Amyloid-β predominant Alzheimer’s disease neuropathologic change
Gábor G. Kovács, Yuriko Katsumata, Xian Wu, Khine Zin Aung, David W. Fardo, Shelley L. Forrest, James D. Bowen, Paul K. Crane, Gail P. Jarvik, C. Dirk Keene, Eric B. Larson, Wayne C. McCormick, Susan M. McCurry, Shubhabrata Mukherjee, Neil W. Kowall, Ann C. McKee, Robert A. Stern, Clinton T. Baldwin, Lindsay A. Farrer, Gyungah Jun, Kathryn L. Lunetta, Lawrence S. Honig, Jean Paul Vonsattel, Jennifer Williamson, Scott A. Small, Sandra Barral, Christiane Reitz, Badri N. Vardarajan, Richard Mayeux, James R. Burke, Christine M. Hulette, Kathleen A. Welsh‐Bohmer, Marla Gearing, James J. Lah, Allan I. Levey, Thomas S. Wingo, Liana G. Apostolova, Martin R. Farlow, Bernardino Ghetti, Andrew J. Saykin, Salvatore Spina, Kelley Faber, Tatiana M. Foroud, Marilyn Albert, Constantine G. Lyketsos, Juan C. Troncoso, Matthew P. Frosch, Robert C. Green, John H. Growdon, Bradley T. Hyman, Rudolph E. Tanzi, Huntington Potter, Dennis W. Dickson, Nilüfer Ertekin‐Taner, Neill R Graff-Radford, Joseph E. Parisi, Ronald C. Petersen, Bradley F Boeve, Mariet Allen, Minerva M. Carrasquillo, Steven G. Younkin, Ranjan Duara, Joseph D. Buxbaum, Alison Goate, Mary Sano, Arjun V. Masurkar, Thomas Wısnıewskı, Eileen H. Bigio, Marsel Mesulam, Sandra Weıntraub, Robert Vassar, Jeffrey Kaye, Joseph F. Quinn, Randall L. Woltjer, Lisa L. Barnes, Lei Yu, Denis A. Evans, Victor W. Henderson, Kenneth B. Fallon, Lindy E. Harrell, Daniel Marson, Erik D. Roberson, Charles DeCarli, Lee‐Way Jin, John Olichney, Ronald Kim, Frank M. LaFerla, Edwin S. Monuki, Elizabeth Head, David L. Sultzer, Daniel H. Geschwind, Harry V. Vinters, Marie‐Françoise Chesselet, Douglas Galasko, James Brewer, Adam L. Boxer, Anna Karydas, Joel H. Kramer, Bruce L. Miller, Howard J. Rosen
Abstract
Different subsets of Alzheimer's disease neuropathologic change (ADNC), including the intriguing set of individuals with severe/widespread amyloid-β (Aβ) plaques but no/mild tau tangles [Aβ-predominant (AP)-ADNC], may have distinct genetic and clinical features. Analysing National Alzheimer's Coordinating Center data, we stratified 1187 participants into AP-ADNC (n = 95), low Braak primary age-related tauopathy (PART; n = 185), typical-ADNC (n = 832) and high-Braak PART (n = 75). AP-ADNC differed in some clinical features and genetic polymorphisms in the APOE, SNX1, WNT3/MAPT and IGH genes. We conclude that AP-ADNC differs from classical ADNC with implications for in vivo studies.