tristram A, Kim, Sungeun, Ainscough, Susan, Schultz, Susan K, Landau, Susan, Mendick, Susan, Rountree, Susan, Ostrowizki, Suzanne, Veillette, Suzanne, van der Lee, Sven J, Desrivieres, Sylvane, Lewis, Lindsay B, Lee, T-Y, Simuni, Tanya, Foroud, Tatiana, Foroud, Tatiana M, Wong, Terence Z, Villena, Teresa, Comery, Thomas, Obisesan, Thomas O, Lopes-Cendes, Iscia, Banaschewski, Tobias, Sherer, Todd, Montine, Tom, Paus, Tomáš, Robbins, Trevor, Bromberg, Uli, Völker, Uwe, Pavlik, Valory, Arnedo, Vanessa, Kiyasova, Vera, Bates, Vernice, Logovinsky, Veronika, Sossi, Vesna, Shibley, Victoria, Frouin, Vincent, Lee, Virginia, Poewe, Werner, Jagust, William, Brooks, William M, Macciardi, Fabio, Pavlosky, William, Potter, William, Kremen, William S, Longstreth, William T, Niessen, Wiro J, Jian, Xueqiu, Stern, Yaakov, Saba, Yasaman, Cabrera, Yuliana, Grimmer, Yvonne, Marquand, Andre F, Khachaturian, Zaven, Mari, Zoltan, Mathias, Samuel R, Melzer, Tracy R, Milaneschi, Yuri, Interdisciplinary Centre Psychopathology and Emotion regulation (ICPE), Guided Treatment in Optimal Selected Cancer Patients (GUTS), Clinical Cognitive Neuropsychiatry Research Program (CCNP), Movement Disorder (MD), Alzheimer’s Disease Neuroimaging Initiative, CHARGE Consortium, EPIGEN Consortium, IMAGEN Consortium, SYS Consortium, Parkinson’s Progression Markers Initiative, Stochastics, Biological Psychology, APH - Health Behaviors & Chronic Diseases, APH - Mental Health, Science and Society, Cognitive Psychology, IBBA, APH - Personalized Medicine, Complex Trait Genetics, APH - Methodology, Clinical Neuropsychology, Sociology and Social Gerontology, Amsterdam Neuroscience - Complex Trait Genetics, RS: MHeNs - R2 - Mental Health, Psychiatrie & Neuropsychologie, Klinische Genetica, RS: GROW - R4 - Reproductive and Perinatal Medicine, MUMC+: DA Klinische Genetica (5), Neurology, Psychiatry, Pediatric surgery, Amsterdam Reproduction & Development (AR&D), Human genetics, APH - Digital Health, Psychology, Precision Medicine Institute of Psychiatry, Child and Adolescent Psychiatry / Psychology, Radiology & Nuclear Medicine, Clinical Genetics, Epidemiology, Medical Informatics, Service NEUROSPIN (NEUROSPIN), Université Paris-Saclay-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA), Neurodegeneratives Diseases Institute (IMN-UMR CNRS 5293), Centre National de la Recherche Scientifique (CNRS), General Paediatrics, ARD - Amsterdam Reproduction and Development, Direction de Recherche Fondamentale (CEA) (DRF (CEA)), and Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay
- Subjects
0301 basic medicine ,Netherlands Twin Register (NTR) ,[SDV]Life Sciences [q-bio] ,LOCI ,Genome-wide association study ,Brain mapping ,0302 clinical medicine ,Cognition ,Cortex (anatomy) ,ComputingMilieux_MISCELLANEOUS ,Cerebral Cortex ,0303 health sciences ,Brain Mapping ,Multidisciplinary ,COMMON VARIANTS ,Parkinson Disease ,Organ Size ,Central sulcus ,Magnetic Resonance Imaging ,medicine.anatomical_structure ,Cerebral cortex ,Neuroinformatics ,EXPRESSION ,endocrine system ,central sulcus ,SURFACE-AREA ,Biology ,Article ,03 medical and health sciences ,SDG 3 - Good Health and Well-being ,Genetic variation ,medicine ,Attention deficit hyperactivity disorder ,Humans ,General ,Gene ,METAANALYSIS ,030304 developmental biology ,Progenitor ,CORTICAL SULCI ,Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7] ,Genetic variants ,Genetic Variation ,Attention Deficit Disorder with Hyperactivity ,Genetic Loci ,Genome-Wide Association Study ,functional annotation ,medicine.disease ,Genetic architecture ,030104 developmental biology ,Evolutionary biology ,OBSERVER-INDEPENDENT CHARACTERIZATION ,Multiple comparisons problem ,ddc:320 ,genome-wide association ,Neuroscience ,030217 neurology & neurosurgery - Abstract
Enhancing NeuroImaging Genetics through Meta-Analysis Consortium (ENIGMA)—Genetics working group., The cerebral cortex underlies our complex cognitive capabilities, yet little is known about the specific genetic loci that influence human cortical structure. To identify genetic variants that affect cortical structure, we conducted a genome-wide association meta-analysis of brain magnetic resonance imaging data from 51,665 individuals. We analyzed the surface area and average thickness of the whole cortex and 34 regions with known functional specializations. We identified 199 significant loci and found significant enrichment for loci influencing total surface area within regulatory elements that are active during prenatal cortical development, supporting the radial unit hypothesis. Loci that affect regional surface area cluster near genes in Wnt signaling pathways, which influence progenitor expansion and areal identity. Variation in cortical structure is genetically correlated with cognitive function, Parkinson's disease, insomnia, depression, neuroticism, and attention deficit hyperactivity disorder.
- Published
- 2020
22. A Metabolomic Aging Clock Using Human Cerebrospinal Fluid.
- Author
-
Hwangbo, Nathan, Zhang, Xinyu, Raftery, Daniel, Gu, Haiwei, Hu, Shu-Ching, Montine, Thomas J, Quinn, Joseph F, Chung, Kathryn A, Hiller, Amie L, Wang, Dongfang, Fei, Qiang, Bettcher, Lisa, Zabetian, Cyrus P, Peskind, Elaine, Li, Gail, Promislow, Daniel E L, and Franks, Alexander
- Subjects
CEREBROSPINAL fluid ,AGE ,METABOLOMICS ,ALZHEIMER'S disease ,PARKINSON'S disease ,BIOCHEMISTRY ,METABOLISM ,AGING ,MASS spectrometry ,RESEARCH funding ,LONGITUDINAL method - Abstract
Quantifying the physiology of aging is essential for improving our understanding of age-related disease and the heterogeneity of healthy aging. Recent studies have shown that, in regression models using "-omic" platforms to predict chronological age, residual variation in predicted age is correlated with health outcomes, and suggest that these "omic clocks" provide measures of biological age. This paper presents predictive models for age using metabolomic profiles of cerebrospinal fluid (CSF) from healthy human subjects and finds that metabolite and lipid data are generally able to predict chronological age within 10 years. We use these models to predict the age of a cohort of subjects with Alzheimer's and Parkinson's disease and find an increase in prediction error, potentially indicating that the relationship between the metabolome and chronological age differs with these diseases. However, evidence is not found to support the hypothesis that our models will consistently overpredict the age of these subjects. In our analysis of control subjects, we find the carnitine shuttle, sucrose, biopterin, vitamin E metabolism, tryptophan, and tyrosine to be the most associated with age. We showcase the potential usefulness of age prediction models in a small data set (n = 85) and discuss techniques for drift correction, missing data imputation, and regularized regression, which can be used to help mitigate the statistical challenges that commonly arise in this setting. To our knowledge, this work presents the first multivariate predictive metabolomic and lipidomic models for age using mass spectrometry analysis of CSF. [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
- View/download PDF
23. Predictive Modeling of Alzheimer's and Parkinson's Disease Using Metabolomic and Lipidomic Profiles from Cerebrospinal Fluid.
- Author
-
Hwangbo, Nathan, Zhang, Xinyu, Raftery, Daniel, Gu, Haiwei, Hu, Shu-Ching, Montine, Thomas J., Quinn, Joseph F., Chung, Kathryn A., Hiller, Amie L., Wang, Dongfang, Fei, Qiang, Bettcher, Lisa, Zabetian, Cyrus P., Peskind, Elaine R., Li, Ge, Promislow, Daniel E. L., Davis, Marie Y., and Franks, Alexander
- Subjects
ALZHEIMER'S disease ,PARKINSON'S disease ,CEREBROSPINAL fluid ,PREDICTION models ,METABOLOMICS ,ALZHEIMER'S patients ,TRYPTOPHAN - Abstract
In recent years, metabolomics has been used as a powerful tool to better understand the physiology of neurodegenerative diseases and identify potential biomarkers for progression. We used targeted and untargeted aqueous, and lipidomic profiles of the metabolome from human cerebrospinal fluid to build multivariate predictive models distinguishing patients with Alzheimer's disease (AD), Parkinson's disease (PD), and healthy age-matched controls. We emphasize several statistical challenges associated with metabolomic studies where the number of measured metabolites far exceeds sample size. We found strong separation in the metabolome between PD and controls, as well as between PD and AD, with weaker separation between AD and controls. Consistent with existing literature, we found alanine, kynurenine, tryptophan, and serine to be associated with PD classification against controls, while alanine, creatine, and long chain ceramides were associated with AD classification against controls. We conducted a univariate pathway analysis of untargeted and targeted metabolite profiles and find that vitamin E and urea cycle metabolism pathways are associated with PD, while the aspartate/asparagine and c21-steroid hormone biosynthesis pathways are associated with AD. We also found that the amount of metabolite missingness varied by phenotype, highlighting the importance of examining missing data in future metabolomic studies. [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
- View/download PDF
24. Familial Idiopathic Basal Ganglia Calcification: A Father-Son Dyad Demonstrate Heterogeneity of Presentation and Disease Progression.
- Author
-
Zahniser, Evan, Bird, Thomas D, Chen, Dong-Hui, Hu, Shu-Ching, Raskind, Wendy H, and Trittschuh, Emily H
- Subjects
BASAL ganglia ,SYMPTOMS ,DISEASE progression ,CALCIFICATION ,NEUROPSYCHOLOGICAL tests ,HYPOPARATHYROIDISM ,BASAL ganglia diseases - Abstract
Objective Familial idiopathic basal ganglia calcification (FIBGC) is a rare, heritable disease characterized by calcium deposition in the basal ganglia and other brain regions. Clinical presentations are diverse, featuring an array of neurologic, psychiatric, and/or cognitive symptoms. This dyad report presents neurogenetic, neuroimaging, neurological, and serial neuropsychological data from a father (S1) and son (S2) with FIBGC. Method/Results The SLC20A2 genetic mutation c.1828-1831delTCCC was identified for each patient, both of whom evidenced similar patterns of brain calcification mainly in the basal ganglia and cerebellum on neuroimaging. S1's onset was in his late 60s with primary motor abnormalities followed by cognitive decline; S2's younger onset (late 30s) was characterized by predominant psychiatric symptoms and mild cognitive changes. Our unique, detailed longitudinal study revealed that both subjects demonstrated largely stable performance across most neuropsychological domains assessed. Conclusions The subjects' differences in presentation demonstrate the variable expressivity in FIBGC even with the same pathogenic variant within a single family. Distinct phenotypes may be associated with age of onset even in persons with the same mutation, consistent with past research. Disease progression may feature an initial period of notable change from baseline followed by relative stability, as seen both on imaging and neuropsychological evaluation. [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
- View/download PDF
25. Effect of deep brain stimulation on postencephalitic parkinsonism: A case report
- Author
-
Hu, Shu-Ching and Hebb, Adam O.
- Published
- 2012
- Full Text
- View/download PDF
26. Feasibility and safety of lumbar puncture in the Parkinson's disease research participants: Parkinson's Progression Marker Initiative (PPMI)
- Author
-
Marek, Kenneth, Siderowf, Andrew, Seibyl, John, Coffey, Christopher, Tanner, Caroline, Tosun-Turgut, Duygu, Simuni, Tanya, Shaw, Leslie, Trojanowski, John, Singleton, Andrew, Kieburtz, Karl, Toga, Arthur, Mollenhauer, Brit, Galasko, Douglas, Poewe, Werner, Foroud, Tatiana, Poston, Kathleen, Sherer, Todd, Chowdhury, Sohini, Frasier, Mark, Kopil, Catherine, Arnedo, Vanessa, Daegele, Nichole, Casaceli, Cynthia, Dorsey, Ray, Wilson, Renee, Mahes, Sugi, Salerno, Christina, Caspell-Garcia, Chelsea, Crawford, Karen, Casalin, Paola, Malferrari, Giulia, Weisz, Mali Gani, Orr-Urtreger, Avi, Montine, Thomas, Russell, David, Dahodwala, Nabila, Giladi, Nir, Factor, Stewart, Hogarth, Penelope, Standaert, David, Hauser, Robert, Jankovic, Joseph, Saint-Hilaire, Marie, Richard, Irene, Shprecher, David, Fernandez, Hubert, Brockmann, Katrina, Rosenthal, Liana, Barone, Paolo, Espay, Alberto, Rowe, Dominic, Marder, Karen, Santiago, Anthony, Bressman, Susan, Hu, Shu-Ching, Isaacson, Stuart, Corvol, Jean-Christophe, Martinez, Javiar Ruiz, Tolosa, Eduardo, Tai, Yen, Politis, Marios, Smejdir, Debra, Rees, Linda, Williams, Karen, Kausar, Farah, Richardson, Whitney, Willeke, Diana, Peacock, Shawnees, Heim, Beatrice, Mirelman, Anat, Sommerfeld, Barbara, Freed, Alison, Wakeman, Katrina, Blair, Courtney, Guthrie, Stephanie, Harrell, Leigh, Hunter, Christine, Thomas, Cathi-Ann, James, Raymond, Zimmerman, Grace, Brown, Victoria, Mule, Jennifer, Hilt, Ella, Ribb, Kori, Ainscough, Susan, Wethington, Misty, Ranola, Madelaine, Santana, Helen Mejia, Moreno, Juliana, Raymond, Deborah, Speketer, Krista, Carvajal, Lisbeth, Carvalho, Stephanie, Croitoru, Ioana, Garrido, Alicia, Payne, Laura Marie, Viswanth, Veena, Severt, Lawrence, Facheris, Maurizio, Soares, Holly, Mintun, Mark A., Cedarbaum, Jesse, Taylor, Peggy, Biglan, Kevin, Vandenbroucke, Emily, Sheikh, Zulfiqar Haider, Bingol, Baris, Fischer, Tanya, Sardi, Pablo, Forrat, Remi, Reith, Alastair, Egebjerg, Jan, Hillert, Gabrielle Ahlberg, Saba, Barbara, Min, Chris, Umek, Robert, Mather, Joe, De Santi, Susan, Post, Anke, Boess, Frank, Taylor, Kirsten, Grachev, Igor, Avbersek, Andreja, Muglia, Pierandrea, Merchant, Kaplana, Tauscher, Johannes, Prakash, Neha, Tanner, Caroline M., Merchant, Kalpana, Chahine, Lana M., Weintraub, Daniel, Casaceli, Cindy, Herzog, Margaret, Marek, Ken, Frank, Samuel, and Jennings, Danna
- Published
- 2019
- Full Text
- View/download PDF
27. Transcriptomic Profiling of Extracellular RNAs Present in Cerebrospinal Fluid Identifies Differentially Expressed Transcripts in Parkinson’s Disease
- Author
-
Hossein-nezhad, Arash, Fatemi, Roya Pedram, Ahmad, Rili, Peskind, Elaine R., Zabetian, Cyrus P., Hu, Shu-Ching, Shi, Min, Wahlestedt, Claes, Zhang, Jing, and Faghihi, Mohammad Ali
- Subjects
Research Report ,Male ,Gene Expression Profiling ,biomarkers ,High-Throughput Nucleotide Sequencing ,RNA sequencing ,Parkinson Disease ,Middle Aged ,Real-Time Polymerase Chain Reaction ,cerebrospinal fluid ,Humans ,RNA ,Female ,long noncoding RNA ,Transcriptome ,Aged - Abstract
Background: Parkinson’s disease (PD) is a debilitating neurological disorder for which prognostic and diagnostic biomarkers are lacking. Cerebrospinal fluid (CSF) is an accessible body fluid that comes into direct contact with the central nervous system (CNS) and acts as a nuclease-free repository where RNA transcripts shed by brain tissues can reside for extended periods of time. Objective: We studied the RNA species present in the CSF of PD patients to identify novel diagnostic biomarkers. Methods: Small volumes of CSF from 27 PD patients and 30 healthy age- and sex-matched controls were used for RNA extraction followed by next-generation sequencing (RNA-seq) using the Illumina platform. CSF contains a number of fragmented RNA species that were individually sequenced and analyzed. Comparing PD to control subjects, we observed a pool of dysregulated sequencing tags that were further analyzed and validated by quantitative real-time PCR (qRT-PCR). Results: A total of 201 differentially expressed sequencing tags (DETs), including 92 up-regulated and 109 down-regulated DETs were identified. We validated the following DETs by real time PCR in the patient samples: Dnmt1, Ezh2, CCR3, SSTR5,PTPRC, UBC, NDUFV2, BMP7, SCN9, SCN9 antisense (AC010127.3), and long noncoding RNAs AC079630 and UC001lva.4 (close to the LRRK2 gene locus), as potential PD biomarkers. Conclusions: The CSF is a unique environment that contains many species of RNA. Our work demonstrates that CSF can potentially be used to identify biomarkers for the detection and tracking of disease progression and evaluation of therapeutic outcomes.
- Published
- 2016
28. Semantic fluency and processing speed are reduced in non-cognitively impaired participants with Parkinson's disease.
- Author
-
Cholerton, Brenna A., Poston, Kathleen L., Yang, Laurice, Rosenthal, Liana S., Dawson, Ted M., Pantelyat, Alexander, Edwards, Karen L., Tian, Lu, Quinn, Joseph F., Chung, Kathryn A., Hiller, Amie L., Hu, Shu-Ching, Montine, Thomas J., and Zabetian, Cyrus P.
- Subjects
PARKINSON'S disease ,MILD cognitive impairment ,COGNITION disorders ,SYMPTOMS ,COGNITIVE testing ,APATHY ,COGNITION ,BLAND-Altman plot - Abstract
Introduction: Parkinson's disease (PD) is associated with a range of cognitive deficits. Few studies have carefully examined the subtle impacts of PD on cognition among patients who do not meet formal criteria for MCI or dementia. The aim of the current study was thus to describe the impact of PD on cognition in those without cognitive impairment in a well-characterized cohort. Methods: Non-cognitively impaired participants (122 with PD, 122 age- and sex-matched healthy volunteers) underwent extensive cognitive testing. Linear regression analyses compared diagnostic group performance across cognitive measures. For cognitive tasks that were significantly different between groups, additional analyses examined group differences restricting the group inclusion to PD participants with mild motor symptoms or disease duration less than 10 years. Results: Processing speed and semantic verbal fluency were significantly lower in the PD group (B = −3.77, 95% CIs [−5.76 to −1.77], p <.001, and B = −2.02, 95% CIs [−3.12, −0.92], p <.001, respectively), even after excluding those with moderate to severe motor symptoms (B = −2.73, 95% CIs [−4.94 to −0.53], p =.015 and B = −2.11, 95% CIs [−3.32 to −0.91], p <.001, respectively) or longer disease duration (B = −3.89, 95% CIs [−6.14 to −1.63], p <.001 and B = −1.58, 95% CIs [−2.78 to −0.37], p =.010, respectively). Semantic verbal fluency remained significantly negatively associated with PD diagnosis after controlling for processing speed (B = −1.66, 95% CIs [−2.79 to −0.53], p =.004). Conclusions: Subtle decline in specific cognitive domains may be present among people diagnosed with PD but without evidence to support a formal cognitive diagnosis. These results suggest the importance of early awareness of the potential for diminishing aspects of cognition in PD even among those without mild cognitive impairment or dementia. [ABSTRACT FROM AUTHOR]
- Published
- 2021
- Full Text
- View/download PDF
29. I-123 DaTscan SPECT Brain Imaging in Parkinsonian Syndromes: Utility of the Putamen-to-Caudate Ratio.
- Author
-
Matesan, Manuela, Gaddikeri, Santhosh, Longfellow, Katelan, Miyaoka, Robert, Elojeimy, Saeed, Elman, Shana, Hu, Shu‐Ching, Minoshima, Satoshi, Lewis, David, and Hu, Shu-Ching
- Subjects
SINGLE-photon emission computed tomography ,BRAIN imaging ,PARKINSONIAN disorders ,IMAGE analysis ,DOPAMINE - Abstract
Background and Purpose: Computer-based analysis of Dopamine transporter imaging (DaTscan) can aid in image interpretation. In this study, we examined the distribution of putamen-to-caudate ratios (PCRs) obtained by using a clinically available semiquantification method.Methods: Medical records of 32 patients (M:16) with a diagnosis of Parkinson's disease (PD) (n = 22) or Parkinson's plus syndromes (PPS) (n = 10) based on clinical follow-up, were retrospectively reviewed. Single photon emission tomography (SPECT) imaging was performed 4 hours after intravenous injection of 3-5 mCi [I-123]-ioflupane. Semiquantitative evaluation using DaTQUANT software was performed. Utility of PCR with a cutoff of .7 and .8 in the diagnosis of nigrostriatal degeneration was assessed. PD and PPS groups based on clinical assessment and caudate-to-background ratio (CBR) were assessed separately.Results: Minimum PCR for both hemispheres was .74 ± .09 (Mean ± SD, range: .58-.89), with 65.63% patients (21/32) having PCR > .7. Mean PCR in mild nigrostriatal degeneration was .77 ± .08 (range: .62-.89) and in advanced nigrostriatal degeneration was .73 ± .09 (range: .58-.89). Mean PCR in PD group was .73 ± .09 (range: .58-.89) and in PPS group was .75 ± .10 (range: .61-.88).Conclusions: Although PCR can intrinsically be a useful indication of disease, this ratio obtained in our analysis by using one of the clinically available automatic semiquantitative methods has large variability and might not be a reliable numeric marker in interpretation of [I-123]ioflupane studies. This may be due to difficulty in separating caudate from putamen on SPECT images, as well as the nonuniform decreased Ioflupane uptake in both putamen and caudate. [ABSTRACT FROM AUTHOR]- Published
- 2018
- Full Text
- View/download PDF
30. Direct Surgery of Carotid Cavernous Fistulae and Dural Arteriovenous Malformations of the Cavernous Sinus
- Author
-
Tu, Yong-Kwang, Liu, Hon-Man, and Hu, Shu-Ching
- Published
- 1997
31. Relationships Between Sensorimotor Inhibition and Mobility in Older Adults With and Without Parkinson's Disease.
- Author
-
Martini, Douglas N, Morris, Rosie, Madhyastha, Tara M, Grabowski, Thomas J, Oakley, John, Hu, Shu-Ching, Zabetian, Cyrus P, Edwards, Karen L, Hiller, Amie, Chung, Kathryn, Ramsey, Katrina, Lapidus, Jodi A, Cholerton, Brenna, Montine, Thomas J, Quinn, Joseph F, and Horak, Fay B
- Subjects
PARKINSON'S disease ,OLDER people ,EXECUTIVE function ,WALKING speed ,COGNITION disorders ,IMPULSE control disorders ,RESPONSE inhibition - Abstract
Background: Reduced cortical sensorimotor inhibition is associated with mobility and cognitive impairments in people with Parkinson's disease (PD) and older adults (OAs). However, there is a lack of clarity regarding the relationships among sensorimotor, cognitive, and mobility impairments. The purpose of this study was to determine how cortical sensorimotor inhibition relates to impairments in mobility and cognition in people with PD and OAs.Method: Cortical sensorimotor inhibition was characterized with short-latency afferent inhibition (SAI) in 81 people with PD and 69 OAs. Six inertial sensors recorded single- and dual-task gait and postural sway characteristics during a 2-minute walk and a 1-minute quiet stance. Cognition was assessed across the memory, visuospatial, executive function, attention, and language domains.Results: SAI was significantly impaired in the PD compared to the OA group. The PD group preformed significantly worse across all gait and postural sway tasks. In PD, SAI significantly correlated with single-task foot strike angle and stride length variability, sway area, and jerkiness of sway in the coronal and sagittal planes. In OAs, SAI significantly related to single-task gait speed and stride length, dual-task stride length, and immediate recall (memory domain). No relationship among mobility, cognition, and SAI was observed.Conclusions: Impaired SAI related to slower gait in OA and to increased gait variability and postural sway in people with PD, all of which have been shown to be related to increased fall risk. [ABSTRACT FROM AUTHOR]- Published
- 2021
- Full Text
- View/download PDF
32. Hallucinations and Development of Dementia in Parkinson's Disease.
- Author
-
Gryc, Wojciech, Roberts, Kathryn A., Zabetian, Cyrus P., Weintraub, Daniel, Trojanowski, John Q., Quinn, Joseph F., Hiller, Amie L., Chung, Kathryn A., Poston, Kathleen L., Yang, Laurice, Hu, Shu-Ching, Edwards, Karen L., Montine, Thomas J., and Cholerton, Brenna A.
- Subjects
PARKINSON'S disease ,HALLUCINATIONS ,DEMENTIA ,SYMPTOMS - Abstract
Neuropsychiatric symptoms are common in Parkinson's disease (PD). We investigated the relationship between neuropsychiatric symptoms and current and future diagnosis of PD dementia (PDD). Individuals with PD who had a study partner were enrolled (n = 696). Study partners were administered the Neuropsychiatric Inventory or Neuropsychiatric Inventory Questionnaire at baseline. Participants were assigned a cognitive diagnosis at baseline and follow up visits. Hallucinations were significantly associated with a diagnosis of PDD cross-sectionally (p < 0.001) and with shortened time to dementia longitudinally among initially nondemented participants (n = 444; p = 0.005). Screening for hallucinations may be useful for assessing risk of dementia in participants with PD. [ABSTRACT FROM AUTHOR]
- Published
- 2020
- Full Text
- View/download PDF
33. Sensorimotor Inhibition and Mobility in Genetic Subgroups of Parkinson's Disease.
- Author
-
Martini, Douglas N., Morris, Rosie, Kelly, Valerie E., Hiller, Amie, Chung, Kathryn A., Hu, Shu-Ching, Zabetian, Cyrus P., Oakley, John, Poston, Kathleen, Mata, Ignacio F., Edwards, Karen L., Lapidus, Jodi A., Grabowski, Thomas J., Montine, Thomas J., Quinn, Joseph F., and Horak, Fay
- Subjects
PARKINSON'S disease ,UROLOGY ,OLDER people ,ALPHA rhythm - Abstract
Background: Mobility and sensorimotor inhibition impairments are heterogeneous in Parkinson's disease (PD). Genetics may contribute to this heterogeneity since the apolipoprotein (APOE) ε4 allele and glucocerebrosidase (GBA) gene variants have been related to mobility impairments in otherwise healthy older adult (OA) and PD cohorts. The purpose of this study is to determine if APOE or GBA genetic status affects sensorimotor inhibition and whether the relationship between sensorimotor inhibition and mobility differs in genetic sub-groups of PD. Methods: Ninety-three participants with idiopathic PD (53 non-carriers; 23 ε4 carriers; 17 GBA variants) and 72 OA (45 non-carriers; 27 ε4 carriers) had sensorimotor inhibition characterized by short-latency afferent inhibition. Mobility was assessed in four gait domains (pace/turning, rhythm, trunk, variability) and two postural sway domains (area/jerkiness and velocity) using inertial sensors. Results: Sensorimotor inhibition was worse in the PD than OA group, with no effect of genetic status. Gait pace/turning was slower and variability was higher (p < 0.01) in PD compared to OA. Postural sway area/jerkiness (p < 0.01) and velocity (p < 0.01) were also worse in the PD than OA group. Genetic status was not significantly related to any gait or postural sway domain. Sensorimotor inhibition was significantly correlated with gait variability (r = 0.27; p = 0.02) and trunk movement (r = 0.23; p = 0.045) in the PD group. In PD non-carriers, sensorimotor inhibition related to variability (r = 0.35; p = 0.010) and trunk movement (r = 0.31; p = 0.025). In the PD ε4 group, sensorimotor inhibition only related to rhythm (r = 0.47; p = 0.024), while sensorimotor inhibition related to pace/turning (r = −0.49; p = 0.046) and rhythm (r = 0.59; p = 0.013) in the PD GBA group. Sensorimotor inhibition was significantly correlated with gait pace/turning (r = −0.27; p = 0.04) in the OA group. There was no relationship between sensorimotor inhibition and postural sway. Conclusion: ε4 and GBA genetic status did not affect sensorimotor inhibition or mobility impairments in this PD cohort. However, worse sensorimotor inhibition was associated with gait variability in PD non-carriers, but with gait rhythm in PD ε4 carriers and with gait rhythm and pace in PD with GBA variants. Impaired sensorimotor inhibition had a larger effect on mobility in people with PD than OA and affected different domains of mobility depending on genetic status. [ABSTRACT FROM AUTHOR]
- Published
- 2020
- Full Text
- View/download PDF
34. Participant and Study Partner Reported Impact of Cognition on Functional Activities in Parkinson's Disease.
- Author
-
Cholerton, Brenna, Poston, Kathleen L., Tian, Lu, Quinn, Joseph F., Chung, Kathryn A., Hiller, Amie L., Hu, Shu‐Ching, Specketer, Krista, Montine, Thomas J., Edwards, Karen L., and Zabetian, Cyrus P.
- Subjects
PARKINSON'S disease ,MILD cognitive impairment ,ACTIVITIES of daily living ,IMPULSE control disorders ,LOGISTIC regression analysis ,COGNITIVE testing ,SEXUAL partners - Abstract
Introduction: Cognitive dysfunction is common in Parkinson's disease (PD) and associated with reduced functional abilities and increased dependence. To date, however, little is known about the relationship between performance of instrumental activities of daily living (IADLs) and cognitive stages in PD, and there are conflicting reports as to whether declines in specific cognitive domains predict IADL impairment. Methods: Participants with PD were drawn from the Pacific Udall Center and included in the study if both participant and study partner IADL ratings and cognitive tests were completed (n = 192). Logistic regression analyses were performed to determine whether participant and/or study partner rating predicted mild cognitive impairment or dementia. Correlations are reported for the relationship between participant/study partner IADL reports as well as for specific cognitive tests. Results: Although both participant and study partner ratings of IADL performance were associated with a diagnosis of PD with dementia, only participant self‐rating of functional ability was significantly associated with a diagnosis of PD with mild cognitive impairment. Functional ability correlated most strongly with measures of processing speed, auditory working memory, and immediate verbal recall for both the participant and study partner ratings. Conclusion: For participants with PD in the early stages of cognitive decline, self‐rating may be more sensitive to the impact of cognitive changes on IADL function than ratings made by a knowledgeable study partner. Changes in executive function, processing speed, and learning may indicate a higher likelihood of IADL impairment. Careful assessment of cognition and IADL performance is recommended to permit individualized interventions prior to significant disability. [ABSTRACT FROM AUTHOR]
- Published
- 2020
- Full Text
- View/download PDF
35. Diagnosis of Parkinson's disease on the basis of clinical and genetic classification: A population-based modelling study
- Author
-
Nalls, Mike A, McLean, Cory Y, Hardy, John, Seppi, Klaus, Reiter, Eva, Shill, Holly, Fernandez, Hubert, Ahmed, Anwar, Berg, Daniela, Wurster, Isabel, Mari, Zoltan, Brooks, David, Pavese, Nicola, Gasser, Thomas, Barone, Paolo, Isaacson, Stuart, Espay, Alberto, Rowe, Dominic, Brandabur, Melanie, Tetrud, James, Liang, Grace, Marder, Karen, Corvol, Jean-Christophe, Martí Masso, Jose Felix, Brice, Alexis, Tolosa, Eduardo, Aasly, Jan O, Giladi, Nir, Stefanis, Leonidas, Leary, Laura, Riordan, Cheryl, Rees, Linda, Sommerfeld, Barbara, Wood-Siverio, Cathy, Portillo, Alicia, Price, T Ryan, Lenahan, Art, Williams, Karen, Guthrie, Stephanie, Rawlins, Ashlee, Harlan, Sherry, Hunter, Christine, Tran, Baochan, Darin, Abigail, Linder, Carly, Todd, Gretchen, Nicolas, Aude, Thomas, Cathi-Ann, James, Raymond, Deeley, Cheryl, Bishop, Courtney, Sprenger, Fabienne, Willeke, Diana, Obradov, Sanja, Mule, Jennifer, Monahan, Nancy, Gauss, Katharina, Keller, Margaux F, Comyns, Kathleen, Fontaine, Deborah, Gigliotti, Christina, McCoy, Arita, Dunlop, Becky, Shah, Bina, Ainscough, Susan, James, Angela, Silverstein, Rebecca, Espay, Kristy, Molony, Cliona, Ranola, Madelaine, Santana, Helen M, Ngono, Nelly, Rezola, Elisabet, Rolan, Delores Vilas, Waro, Bjorg, Mirlman, Anat, Stamelou, Maria, Comery, Thomas, Papapetropoulos, Spyros, Gibbs, J Raphael, Ravina, Bernard, Grachev, Igor D, Dubow, Jordan S, Ahlijanian, Michael, Soares, Holly, Ostrowizki, Suzanne, Fontoura, Paulo, Chalker, Alison, Hewitt, David L, van der Brug, Marcel, Chen-Plotkin, Alice, Reith, Alastair D, Taylor, Peggy, Egebjerg, Jan, Minton, Mark, Siderowf, Andrew, Muglia, Pierandrea, Umek, Robert, Catafau, Ana, Suh, Eunran, Rick, Jacqueline, Letson, Christopher, Fiandaca, Massimo S, Mapstone, Mark, Federoff, Howard J, Noyce, Alastair J, Morris, Huw, Van Deerlin, Vivianna M, Weintraub, Daniel, Zabetian, Cyrus, Hernandez, Dena G, Eberly, Shirley, Lesage, Suzanne, Mullins, Meghan, Conley, Emily Drabant, Northover, Carrie A M, Frasier, Mark, Marek, Ken, Day-Williams, Aaron G, Stone, David J, Ioannidis, John P A, Singleton, Andrew B, Hutten, Samantha J, investigators, Parkinson's Disease Biomarkers Program and Parkinson's Progression Marker Initiative, Bowman, Dubois, Dawson, Ted, Dewey, Richard, German, Dwight Charles, Huang, Xuemei, Petyuk, Vladislav, Scherzer, Clemens, Vaillancourt, David, Gwinn, Katrina, West, Andrew, Zhang, Jing, Marek, Kenneth, Jennings, Danna, Lasch, Shirley, Tanner, Caroline, Simuni, Tanya, Coffey, Christopher, Kieburtz, Karl, Wilson, Renee, Sutherland, Margaret, Poewe, Werner, Mollenhauer, Brit, Galasko, Douglas, Foroud, Tatiana, Sherer, Todd, Chowdhury, Sohini, Kopil, Catherine, Arnedo, Vanessa, Casaceli, Cynthia, Martinez, Maria, Seibyl, John, Mendick, Susan, Schuff, Norbert, Caspell, Chelsea, Uribe, Liz, Foster, Eric, Gloer, Katherine, Yankey, Jon, Toga, Arthur, Crawford, Karen, Heutink, Peter, Smith, Danielle Elise, Casalin, Paola, Malferrari, Giulia, Trojanowski, John, Shaw, Les, Singleton, Andrew, Halter, Cheryl, Russell, David, Factor, Stewart, Hogarth, Penelope, Williams, Nigel M, Standaert, David, Hauser, Robert, Jankovic, Joseph, Stern, Matthew, Chahine, Lama, Hu, Shu-Ching, Frank, Samuel, Trenkwalder, Claudia, Oertel, Wolfgang, and Richard, Irene
- Subjects
Male ,Aging ,Parkinson's disease ,Genome-wide association study ,Disease ,Neurodegenerative ,Cohort Studies ,genetics [Parkinson Disease] ,Models ,2.1 Biological and endogenous factors ,Family history ,Aetiology ,education.field_of_study ,screening and diagnosis ,Parkinson's Disease ,Aged ,Disease Progression ,Female ,Humans ,Middle Aged ,Parkinson Disease ,Prodromal Symptoms ,Models, Statistical ,Neurology (clinical) ,Statistical ,Detection ,Cohort ,Neurological ,Biomarker (medicine) ,diagnosis [Parkinson Disease] ,Cohort study ,4.2 Evaluation of markers and technologies ,medicine.medical_specialty ,Population ,Clinical Sciences ,Parkinson's Disease Biomarkers Program and Parkinson's Progression Marker Initiative investigators ,Article ,Clinical Research ,Internal medicine ,medicine ,ddc:610 ,education ,Neurology & Neurosurgery ,business.industry ,Prevention ,Neurosciences ,medicine.disease ,Brain Disorders ,4.1 Discovery and preclinical testing of markers and technologies ,Good Health and Well Being ,Physical therapy ,business - Abstract
Summary Background Accurate diagnosis and early detection of complex diseases, such as Parkinson's disease, has the potential to be of great benefit for researchers and clinical practice. We aimed to create a non-invasive, accurate classification model for the diagnosis of Parkinson's disease, which could serve as a basis for future disease prediction studies in longitudinal cohorts. Methods We developed a model for disease classification using data from the Parkinson's Progression Marker Initiative (PPMI) study for 367 patients with Parkinson's disease and phenotypically typical imaging data and 165 controls without neurological disease. Olfactory function, genetic risk, family history of Parkinson's disease, age, and gender were algorithmically selected by stepwise logistic regression as significant contributors to our classifying model. We then tested the model with data from 825 patients with Parkinson's disease and 261 controls from five independent cohorts with varying recruitment strategies and designs: the Parkinson's Disease Biomarkers Program (PDBP), the Parkinson's Associated Risk Study (PARS), 23andMe, the Longitudinal and Biomarker Study in PD (LABS-PD), and the Morris K Udall Parkinson's Disease Research Center of Excellence cohort (Penn-Udall). Additionally, we used our model to investigate patients who had imaging scans without evidence of dopaminergic deficit (SWEDD). Findings In the population from PPMI, our initial model correctly distinguished patients with Parkinson's disease from controls at an area under the curve (AUC) of 0·923 (95% CI 0·900–0·946) with high sensitivity (0·834, 95% CI 0·711–0·883) and specificity (0·903, 95% CI 0·824–0·946) at its optimum AUC threshold (0·655). All Hosmer-Lemeshow simulations suggested that when parsed into random subgroups, the subgroup data matched that of the overall cohort. External validation showed good classification of Parkinson's disease, with AUCs of 0·894 (95% CI 0·867–0·921) in the PDBP cohort, 0·998 (0·992–1·000) in PARS, 0·955 (no 95% CI available) in 23andMe, 0·929 (0·896–0·962) in LABS-PD, and 0·939 (0·891–0·986) in the Penn-Udall cohort. Four of 17 SWEDD participants who our model classified as having Parkinson's disease converted to Parkinson's disease within 1 year, whereas only one of 38 SWEDD participants who were not classified as having Parkinson's disease underwent conversion (test of proportions, p=0·003). Interpretation Our model provides a potential new approach to distinguish participants with Parkinson's disease from controls. If the model can also identify individuals with prodromal or preclinical Parkinson's disease in prospective cohorts, it could facilitate identification of biomarkers and interventions. Funding National Institute on Aging, National Institute of Neurological Disorders and Stroke, and the Michael J Fox Foundation.
- Published
- 2015
36. Visuospatial functioning is associated with sleep disturbance and hallucinations in nondemented patients with Parkinson's disease.
- Author
-
Specketer, Krista, Zabetian, Cyrus P., Edwards, Karen L., Tian, Lu, Quinn, Joseph F., Peterson-Hiller, Amie L., Chung, Kathryn A., Hu, Shu-Ching, Montine, Thomas J., and Cholerton, Brenna A.
- Subjects
SLEEP interruptions ,PARKINSON'S disease ,VISUAL learning ,HALLUCINATIONS ,DISEASE progression ,VERBAL memory - Abstract
Introduction: Cognitive impairment is a common symptom of Parkinson's disease (PD) associated with reduced quality of life and a more severe disease state. Previous research has shown an association between visuospatial dysfunction and worse disease course; however, it is not clear whether this is separable from executive dysfunction and/or dementia. This study sought to determine whether distinct cognitive factors could be measured in a large PD cohort, and if those factors were differentially associated with other PD-related features, specifically to provide insight into visuospatial dysfunction. Methods: Non-demented participants with PD from the Pacific Udall Center were enrolled (n = 197). Co-participants (n = 104) completed questionnaires when available. Principal components factor analysis (PCFA) was utilized to group the neuropsychological test scores into independent factors by considering those with big factor loading (≥.40). Linear and logistic regression analyses were performed to examine the relationship between the cognitive factors identified in the PCFA and other clinical features of PD. Results: Six factors were extracted from the PCFA: 1) executive/processing speed, 2) visual learning & memory/visuospatial, 3) auditory working memory, 4) contextual verbal memory, 5) semantic learning & memory, and 6) visuospatial. Motor severity (p = 0.001), mood (p < 0.001), and performance on activities of daily living scores (informant: p < 0.001, patient: p = 0.009) were primarily associated with frontal and executive factors. General sleep disturbance (p < 0.006) and hallucinations (p = 0.002) were primarily associated with visuospatial functioning and visual learning/memory. Conclusions: Motor symptoms, mood, and performance on activities of daily living were primarily associated with frontal/executive factors. Sleep disturbance and hallucinations were associated with visuospatial functioning and visual learning/memory only, over and above executive functioning and regardless of cognitive disease severity. These findings support that visuospatial function in PD may indicate a more severe disease course, and that symptom management should be guided accordingly. [ABSTRACT FROM AUTHOR]
- Published
- 2019
- Full Text
- View/download PDF
37. Diagnostic Validation for Participants in the Washington State Parkinson Disease Registry.
- Author
-
Kim, Hojoong M., Leverenz, James B., Burdick, Daniel J., Srivatsal, Sindhu, Pate, Jennifer, Hu, Shu-Ching, Millard, Steven P., Davis, Marie Y., Samii, Ali, and Zabetian, Cyrus P.
- Subjects
PARKINSON'S disease diagnosis ,CONFIDENCE intervals ,REPORTING of diseases ,INTERVIEWING ,MEDICAL research ,NEUROLOGIC examination ,STATISTICAL sampling ,SELF-evaluation ,DESCRIPTIVE statistics - Abstract
Background. The Washington State Parkinson Disease Registry (WPDR) was created to facilitate recruitment for Parkinson’s disease (PD) research studies conducted in the Pacific Northwest. The success of registries that rely on self-report is dependent on the accuracy of the information provided by participants, particularly diagnosis. Objective and Methods. Our goal was to assess diagnostic accuracy within the WPDR cohort. We randomly selected and attempted to contact 168 of the 1,278 actively enrolled WPDR participants. Those who responded were invited to undergo an interview and neurological examination performed by a PD specialist. If an in-person assessment was not possible, we sought information collected during participation in prior research studies or from review of medical records. A diagnosis was considered “validated” if the individual met UK Parkinson’s Disease Society Brain Bank (UKBB) clinical diagnostic criteria for PD. Results. Data were ascertained for 106 participants; 77 underwent an in-person assessment, 21 had data available from a prior research study, and 8 provided access to medical records. Diagnostic accuracy within the overall sample was 93.4% (95% confidence interval (86.4%, 97.1%)). Seven patients did not fulfill UKBB criteria for the following reasons: early severe autonomic involvement (n=3), history of neuroleptic treatment (n=1), presence of the Babinski sign (n=1), or insufficient supportive criteria (n=2). Conclusions. Our results indicate that studies which use the WPDR for recruitment will rarely encounter patients who are misdiagnosed. This further supports the utility of the WPDR as an effective recruitment tool for PD research in the Pacific Northwest. [ABSTRACT FROM AUTHOR]
- Published
- 2018
- Full Text
- View/download PDF
38. Occupational exposures and parkinsonism among Shanghai women textile workers.
- Author
-
Checkoway, Harvey, Ilango, Sindana, Li, Wenjin, Ray, Roberta M., Tanner, Caroline M., Hu, Shu‐Ching, Wang, Xin, Nielsen, Susan, Gao, Dao L., and Thomas, David B.
- Subjects
WOMEN textile workers ,PARKINSONIAN disorders ,ENDOTOXINS ,THRESHOLD limit values (Industrial toxicology) ,TEXTILE workers - Abstract
Background: Endotoxin, a contaminant of cotton dust, is an experimental model for parkinsonism (PS). Methods: We investigated associations between exposures to endotoxin, solvents, magnetic fields, and night shift work, and neurologist‐determined PS among Shanghai women textile workers, including 537 retired cotton factory workers ages ≥50 years and an age‐matched reference group of 286 retired textile workers not exposed to cotton dust. Repeat exams were conducted 2.5 years after enrollment among 467 cotton workers and 229 reference workers. Results: We identified 39 prevalent PS cases and 784 non‐cases. No consistent or statistically significant associations were observed for endotoxin, solvents, magnetic fields, or shift work with PS risk, severity, or progression. Conclusions: Despite the null findings, additional studies of endotoxin exposure and risk of PS in other well‐characterized occupational cohorts are warranted in view of toxicological evidence that endotoxin is a pathogenic agent and its widespread occurrence in multiple industries worldwide. [ABSTRACT FROM AUTHOR]
- Published
- 2018
- Full Text
- View/download PDF
39. Parkinsonism Signs and Symptoms in Agricultural Pesticide Handlers in Washington State.
- Author
-
Searles Nielsen, Susan, Hu, Shu-Ching, Checkoway, Harvey, Negrete, Maria, Palmández, Pablo, Bordianu, Theresa, Racette, Brad A., and Simpson, Christopher D.
- Subjects
- *
AGRICULTURAL laborers , *AGRICULTURE , *STATISTICAL correlation , *HISPANIC Americans , *INSECTICIDES , *PESTICIDES , *QUESTIONNAIRES , *RESEARCH , *SELF-evaluation , *OCCUPATIONAL hazards , *ENVIRONMENTAL exposure , *PARKINSONIAN disorders , *SYMPTOMS - Abstract
Objectives: Examine associations between pesticide exposure and signs or symptoms of parkinsonism. Methods: Prior to the 2014 pesticide spray season, the authors examined 38 active pesticide handlers aged 35 to 65 (median: 43.5) who participated in the State of Washington’s cholinesterase monitoring program in the Yakima Valley, where cholinesterase-inhibiting insecticides are applied in fruit orchards. A movement disorder specialist assessed the workers using the Unified Parkinson’s Disease Rating Scale (UPDRS) motor subscore 3 (UPDRS3). Participants also self-reported work and medical histories, including the UPDRS activities of daily living subscore 2 (UPDRS2). The authors explored the relation between these scores and lifetime occupational pesticide exposure while accounting for age. Results: All participants were Hispanic men born in Mexico who had worked in agriculture for 4 to 43 years (median: 21 years, including 11 years applying pesticides, mostly in the United States). Ten participants (26%) reported difficulty with one or more UPDRS2 activities of daily living (maximum = 2), and nine (24%) had a UPDRS3 >0 (maximum = 10). The most common symptom and sign, respectively, were excess saliva (n= 6) and action tremor (n= 5). UPDRS2 and UPDRS3 scores were unrelated to the number of years applying pesticides, but UPDRS3, especially action tremor, was positively associated with living on or by a farm. Conclusions: Symptoms and signs of parkinsonism were absent to mild in this small sample of active workers who apply cholinesterase-inhibiting insecticides in Washington State, USA. Future studies should be larger and examine older, retired workers with greater cumulative exposure to agricultural pesticides at work and home, including other types of agricultural pesticides. [ABSTRACT FROM AUTHOR]
- Published
- 2017
- Full Text
- View/download PDF
40. An alpha-synuclein MRM assay with diagnostic potential for Parkinson's disease and monitoring disease progression.
- Author
-
Yang, Li, Stewart, Tessandra, Shi, Min, Pottiez, Gwenael, Dator, Romel, Wu, Rui, Aro, Patrick, Schuster, Robert J., Ginghina, Carmen, Pan, Catherine, Gao, Yuqian, Qian, Weijun, Zabetian, Cyrus P., Hu, Shu‐Ching, Quinn, Joseph F., and Zhang, Jing
- Published
- 2017
- Full Text
- View/download PDF
41. CNS tau efflux via exosomes is likely increased in Parkinson's disease but not in Alzheimer's disease.
- Author
-
Shi, Min, Kovac, Andrej, Korff, Ane, Cook, Travis J., Ginghina, Carmen, Bullock, Kristin M., Yang, Li, Stewart, Tessandra, Zheng, Danfeng, Aro, Patrick, Atik, Anzari, Kerr, Kathleen F., Zabetian, Cyrus P., Peskind, Elaine R., Hu, Shu-Ching, Quinn, Joseph F., Galasko, Douglas R., Montine, Thomas J., Banks, William A., and Zhang, Jing
- Abstract
Introduction Alzheimer's disease (AD) and Parkinson's disease (PD) involve tau pathology. Tau is detectable in blood, but its clearance from neuronal cells and the brain is poorly understood. Methods Tau efflux from the brain to the blood was evaluated by administering radioactively labeled and unlabeled tau intracerebroventricularly in wild-type and tau knock-out mice, respectively. Central nervous system (CNS)–derived tau in L1CAM-containing exosomes was further characterized extensively in human plasma, including by single molecule array technology with 303 subjects. Results The efflux of Tau, including a fraction via CNS-derived L1CAM exosomes, was observed in mice. In human plasma, tau was explicitly identified within L1CAM exosomes. In contrast to AD patients, L1CAM exosomal tau was significantly higher in PD patients than controls and correlated with cerebrospinal fluid tau. Conclusions Tau is readily transported from the brain to the blood. The mechanisms of CNS tau efflux are likely different between AD and PD. [ABSTRACT FROM AUTHOR]
- Published
- 2016
- Full Text
- View/download PDF
42. Response to the letter “Haptoglobin phenotype and Parkinson disease risk” by Delanghe et al.
- Author
-
Costa-Mallen, Paola, Zabetian, Cyrus P., Agarwal, Pinky, Hu, Shu-Ching, Yearout, Dora, Samii, Ali, Leverenz, James B., Roberts, John W., and Checkoway, Harvey
- Published
- 2016
- Full Text
- View/download PDF
43. The discovery of LRRK2 p.R1441S, a novel mutation for Parkinson's disease, adds to the complexity of a mutational hotspot.
- Author
-
Mata, Ignacio F., Davis, Marie Y., Lopez, Alexis N., Dorschner, Michael O., Martinez, Erica, Yearout, Dora, Cholerton, Brenna A., Hu, Shu‐Ching, Edwards, Karen L., Bird, Thomas D., and Zabetian, Cyrus P.
- Published
- 2016
- Full Text
- View/download PDF
44. CHAPTER 5 - Animal Models of Parkinson's Disease to Aid Drug Discovery and Development
- Author
-
Merchant, Kalpana M., Chesselet, Marie-Françoise, Hu, Shu-Ching, and Fahn, Stanley
- Published
- 2008
- Full Text
- View/download PDF
45. Pacific Northwest Udall Center of Excellence Clinical Consortium: Study Design and Baseline Cohort Characteristics.
- Author
-
Cholerton, Brenna A., Zabetian, Cyrus P., Quinn, Joseph F., Chung, Kathryn A., Peterson, Amie, Espay, Alberto J., Revilla, Fredy J., Devoto, Johnna, Watson, G. Stennis, Hu, Shu-Ching, Edwards, Karen L., Montine, Thomas J., and Leverenz, James B.
- Subjects
MILD cognitive impairment ,NEUROPSYCHOLOGY ,QUALITY of life ,DEMENTIA ,DISEASE prevalence - Abstract
Background: The substantial proportion of individuals with Parkinson's disease (PD) who have or are expected to develop concomitant cognitive impairment emphasizes the need for large, well-characterized participant cohorts to serve as a basis for research into the causes, manifestations, and potential treatments of cognitive decline in those with PD. Objective: To establish a multi-site clinical core that cognitively and clinically characterizes patients with PD by obtaining quality longitudinal clinical, neuropsychological, and validated biomarker data. Methods: Six hundred nineteen participants with idiopathic PD (68.0 ± 9.1 years, 7.1 ± 6.2 years since diagnosis, 70% males) were enrolled in the Pacific Northwest Udall Center (PANUC), one of the Morris K. Udall Centers of Excellence for Parkinson's Research, Clinical Consortium and underwent comprehensive clinical and neuropsychological assessment. Participants were diagnosed with no cognitive impairment (PD-NCI), mild cognitive impairment (PD-MCI), or dementia (PDD) at a diagnostic consensus conference. Results: A substantial proportion of the overall sample was diagnosed with cognitive impairment at baseline: 22% with PDD and 59% with PD-MCI. A higher rate of cognitive impairment was observed in men than women (87% vs. 68%, p < 0.0001), despite a higher level of education. Most patients older than 50 years at the time of diagnosis and with disease duration greater than 10 years were cognitively impaired or demented. Conclusions: The PANUC Clinical Consortium is a clinically and cognitively well-characterized cohort of patients with PD. Baseline cohort characteristics demonstrate a high rate of cognitive impairment in the sample, as well as potential sex differences with regard to cognitive diagnosis. The PANUC Clinical Consortium, with its access to biomarker, genetic, and autopsy data, provides an excellent foundation for detailed research related to cognitive impairment in PD. [ABSTRACT FROM AUTHOR]
- Published
- 2013
- Full Text
- View/download PDF
46. Dendrite Development Regulated by CREST, aCalcium-Regulated Transcriptional Activator.
- Author
-
Aizawa, Hiroyuki, Hu, Shu-Ching, Bobb, Kathryn, Balakrishnan, Karthik, Ince, Culayse, Gurevich, Inga, Cowan, Mitra, and Ghosh, Anirvan
- Subjects
- *
DENDRITES , *NEURAL stem cells , *CALCIUM , *BRAIN , *GENE expression , *GENETIC regulation - Abstract
The lasting effects of neuronal activity on brain development involve calcium-dependent gene expression. Using a strategy called transactivator trap, we cloned a calcium-responsive transactivator called CREST (for calcium-responsive transactivator). CREST is a SYT-related nuclear protein that interacts with adenosine 3',5'-monophosphate (cAMP) response elementbinding protein (CREB)-binding protein (CBP) and is expressed in the developing brain. Mice that have a targeted disruption of the crest gene are viable but display defects in cortical and hippocampal dendrite development. Cortical neurons from crest mutant mice are compromised in calciumdependent dendritic growth. Thus, calcium activation of CREST-mediated transcription helps regulate neuronal morphogenesis. [ABSTRACT FROM AUTHOR]
- Published
- 2004
- Full Text
- View/download PDF
47. The RAB39B p.G192R mutation causes X-linked dominant Parkinson’s disease
- Author
-
Mata, Ignacio F., Jang, Yongwoo, Kim, Chun-Hyung, Hanna, David S., Dorschner, Michael O., Samii, Ali, Agarwal, Pinky, Roberts, John W., Klepitskaya, Olga, Shprecher, David R., Chung, Kathryn A., Factor, Stewart A., Espay, Alberto J., Revilla, Fredy J., Higgins, Donald S., Litvan, Irene, Leverenz, James B., Yearout, Dora, Inca-Martinez, Miguel, Martinez, Erica, Thompson, Tiffany R., Cholerton, Brenna A., Hu, Shu-Ching, Edwards, Karen L., Kim, Kwang-Soo, and Zabetian, Cyrus P.
- Abstract
Objective: To identify the causal gene in a multi-incident U.S. kindred with Parkinson’s disease (PD). Methods: We characterized a family with a classical PD phenotype in which 7 individuals (5 males and 2 females) were affected with a mean age at onset of 46.1 years (range, 29-57 years). We performed whole exome sequencing on 4 affected and 1 unaffected family members. Sanger-sequencing was then used to verify and genotype all candidate variants in the remainder of the pedigree. Cultured cells transfected with wild-type or mutant constructs were used to characterize proteins of interest. Results: We identified a missense mutation (c.574G > A; p.G192R) in the RAB39B gene that closely segregated with disease and exhibited X-linked dominant inheritance with reduced penetrance in females. The mutation occurred in a highly conserved amino acid residue and was not observed among 87,725 X chromosomes in the Exome Aggregation Consortium dataset. Sequencing of the RAB39B coding region in 587 familial PD cases yielded two additional mutations (c.428C > G [p.A143G] and c.624_626delGAG [p.R209del]) that were predicted to be deleterious in silico but occurred in families that were not sufficiently informative to assess segregation with disease. Experiments in PC12 and SK-N-BE(2)C cells demonstrated that p.G192R resulted in mislocalization of the mutant protein, possibly by altering the structure of the hypervariable C-terminal domain which mediates intracellular targeting. Conclusions: Our findings implicate RAB39B, an essential regulator of vesicular-trafficking, in clinically typical PD. Further characterization of normal and aberrant RAB39B function might elucidate important mechanisms underlying neurodegeneration in PD and related disorders. Electronic supplementary material The online version of this article (doi:10.1186/s13024-015-0045-4) contains supplementary material, which is available to authorized users.
- Published
- 2015
- Full Text
- View/download PDF
48. List of Contributors
- Author
-
Acosta, M., Bendotti, Caterina, Blaugrund, Eran, Brunner, Daniela, Borsini, Franco, Cheroni, Cristina, Chesselet, Marie-Françoise, Deadwyler, Sam A., Elgersma, Y., Fahn, Stanley, Gordon, Paul H., Goren, Sari, Goumeniouk, Alexander D., Hallak, Hussein, Hampson, Robert E., Hannan, F., Hardt, M., Hu, Shu-Ching, Hunter, A. Jackie, Hunter-Schaedle, K., Klitgaard, Henrik, Krab, L.C., Leavitt, Blair R., Legius, E., Li, Weidong, Lindner, Mark D., Matagne, Alain, McArthur, Robert A., Menalled, Liliana, Merchant, Kalpana M., Montes, Jacqueline, Schachter, Steven C., Schneider, Lon S., Shilyansky, Carrie, Silva, Alcino J., Speiser, Zipora, Tariot, Pierre N., Tortarolo, Massimo, Wagner, Laura A., White, H. Steve, Wiltgen, B., and Willner, Paul
- Published
- 2008
- Full Text
- View/download PDF
49. The discovery of LRRK2 p.R1441S, a novel mutation for Parkinson's disease, adds to the complexity of a mutational hotspot.
- Author
-
Mata, Ignacio F., Davis, Marie Y., Lopez, Alexis N., Dorschner, Michael O., Martinez, Erica, Yearout, Dora, Cholerton, Brenna A., Hu, Shu‐Ching, Edwards, Karen L., Bird, Thomas D., and Zabetian, Cyrus P.
- Published
- 2017
- Full Text
- View/download PDF
50. Regulation of Thalamocortical Patterning and Synaptic Maturation by NeuroD2
- Author
-
Ince-Dunn, Gulayse, Hall, Benjamin J., Hu, Shu-Ching, Ripley, Beth, Huganir, Richard L., Olson, James M., Tapscott, Stephen J., and Ghosh, Anirvan
- Subjects
- *
TRANSCRIPTION factors , *SYNAPSES , *NEURAL transmission , *NEUROPHYSIOLOGY , *NEURAL circuitry , *NEUROSCIENCES - Abstract
Summary: During cortical development, both activity-dependent and genetically determined mechanisms are required to establish proper neuronal connectivity. While activity-dependent transcription may link the two processes, specific transcription factors that mediate such a process have not been identified. We identified the basic helix-loop-helix (bHLH) transcription factor Neurogenic Differentiation 2 (NeuroD2) in a screen for calcium-regulated transcription factors and report that it is required for the proper development of thalamocortical connections. In neuroD2 null mice, thalamocortical axon terminals fail to segregate in the somatosensory cortex, and the postsynaptic barrel organization is disrupted. Additionally, synaptic transmission is defective at thalamocortical synapses in neuroD2 null mice. Total excitatory synaptic currents are reduced in layer IV in the knockouts, and the relative contribution of AMPA and NMDA receptor-mediated currents to evoked responses is decreased. These observations indicate that NeuroD2 plays a critical role in regulating synaptic maturation and the patterning of thalamocortical connections. [Copyright &y& Elsevier]
- Published
- 2006
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.