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2. γ-Secretase activity, clinical features, and biomarkers of autosomal dominant Alzheimer's disease: cross-sectional and longitudinal analysis of the Dominantly Inherited Alzheimer Network observational study (DIAN-OBS)

Author

Aguillon, David, Allegri, Ricardo F., Aschenbrenner, Andrew J., Baker, Bryce, Barthelemy, Nicolas, Bechara, Jacob A., Berman, Sarah B., Brooks, William S., Cash, David M., Chen, Allison, Chrem Mendez, Patricio, Courtney, Laura, Cruchaga, Carlos, Daniels, Alisha J., Fagan, Anne M., Flores, Shaney, Fox, Nick C., Franklin, Erin, Goate, Alison M., Graber-Sultan, Susanne, Graff-Radford, Neill R., Gremminger, Emily, Herries, Elizabeth, Hofmann, Anna, Holtzman, David M., Hornbeck, Russ, Huey, Edward D., Ibanez, Laura, Ikeuchi, Takeshi, Ikonomovic, Snezana, Jackson, Kelley, Jarman, Steve, Jerome, Gina, Johnson, Erik C.B, Kasuga, Kensaku, Keefe, Sarah, Koudelis, Deborah, Kuder-Buletta, Elke, Laske, Christoph, Leon, Yudy Milena, Levey, Allan I., Li, Yan, Llibre-Guerra, Jorge J., Lopera, Francisco, Lu, Ruijin, Marsh, Jacob, Martins, Ralph, Massoumzadeh, Parinaz, Masters, Colin, McCullough, Austin, McKay, Nicole, Minton, Matthew, Mori, Hiroshi, Morris, John C., Nadkarni, Neelesh K., Nicklaus, Joyce, Niimi, Yoshiki, Noble, James M., Obermueller, Ulrike, Picarello, Danielle M., Pulizos, Christine, Ramirez, Laura, Renton, Alan E., Ringman, John, Rizzo, Jacqueline, Roedenbeck, Yvonne, Roh, Jee Hoon, Rosa-Neto, Pedro, Ryan, Natalie S., Sabaredzovic, Edita, Salloway, Stephen, Sanchez-Valle, Raquel, Scott, Jalen, Seyfried, Nicholas T., Simmons, Ashlee, Smith, Jennifer, Smith, Hunter, Stauber, Jennifer, Stout, Sarah, Supnet-Bell, Charlene, Surace, Ezequiel, Vazquez, Silvia, Vöglein, Jonathan, Wang, Guoqiao, Wang, Qing, Xu, Xiong, Xu, Jinbin, Schultz, Stephanie A, Liu, Lei, Schultz, Aaron P, Fitzpatrick, Colleen D, Levin, Raina, Bellier, Jean-Pierre, Shirzadi, Zahra, Joseph-Mathurin, Nelly, Chen, Charles D, Benzinger, Tammie L S, Day, Gregory S, Farlow, Martin R, Gordon, Brian A, Hassenstab, Jason J, Jack, Clifford R, Jr, Jucker, Mathias, Karch, Celeste M, Lee, Jae-Hong, Levin, Johannes, Perrin, Richard J, Schofield, Peter R, Xiong, Chengjie, Johnson, Keith A, McDade, Eric, Bateman, Randall J, Sperling, Reisa A, Selkoe, Dennis J, and Chhatwal, Jasmeer P

Published
2024
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3. Comparison of tau spread in people with Down syndrome versus autosomal-dominant Alzheimer's disease: a cross-sectional study

Author

Aizenstein, Howard J., Andrews, Howard F., Bell, Karen, Birn, Rasmus M., Bulova, Peter, Cheema, Amrita, Chen, Kewei, Clare, Isabel, Clark, Lorraine, Cohen, Ann D., Constantino, John N., Doran, Eric W., Feingold, Eleanor, Foroud, Tatiana M., Hartley, Sigan L., Hom, Christy, Honig, Lawrence, Ikonomovic, Milos D., Johnson, Sterling C., Jordan, Courtney, Kamboh, M. Ilyas, Keator, David, Klunk, William E., Kofler, Julia K., Kreisl, William C., Krinsky-McHale, Sharon J., Lao, Patrick, Laymon, Charles, Lott, Ira T., Lupson, Victoria, Mathis, Chester A., Minhas, Davneet S., Nadkarni, Neelesh, Pang, Deborah, Petersen, Melissa, Price, Julie C., Pulsifer, Margaret, Reiman, Eric, Rizvi, Batool, Sabbagh, Marwan N., Schupf, Nicole, Tudorascu, Dana L., Tumuluru, Rameshwari, Tycko, Benjamin, Varadarajan, Badri, White, Desiree A., Yassa, Michael A., Zaman, Shahid, Zhang, Fan, Bateman, Randall, Daniels, Alisha J., Courtney, Laura, McDade, Eric, Llibre-Guerra, Jorge J., Supnet-Bell, Charlene, Xiong, Chengie, Xu, Xiong, Lu, Ruijin, Wang, Guoqiao, Li, Yan, Gremminger, Emily, Perrin, Richard J., Franklin, Erin, Ibanez, Laura, Jerome, Gina, Herries, Elizabeth, Stauber, Jennifer, Baker, Bryce, Minton, Matthew, Cruchaga, Carlos, Goate, Alison M., Renton, Alan E., Picarello, Danielle M., Benzinger, Tammie, Gordon, Brian A., Hornbeck, Russall, Hassenstab, Jason, Smith, Jennifer, Stout, Sarah, Aschenbrenner, Andrew J., Karch, Celeste M., Marsh, Jacob, Morris, John C., Holtzman, David M., Barthelemy, Nicolas, Xu, Jinbin, Noble, James M., Berman, Sarah B., Ikonomovic, Snezana, Nadkarni, Neelesh K., Day, Gregory, Graff-Radford, Neill R., Farlow, Martin, Chhatwal, Jasmeer P., Ikeuchi, Takeshi, Kasuga, Kensaku, Niimi, Yoshiki, Huey, Edward D., Salloway, Stephen, Schofield, Peter R., Brooks, William S., Bechara, Jacob A., Martins, Ralph, Fox, Nick C., Cash, David M., Ryan, Natalie S., Jucker, Mathias, Laske, Christoph, Hofmann, Anna, Kuder-Buletta, Elke, Graber-Sultan, Susanne, Obermueller, Ulrike, Levin, Johannes, Roedenbeck, Yvonne, Vöglein, Jonathan, Lee, Jae-Hong, Roh, Jee Hoon, Sanchez-Valle, Raquel, Rosa-Neto, Pedro, Allegri, Ricardo F., Chrem Mendez, Patricio, Surace, Ezequiel, Vazquez, Silvia, Lopera, Francisco, Leon, Yudy Milena, Ramirez, Laura, Aguillon, David, Levey, Allan I., Johnson, Erik C.B, Seyfried, Nicholas T., Ringman, John, Mori, Hiroshi, Wisch, Julie K, McKay, Nicole S, Boerwinkle, Anna H, Kennedy, James, Flores, Shaney, Handen, Benjamin L, Christian, Bradley T, Head, Elizabeth, Mapstone, Mark, Rafii, Michael S, O’Bryant, Sid E, Price, Julie C, Laymon, Charles M, Krinsky-McHale, Sharon J, Lai, Florence, Rosas, H Diana, Hartley, Sigan L, Lott, Ira T, Tudorascu, Dana, Zammit, Matthew, Brickman, Adam M, Lee, Joseph H, Bird, Thomas D, Cohen, Annie, Chrem, Patricio, Daniels, Alisha, Chhatwal, Jasmeer P, Karch, Celeste M, Day, Gregory S, Llibre-Guerra, Jorge, Ringman, John M, van Dyck, Christopher H, Xiong, Chengjie, Morris, John C, Bateman, Randall J, Benzinger, Tammie L S, Gordon, Brian A, and Ances, Beau M

Published
2024
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4. Deconstructing pathological tau by biological process in early stages of Alzheimer disease: a method for quantifying tau spatial spread in neuroimaging

Author

Noble, James M., Day, Gregory S., Graff-Radford, Neill R., Voglein, Jonathan, Levin, Johannes, Allegri, Ricardo F., Mendez, Patricio Chrem, Surace, Ezequiel, Berman, Sarah B., Ikonomovic, Snezana, Nadkarni, Neelesh K., Lopera, Francisco, Ramirez, Laura, Aguillon, David, Leon, Yudy, Ramos, Claudia, Alzate, Diana, Baena, Ana, Londono, Natalia, Moreno, Sonia, Jucker, Mathias, Laske, Christoph, Kuder-Buletta, Elke, Graber-Sultan, Susanne, Preische, Oliver, Hofmann, Anna, Ikeuchi, Takeshi, Kasuga, Kensaku, Niimi, Yoshiki, Ishii, Kenji, Senda, Michio, Sanchez-Valle, Raquel, Rosa-Neto, Pedro, Fox, Nick C., Cash, Dave, Lee, Jae-Hong, Roh, Jee Hoon, Salloway, Stephen, Riddle, Meghan C., Menard, William, Bodge, Courtney, Surti, Mustafa, Takada, Leonel Tadao, Farlow, Martin, Chhatwal, Jasmeer P., Sanchez-Gonzalez, V.J., Orozco-Barajas, Maribel, Goate, Alison M., Renton, Alan E., Esposito, Bianca T., Karch, Celeste M., Marsh, Jacob, Cruchaga, Carlos, Fernanadez, Victoria, Gordon, Brian A., Fagan, Anne M., Jerome, Gina, Herries, Elizabeth, Llibre-Guerra, Jorge, Levey, Allan I., Johnson, Erik C.B., Seyfried, Nicholas T., Schofield, Peter R., Brooks, William S., Bechara, Jacob A., Bateman, Randall, McDade, Eric, Hassenstab, Jason, Perrin, Richard J., Franklin, Erin E., Benzinger, Tammie, Chen, Allison, Chen, Charles, Flores, Shaney, Friedrichsen, Nelly, Gordon, Brian, Hantler, Nancy, Hornbeck, Russ, Jarman, Steve, Keefe, Sarah, Koudelis, Deborah, Massoumzadeh, Parinaz, McCullough, Austin, McKay, Nicole, Nicklaus, Joyce, Pulizos, Christine, Wang, Qing, Mishall, Sheetal, Sabaredzovic, Edita, Deng, Emily, Candela, Madison, Smith, Hunter, Hobbs, Diana, Scott, Jalen, Xiong, Chengjie, Wang, Peter, Xu, Xiong, Li, Yan, Gremminger, Emily, Ma, Yinjiao, Bui, Ryan, Lu, Ruijin, Martins, Ralph, Sosa Ortiz, Ana Luisa, Daniels, Alisha, Courtney, Laura, Mori, Hiroshi, Supnet-Bell, Charlene, Xu, Jinbin, Ringman, John, Barthelemy, Nicolas, Morris, John, Smith, Jennifer, Doering, Stephanie, Chen, Charles D., Jarman, Stephen, Jackson, Kelley, Hornbeck, Russ C., Ances, Beau M., Aschenbrenner, Andrew J., Bateman, Randall J., Morris, John C., and Benzinger, Tammie L.S.

Published
2024
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5. Deconstructing pathological tau by biological process in early stages of Alzheimer disease: a method for quantifying tau spatial spread in neuroimaging

Author

Doering, Stephanie, primary, McCullough, Austin, additional, Gordon, Brian A., additional, Chen, Charles D., additional, McKay, Nicole, additional, Hobbs, Diana, additional, Keefe, Sarah, additional, Flores, Shaney, additional, Scott, Jalen, additional, Smith, Hunter, additional, Jarman, Stephen, additional, Jackson, Kelley, additional, Hornbeck, Russ C., additional, Ances, Beau M., additional, Xiong, Chengjie, additional, Aschenbrenner, Andrew J., additional, Hassenstab, Jason, additional, Cruchaga, Carlos, additional, Daniels, Alisha, additional, Bateman, Randall J., additional, Noble, James M., additional, Day, Gregory S., additional, Graff-Radford, Neill R., additional, Voglein, Jonathan, additional, Levin, Johannes, additional, Allegri, Ricardo F., additional, Mendez, Patricio Chrem, additional, Surace, Ezequiel, additional, Berman, Sarah B., additional, Ikonomovic, Snezana, additional, Nadkarni, Neelesh K., additional, Lopera, Francisco, additional, Ramirez, Laura, additional, Aguillon, David, additional, Leon, Yudy, additional, Ramos, Claudia, additional, Alzate, Diana, additional, Baena, Ana, additional, Londono, Natalia, additional, Moreno, Sonia, additional, Jucker, Mathias, additional, Laske, Christoph, additional, Kuder-Buletta, Elke, additional, Graber-Sultan, Susanne, additional, Preische, Oliver, additional, Hofmann, Anna, additional, Ikeuchi, Takeshi, additional, Kasuga, Kensaku, additional, Niimi, Yoshiki, additional, Ishii, Kenji, additional, Senda, Michio, additional, Sanchez-Valle, Raquel, additional, Rosa-Neto, Pedro, additional, Fox, Nick C., additional, Cash, Dave, additional, Lee, Jae-Hong, additional, Roh, Jee Hoon, additional, Salloway, Stephen, additional, Riddle, Meghan C., additional, Menard, William, additional, Bodge, Courtney, additional, Surti, Mustafa, additional, Takada, Leonel Tadao, additional, Farlow, Martin, additional, Chhatwal, Jasmeer P., additional, Sanchez-Gonzalez, V.J., additional, Orozco-Barajas, Maribel, additional, Goate, Alison M., additional, Renton, Alan E., additional, Esposito, Bianca T., additional, Karch, Celeste M., additional, Marsh, Jacob, additional, Fernanadez, Victoria, additional, Fagan, Anne M., additional, Jerome, Gina, additional, Herries, Elizabeth, additional, Llibre-Guerra, Jorge, additional, Levey, Allan I., additional, Johnson, Erik C.B., additional, Seyfried, Nicholas T., additional, Schofield, Peter R., additional, Brooks, William S., additional, Bechara, Jacob A., additional, Bateman, Randall, additional, McDade, Eric, additional, Perrin, Richard J., additional, Franklin, Erin E., additional, Benzinger, Tammie, additional, Chen, Allison, additional, Chen, Charles, additional, Friedrichsen, Nelly, additional, Gordon, Brian, additional, Hantler, Nancy, additional, Hornbeck, Russ, additional, Jarman, Steve, additional, Koudelis, Deborah, additional, Massoumzadeh, Parinaz, additional, Nicklaus, Joyce, additional, Pulizos, Christine, additional, Wang, Qing, additional, Mishall, Sheetal, additional, Sabaredzovic, Edita, additional, Deng, Emily, additional, Candela, Madison, additional, Wang, Peter, additional, Xu, Xiong, additional, Li, Yan, additional, Gremminger, Emily, additional, Ma, Yinjiao, additional, Bui, Ryan, additional, Lu, Ruijin, additional, Martins, Ralph, additional, Sosa Ortiz, Ana Luisa, additional, Courtney, Laura, additional, Mori, Hiroshi, additional, Supnet-Bell, Charlene, additional, Xu, Jinbin, additional, Ringman, John, additional, Barthelemy, Nicolas, additional, Morris, John, additional, Smith, Jennifer, additional, Morris, John C., additional, and Benzinger, Tammie L.S., additional

Published
2024
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20. Change in cerebrospinal fluid tau microtubule binding region detects symptom onset, cognitive decline, tangles, and atrophy in Dominantly Inherited Alzheimer's Disease

Author

Horie, Kanta, Li, Yan, Allegri, Ricardo, Mendez, Patricio Chrem, Ikeuchi, Takeshi, Kasuga, Kensaku, Noble, James, Farlow, Martin, Chhatwal, Jasmeer, Day, Gregory S, Schofield, Peter R, Masters, Colin L, Barthélemy, Nicolas R, Levin, Johannes, Jucker, Mathias, Lee, Jae-Hong, Roh, Jee Hoon, Sato, Chihiro, Sachdev, Pallavi, Koyama, Akihiko, Reyderman, Larisa, Bateman, Randall J, McDade, Eric, Gordon, Brian A, Network, Dominantly Inherited Alzheimer, Hassenstab, Jason, Benzinger, Tammie L S, Fagan, Anne M, Morris, John C, Karch, Celeste M, and Xiong, Chengjie

Subjects
Neurology, Neurology (clinical), ddc:610
Abstract

Identifying cerebrospinal fluid measures of the microtubule binding region of tau (MTBR-tau) species that reflect tau aggregation could provide fluid biomarkers that track Alzheimer disease related neurofibrillary tau pathological changes. We examined CSF MTBR-tau species in dominantly inherited Alzheimer disease (DIAD) mutation carriers to assess the association with AD biomarkers and clinical symptoms.Cross-sectional and longitudinal CSF from 229 DIAD mutation and 130 mutation non-carriers had sequential characterization of N-terminal/mid-domain phosphorylated tau (p-tau) followed by MTBR-tau species and tau-PET, other soluble tau and amyloid biomarkers, comprehensive clinical and cognitive assessments, and brain magnetic resonance imaging of atrophy.CSF MTBR-tau species located within the putative 'border' region and one species corresponding to the 'core' region of aggregates in neurofibrillary tangles increased during the presymptomatic stage and decreased during the symptomatic stage. The 'border' MTBR-tau species were associated with amyloid pathology and CSF p-tau; while the 'core' MTBR-tau species were associated stronger with tau-PET and CSF measures of neurodegeneration. The ratio of the border to the core species provided a continuous measure of increasing amounts that tracked clinical progression and NFT.Changes in CSF soluble MTBR-tau species preceded the onset of dementia, tau tangle increase, and atrophy in DIAD. The ratio of 4R-specific MTBR-tau (border) to the NFT (core) MTBR-tau species corresponds to the pathology of NFT in DIAD and change with disease progression. The dynamics between different MTBR-tau species in the CSF may serve as a marker of tau-related disease progression and target engagement of anti-tau therapeutics. This article is protected by copyright. All rights reserved.

Published
2023

21. Genetic Screening in Korean Patients with Frontotemporal Dementia Syndrome

Author

Kim, Eun-Joo, primary, Na, Duk L., additional, Kim, Hee-Jin, additional, Park, Kyung Won, additional, Lee, Jae-Hong, additional, Roh, Jee Hoon, additional, Kwon, Jay C., additional, Yoon, Soo Jin, additional, Jung, Na-Yeon, additional, Jeong, Jee Hyang, additional, Jang, Jae-Won, additional, Park, Kee Hyung, additional, Choi, Seong Hye, additional, Kim, SangYun, additional, Park, Young Ho, additional, Kim, Byeong C., additional, Youn, Young Chul, additional, Ki, Chang-Seok, additional, Kim, Seung Hyun, additional, Seo, Sang Won, additional, and Kim, Young-Eun, additional

Published
2022
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26. Survival in Korean Patients with Frontotemporal Dementia Syndrome: Association with Behavioral Features and Parkinsonism

Author

Jung, Na-Yeon, primary, Park, Kee Hyung, additional, Seo, Sang Won, additional, Kim, Hee Jin, additional, Roh, Jee Hoon, additional, Lee, Jae-Hong, additional, Park, Kyung Won, additional, Kwon, Jay C., additional, Jeong, Jee Hyang, additional, Yoon, Soo Jin, additional, Kim, Byeong C., additional, Park, Young Ho, additional, Kim, SangYun, additional, Jang, Jae-Won, additional, Youn, Young Chul, additional, Yang, Dong Won, additional, Choi, Seong Hye, additional, Na, Duk L., additional, and Kim, Eun-Joo, additional

Published
2022
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27. Role of White Matter Abnormalities in the Relationship Between Microbleed Burden and Cognitive Impairment in Cerebral Amyloid Angiopathy

Author

Jo, Sungyang, primary, Cheong, E-Nae, additional, Kim, Nayoung, additional, Oh, Jungsu S., additional, Shim, Woo Hyun, additional, Kim, Hyung-Ji, additional, Lee, Sun Ju, additional, Lee, Yoojin, additional, Oh, Minyoung, additional, Kim, Jae Seung, additional, Kim, Bum Joon, additional, Roh, Jee Hoon, additional, Kim, Sang Joon, additional, and Lee, Jae-Hong, additional

Published
2022
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30. 18F-THK5351 PET Positivity and Longitudinal Changes in Cognitive Function in β-Amyloid-Negative Amnestic Mild Cognitive Impairment

Author

Chun, Min Young, primary, Lee, Jongmin, additional, Jeong, Jee Hyang, additional, Roh, Jee Hoon, additional, Oh, Seung Jun, additional, Oh, Minyoung, additional, Oh, Jungsu S., additional, Kim, Jae Seung, additional, Moon, Seung Hwan, additional, Woo, Sook-young, additional, Kim, Young Ju, additional, Choe, Yeong Sim, additional, Kim, Hee Jin, additional, Na, Duk L., additional, Jang, Hyemin, additional, and Seo, Sang Won, additional

Published
2022
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32. Circadian clock proteins regulate neuronal redox homeostasis and neurodegeneration

Author

Musiek, Erik S., Lim, Mirand M., Yang, Guangrui, Bauer, Adam Q., Qi, Laura, Lee, Yool, Roh, Jee Hoon, Ortiz-Gonzalez, Xilma, Dearborn, Joshua T., Culver, Joseph P., Herzog, Erik D., Hogenesch, John B., Wozniak, David F., Dikranian, Krikor, Giasson, Benoit I., Weaver, David R., Holtzman, David M., and FitzGerald, Garret A.

Subjects
Homeostasis -- Research, Nervous system -- Degeneration, Circadian rhythms -- Physiological aspects, Health care industry
Abstract

Brain aging is associated with diminished circadian clock output and decreased expression of the core clock proteins, which regulate many aspects of cellular biochemistry and metabolism. The genes encoding clock [...]

Published
2013

33. Increased telomere length in patients with frontotemporal dementia syndrome

Author

Kim, Eun-Joo, Koh, Seong-Ho, Ha, Jungsoon, Na, Duk L., Seo, Sang Won, Kim, Hee-Jin, Park, Kyung Won, Lee, Jae-Hong, Roh, Jee Hoon, Kwon, Jay C., Yoon, Soo Jin, Jung, Na-Yeon, Jeong, Jee H., Jang, Jae-Won, Park, Kee Hyung, Choi, Seong Hye, Kim, SangYun, Park, Young Ho, Kim, Byeong C., Kim, Young-Eun, Kwon, Hyuk Sung, Park, Hyun-Hee, and Jin, Jeong-Hwa

Published
2021
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36. Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease

Author

Preische, Oliver, Schultz, Stephanie A, Vöglein, Jonathan, Raichle, Marc, Ringman, John, Roh, Jee Hoon, Salloway, Stephen, Schofield, Peter, Shimada, Hiroyuki, Shiroto, Tomoyo, Shoji, Mikio, Sigurdson, Wendy, Sohrabi, Hamid, Levin, Johannes, Sparks, Paige, Suzuki, Kazushi, Swisher, Laura, Taddei, Kevin, Wang, Jen, Wang, Peter, Weiner, Mike, Wolfsberger, Mary, Xiong, Chengjie, Xu, Xiong, Masters, Colin L, Martins, Ralph, Schofield, Peter R, Rossor, Martin N, Graff-Radford, Neill R, Ghetti, Bernardino, Ringman, John M, Apel, Anja, Noble, James M, Chhatwal, Jasmeer, Goate, Alison M, Benzinger, Tammie L S, Morris, John C, Bateman, Randall J, Wang, Guoqiao, Fagan, Anne M, McDade, Eric M, Gordon, Brian A, Kuhle, Jens, Jucker, Mathias, Network, Dominantly Inherited Alzheimer, Allegri, Ricardo, Amtashar, Fatima, Bateman, Randall, Benzinger, Tammie, Berman, Sarah, Bodge, Courtney, Brandon, Susan, Brooks, William, Kaeser, Stephan A, Buck, Jill, Buckles, Virginia, Chea, Sochenda, Chrem, Patricio, Chui, Helena, Cinco, Jake, Clifford, Jack, Cruchaga, Carlos, D'Mello, Mirelle, Barro, Christian, Donahue, Tamara, Douglas, Jane, Edigo, Noelia, Erekin-Taner, Nilufer, Fagan, Anne, Farlow, Marty, Farrar, Angela, Feldman, Howard, Flynn, Gigi, Fox, Nick, Gräber, Susanne, Franklin, Erin, Fujii, Hisako, Gant, Cortaiga, Gardener, Samantha, Goate, Alison, Goldman, Jill, Gordon, Brian, Graff-Radford, Neill, Gray, Julia, Kuder-Buletta, Elke, Gurney, Jenny, Hassenstab, Jason, Hirohara, Mie, Holtzman, David, Hornbeck, Russ, DiBari, Siri Houeland, Ikeuchi, Takeshi, Ikonomovic, Snezana, Jerome, Gina, Karch, Celeste, la Fougère, Christian, Kasuga, Kensaku, Kawarabayashi, Takeshi, Klunk, William, Koeppe, Robert, Lee, Jae-Hong, Marcus, Daniel, Mason, Neal Scott, Masters, Colin, Laske, Christoph, Maue-Dreyfus, Denise, McDade, Eric, Montoya, Lucy, Mori, Hiroshi, Morris, John, Nagamatsu, Akem, Neimeyer, Katie, Noble, James, Norton, Joanne, and Perrin, Richard

Subjects
0301 basic medicine, Oncology, Aging, blood [Neurofilament Proteins], Neurofilament, Medicina Clínica, Disease, Neurodegenerative, Alzheimer's Disease, Medical and Health Sciences, pathology [Alzheimer Disease], 0302 clinical medicine, Cerebrospinal fluid, Neurofilament Proteins, 2.1 Biological and endogenous factors, Aetiology, screening and diagnosis, medicine.diagnostic_test, Neurodegeneration, General Medicine, genetics [Neurofilament Proteins], cerebrospinal fluid [Alzheimer Disease], Detection, Editorial Commentary, Positron emission tomography, 030220 oncology & carcinogenesis, Neurological, Disease Progression, Biomarker (medicine), Alzheimer's disease, medicine.medical_specialty, CIENCIAS MÉDICAS Y DE LA SALUD, Immunology, blood [Nerve Degeneration], genetics [Mutation], General Biochemistry, Genetics and Molecular Biology, 03 medical and health sciences, blood [Alzheimer Disease], Clinical Research, Alzheimer Disease, Internal medicine, Acquired Cognitive Impairment, medicine, Humans, ddc:610, neurofilament protein L, business.industry, Multiple sclerosis, Neurosciences, Neurología Clínica, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Magnetic resonance imaging, medicine.disease, Brain Disorders, 4.1 Discovery and preclinical testing of markers and technologies, cerebrospinal fluid [Neurofilament Proteins], Good Health and Well Being, 030104 developmental biology, Dominantly Inherited Alzheimer Network, Mutation, Nerve Degeneration, Alzheimer, Dementia, business, Biomarkers
Abstract

Neurofilament light chain (NfL) is a promising fluid biomarker of disease progression for various cerebral proteopathies. Here we leverage the unique characteristics of the Dominantly Inherited Alzheimer Network and ultrasensitive immunoassay technology to demonstrate that NfL levels in the cerebrospinal fluid (n = 187) and serum (n = 405) are correlated with one another and are elevated at the presymptomatic stages of familial Alzheimer's disease. Longitudinal, within-person analysis of serum NfL dynamics (n = 196) confirmed this elevation and further revealed that the rate of change of serum NfL could discriminate mutation carriers from non-mutation carriers almost a decade earlier than cross-sectional absolute NfL levels (that is, 16.2 versus 6.8 years before the estimated symptom onset). Serum NfL rate of change peaked in participants converting from the presymptomatic to the symptomatic stage and was associated with cortical thinning assessed by magnetic resonance imaging, but less so with amyloid-β deposition or glucose metabolism (assessed by positron emission tomography). Serum NfL was predictive for both the rate of cortical thinning and cognitive changes assessed by the Mini-Mental State Examination and Logical Memory test. Thus, NfL dynamics in serum predict disease progression and brain neurodegeneration at the early presymptomatic stages of familial Alzheimer's disease, which supports its potential utility as a clinically useful biomarker. Fil: Preische, Oliver. German Center For Neurodegenerative Disease; Alemania. Eberhard Karls Universität Tübingen.; Alemania Fil: Schultz, Stephanie A.. Washington University in St. Louis; Estados Unidos Fil: Apel, Anja. German Center For Neurodegenerative Disease; Alemania. Eberhard Karls Universität Tübingen.; Alemania Fil: Kuhle, Jens. University of Basel; Suiza Fil: Kaeser, Stephan A.. German Center For Neurodegenerative Disease; Alemania. Eberhard Karls Universität Tübingen.; Alemania Fil: Barro, Christian. University of Basel; Suiza Fil: Gräber, Susanne. German Center For Neurodegenerative Disease; Alemania Fil: Kuder Buletta, Elke. German Center For Neurodegenerative Disease; Alemania Fil: LaFougere, Christian. German Center For Neurodegenerative Disease; Alemania Fil: Laske, Christoph. German Center For Neurodegenerative Disease; Alemania. Eberhard Karls Universität Tübingen.; Alemania Fil: Vöglein, Jonathan. German Center for Neurodegenerative Diseases; Alemania. Ludwig Maximilians Universitat; Alemania Fil: Levin, Johannes. German Center for Neurodegenerative Diseases; Alemania. Ludwig Maximilians Universitat; Alemania Fil: Masters, Colin. University of Melbourne; Australia Fil: Martins, Ralph. Edith Cowan University; Australia. Macquarie University; Australia Fil: Schofield, Peter. Neuroscience Research Australia; Australia. University of New South Wales; Australia Fil: Rossor, Martin N.. University College London; Estados Unidos Fil: Graff Radford, Neill. Mayo Clinic Jacksonville. Department of Neurology; Estados Unidos Fil: Salloway, Stephen. Brown University; Estados Unidos Fil: Ghetti, Bernardino. Indiana University. School of Medicine; Estados Unidos Fil: Ringman, John M.. Indiana University. School of Medicine; Estados Unidos Fil: Noble, James M.. Columbia University; Estados Unidos Fil: Chhatwal, Jasmeer. Harvard Medical School; Estados Unidos Fil: Goate, Alison. Icahn School of Medicine at Mount Sinai. Department of Neuroscience; Estados Unidos Fil: Benzinger, Tammie L. S.. Washington University in St. Louis; Estados Unidos Fil: Morris, John. Washington University in St. Louis; Estados Unidos Fil: Bateman, Randall J.. Washington University in St. Louis; Estados Unidos Fil: Wang, Guoqiao. Washington University in St. Louis; Estados Unidos Fil: Fagan, Anne M.. Washington University in St. Louis; Estados Unidos Fil: McDade, Eric M.. Washington University in St. Louis; Estados Unidos Fil: Gordon, Brian. Washington University in St. Louis; Estados Unidos Fil: Jucker, Mathias. University of Tübingen. Hertie Institute for Clinical Brain Research. Department of Cellular Neurology and Department of Psychiatry and Psychotherapy; Alemania. German Center For Neurodegenerative Disease; Alemania Fil: Allegri, Ricardo Francisco. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Fundación para la Lucha contra las Enfermedades Neurológicas de la Infancia; Argentina

Published
2019

39. Patterns of Focal Amyloid Deposition Using 18 F-Florbetaben PET in Patients with Cognitive Impairment.

Author

Chung, Sung-eun, Kim, Hyung-Ji, Jo, Sungyang, Lee, Sunju, Lee, Yoojin, Roh, Jee Hoon, and Lee, Jae-Hong

Subjects
CEREBRAL amyloid angiopathy, COGNITION disorders, CINGULATE cortex, MILD cognitive impairment, TEMPORAL lobe, PARIETAL lobe, AMYLOID
Abstract

Accumulation of aggregated amyloid-β (Aβ) in the brain is considered the first pathological event within the pathogenesis of Alzheimer's disease (AD). It is difficult to accurately identify the initial brain regions of Aβ accumulation due to the time-lag between the start of the pathophysiology and symptom onset. However, focal regional amyloid uptake on amyloid PET scans may provide insights into this. Hence, we aimed to evaluate the topographic distribution of amyloid deposition in patients with cognitive impairment and to identify the starting order of amyloid accumulation in the brain using conditional probability. We enrolled 58 patients composed of 9 normal cognition (NC), 32 mild cognitive impairment (MCI), and 17 dementia showing focal regional amyloid deposition corresponding to a brain amyloid plaque load (BAPL) score of 2 among those who visited the Memory Clinic of Asan Medical Center and underwent an 18F-florbetaben PET scan (March 2013 to April 2019). Regions of interest (ROI) included the frontal, parietal, lateral temporal, and occipital cortices, the posterior cingulate/precuneus, and the striatum. The most frequent occurrence of Aβ deposition was in the posterior cingulate/precuneus (n = 41, 68.3%). The second most frequent site was the lateral temporal cortex (n = 24, 40.0%), followed by the lateral parietal cortex (n = 21, 35.6%) and other lesions, such as the frontal and occipital cortices. The striatum was the least frequently affected. Our study found that the posterior cingulate/precuneus and the lateral temporal and parietal cortices may be the earliest areas to be affected by Aβ accumulation. Longitudinal follow-up of focal brain amyloid deposition may help elucidate the evolutionary pattern of Aβ accumulation in the brain of people with AD continuum. [ABSTRACT FROM AUTHOR]

Published
2022
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41. Amyloid and Tau Pathology Associations With Personality Traits, Neuropsychiatric Symptoms, and Cognitive Lifestyle in the Preclinical Phases of Sporadic and Autosomal Dominant Alzheimer’s Disease

Author

Pichet Binette, Alexa, primary, Vachon-Presseau, Étienne, additional, Morris, John, additional, Bateman, Randall, additional, Benzinger, Tammie, additional, Collins, D. Louis, additional, Poirier, Judes, additional, Breitner, John C.S., additional, Villeneuve, Sylvia, additional, Allegri, Ricardo, additional, Amtashar, Fatima, additional, Bateman, Randy, additional, Berman, Sarah, additional, Bodge, Courtney, additional, Brandon, Susan, additional, Brooks, William (Bill), additional, Buck, Jill, additional, Buckles, Virginia, additional, Chea, Sochenda, additional, Chhatwal, Jasmeer, additional, Chrem, Patricio, additional, Chui, Helena, additional, Cinco, Jake, additional, Clifford, Jack, additional, Cruchaga, Carlos, additional, D‘Mello, Mirelle, additional, Donahue, Tamara, additional, Douglas, Jane, additional, Edigo, Noelia, additional, Erekin-Taner, Nilufer, additional, Fagan, Anne, additional, Farlow, Marty, additional, Farrar, Angela, additional, Feldman, Howard, additional, Flynn, Gigi, additional, Fox, Nick, additional, Franklin, Erin, additional, Fujii, Hisako, additional, Gant, Cortaiga, additional, Gardener, Samantha, additional, Ghetti, Bernardino, additional, Goate, Alison, additional, Goldman, Jill, additional, Gordon, Brian, additional, Graff-Radford, Neill, additional, Gray, Julia, additional, Gurney, Jenny, additional, Hassenstab, Jason, additional, Hirohara, Mie, additional, Holtzman, David, additional, Hornbeck, Russ, additional, DiBari, Siri Houeland, additional, Ikeuchi, Takeshi, additional, Ikonomovic, Snezana, additional, Jerome, Gina, additional, Jucker, Mathias, additional, Karch, Celeste, additional, Kasuga, Kensaku, additional, Kawarabayashi, Takeshi, additional, Klunk, William (Bill), additional, Koeppe, Robert, additional, Kuder-Buletta, Elke, additional, Laske, Christoph, additional, Lee, Jae-Hong, additional, Levin, Johannes, additional, Marcus, Daniel, additional, Martins, Ralph, additional, Mason, Neal Scott, additional, Masters, Colin, additional, Maue-Dreyfus, Denise, additional, McDade, Eric, additional, Montoya, Lucy, additional, Mori, Hiroshi, additional, Nagamatsu, Akem, additional, Neimeyer, Katie, additional, Noble, James, additional, Norton, Joanne, additional, Perrin, Richard, additional, Raichle, Marc, additional, Ringman, John, additional, Roh, Jee Hoon, additional, Salloway, Stephen, additional, Schofield, Peter, additional, Shimada, Hiroyuki, additional, Shiroto, Tomoyo, additional, Shoji, Mikio, additional, Sigurdson, Wendy, additional, Sohrabi, Hamid, additional, Sparks, Paige, additional, Suzuki, Kazushi, additional, Swisher, Laura, additional, Taddei, Kevin, additional, Wang, Jen, additional, Wang, Peter, additional, Weiner, Mike, additional, Wolfsberger, Mary, additional, Xiong, Chengjie, additional, Xu, Xiong, additional, Tam, Angela, additional, Labonté, Anne, additional, Pichet Binette, Alexa, additional, Faubert, Anne-Marie, additional, Mathieu, Axel, additional, Madjar, Cécile, additional, Carrier, Charles Edouard, additional, Dansereau, Christian, additional, Kazazian, Christina, additional, Lepage, Claude, additional, Picard, Cynthia, additional, Maillet, David, additional, Michaud, Diane, additional, Couture, Doris, additional, Dea, Doris, additional, Cuello, Claudio, additional, Barkun, Alan, additional, Evans, Alan, additional, Courcot, Blandine, additional, Tardif, Christine, additional, Debacker, Clément, additional, Jack, Clifford R., additional, Fontaine, David, additional, Knopman, David S., additional, Maultaup, Gerhard, additional, Near, Jamie, additional, Leoutsakos, Jeannie-Marie, additional, Maltais, Jean-Robert, additional, Brandt, Jason, additional, Pruessner, Jens, additional, Morris, John C., additional, Cheewakriengkrai, Laksanun, additional, Münter, Lisa-Marie, additional, Collins, Louis, additional, Chakravarty, Mallar, additional, Sager, Mark A., additional, Dauar-Tedeschi, Marina, additional, Eisenberg, Mark, additional, Rajah, Natasha, additional, Aisen, Paul, additional, Toussaint, Joanne, additional, Rosa-Neto, Pedro, additional, Bellec, Pierre, additional, Kostopoulos, Penelope, additional, Etienne, Pierre, additional, Tariot, Pierre N., additional, Orban, Pierre, additional, Sperling, Reisa A., additional, Hoge, Rick, additional, Thomas, Ronald G., additional, Gauthier, Serge, additional, Craft, Suzanne, additional, Montine, Thomas J., additional, Nair, Vasavan, additional, Bohbot, Véronique, additional, Venugopalan, Vinod, additional, Fonov, Vladimir, additional, Ituria-Medina, Yasser, additional, Khachaturian, Zaven S., additional, Teigner, Eduard, additional, Anthal, Elena, additional, Yu, Elsa, additional, Ferdinand, Fabiola, additional, Pogossova, Galina, additional, Mayrand, Ginette, additional, Duclair, Guerda, additional, Gagné, Guylaine, additional, Newbold-Fox, Holly, additional, Leppert, Illana, additional, Vallée, Isabelle, additional, Vogel, Jacob W., additional, Tremblay-Mercier, Jennifer, additional, Frenette, Joanne, additional, Frappier, Josée, additional, Kat, Justin, additional, Miron, Justin, additional, Wan, Karen, additional, Mahar, Laura, additional, Carmo, Leopoldina, additional, Théroux, Louise, additional, Dadar, Mahsa, additional, Dufour, Marianne, additional, Lafaille-Magnan, Marie-Elyse, additional, Appleby, Melissa, additional, Savard, Mélissa, additional, Tuwaig, Miranda, additional, Petkova, Mirela, additional, Rioux, Pierre, additional, Meyer, Pierre-François, additional, El-Khoury, Rana, additional, Gordon, Renee, additional, Giles, Renuka, additional, Das, Samir, additional, Wang, Seqian, additional, Tabrizi, Shirin, additional, Mathotaarachchi, Sulantha, additional, Dubuc, Sylvie, additional, Lee, Tanya, additional, Beaudry, Thomas, additional, Gervais, Valérie, additional, Pagé, Véronique, additional, Gonneaud, Julie, additional, Ayranci, Gülebru, additional, Pascoal, Tharick A., additional, Desautels, René, additional, Benbouhoud, Fatiha, additional, Saint-Fort, Eunice Farah, additional, Verfaillie, Sander C.J., additional, Farzin, Sarah, additional, Salaciak, Alyssa, additional, Tullo, Stephanie, additional, Vachon-Presseau, Etienne, additional, Daoust, Leslie-Ann, additional, Köbe, Theresa, additional, Spreng, Nathan, additional, McSweeney, Melissa, additional, Nilsson, Nathalie, additional, Pishnamazi, Morteza, additional, and Bedetti, Christophe, additional

Published
2021
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42. A soluble phosphorylated tau signature links tau, amyloid and the evolution of stages of dominantly inherited Alzheimer’s disease

Author

Barthélemy, Nicolas R, Li, Yan, Morris, John C, Neimeyer, Katie, Noble, James, Norton, Joanne, Perrin, Richard, Raichle, Marc, Renton, Alan, Ringman, John, Roh, Jee Hoon, Salloway, Stephen, Schofield, Peter, Karch, Celeste M, Shimada, Hiroyuki, Sigurdson, Wendy, Sohrabi, Hamid, Sparks, Paige, Suzuki, Kazushi, Taddei, Kevin, Wang, Peter, Xiong, Chengjie, Xu, Xiong, Allegri, Ricardo, Mendez, Patricio Chrem, Berman, Sarah B, Ikeuchi, Takeshi, Mori, Hiroshi, Shoji, Mikio, Joseph-Mathurin, Nelly, Farlow, Martin, Chhatwal, Jasmeer, Graff-Radford, Neill R, Schofield, Peter R, Masters, Colin L, Martins, Ralph N, O'Connor, Antoinette, Gordon, Brian A, Fox, Nick C, Levin, Johannes, Jucker, Mathias, Gabelle, Audrey, Lehmann, Sylvain, Sato, Chihiro, Bateman, Randall J, McDade, Eric, Network, Dominantly Inherited Alzheimer, Hassenstab, Jason, Bateman, Randy, Bechara, Jacob, Benzinger, Tammie, Berman, Sarah, Bodge, Courtney, Brandon, Susan, Brooks, William Bill, Buck, Jill, Buckles, Virginia, Chea, Sochenda, Benzinger, Tammie L S, Chrem Mendez, Patricio, Chui, Helena, Cinco, Jake, Clifford, Jack, Cruchaga, Carlos, Donahue, Tamara, Douglas, Jane, Edigo, Noelia, Erekin-Taner, Nilufer, Fagan, Anne, Fitzpatrick, Colleen, Flynn, Gigi, Fox, Nick, Franklin, Erin, Fujii, Hisako, Gant, Cortaiga, Gardener, Samantha, Ghetti, Bernardino, Fagan, Anne M, Goate, Alison, Goldman, Jill, Gordon, Brian, Graff-Radford, Neill, Gray, Julia, Groves, Alexander, Hoechst-Swisher, Laura, Holtzman, David, Hornbeck, Russ, Perrin, Richard J, DiBari, Siri Houeland, Ikonomovic, Snezana, Jerome, Gina, Karch, Celeste, Kasuga, Kensaku, Kawarabayashi, Takeshi, Klunk, William Bill, Koeppe, Robert, Kuder-Buletta, Elke, Goate, Alison M, Laske, Christoph, Lee, Jae-Hong, Martins, Ralph, Mason, Neal Scott, Masters, Colin, Maue-Dreyfus, Denise, Morris, John, Nagamatsu, Akem, Washington University School of Medicine in St. Louis, Washington University in Saint Louis (WUSTL), Icahn School of Medicine at Mount Sinai [New York] (MSSM), Fundación para la Lucha contra las Enfermedades Neurológicas de la Infancia [Buenos Aires] (FLENI), FLENI, University of Pittsburgh School of Medicine, Pennsylvania Commonwealth System of Higher Education (PCSHE), Niigata University, Osaka City University (OCU), Hirosaki University, The University of Tokyo (UTokyo), Columbia University [New York], Indiana University - Purdue University Indianapolis (IUPUI), Indiana University System, Harvard Medical School [Boston] (HMS), Mayo Clinic [Jacksonville], Brown University, Neuroscience Research Australia (NeuRA), University of New South Wales [Sydney] (UNSW), The Florey Institute of Neuroscience and Mental Health, University of Melbourne, Edith Cowan University (ECU), Commonwealth Scientific and Industrial Research Organisation [Canberra] (CSIRO)-Planning and Transport Research Centre (PATREC), University College of London [London] (UCL), German Research Center for Neurodegenerative Diseases - Deutsches Zentrum für Neurodegenerative Erkrankungen (DZNE), Ludwig-Maximilians-Universität München (LMU), Munich Cluster for systems neurology [Munich] (SyNergy), Technische Universität Munchen - Université Technique de Munich [Munich, Allemagne] (TUM)-Ludwig-Maximilians-Universität München (LMU), University of Tübingen, Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), BioCampus Montpellier (BCM), Université Montpellier 1 (UM1)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Dominantly Inherited Alzheimer Network: Ricardo Allegri, Randy Bateman, Jacob Bechara, Tammie Benzinger, Sarah Berman, Courtney Bodge, Susan Brandon, William Bill Brooks, Jill Buck, Virginia Buckles, Sochenda Chea, Jasmeer Chhatwal, Patricio Chrem Mendez, Helena Chui, Jake Cinco, Jack Clifford, Carlos Cruchaga, Tamara Donahue, Jane Douglas, Noelia Edigo, Nilufer Erekin-Taner, Anne Fagan, Martin Farlow, Colleen Fitzpatrick, Gigi Flynn, Nick Fox, Erin Franklin, Hisako Fujii, Cortaiga Gant, Samantha Gardener, Bernardino Ghetti, Alison Goate, Jill Goldman, Brian Gordon, Neill Graff-Radford, Julia Gray, Alexander Groves, Jason Hassenstab, Laura Hoechst-Swisher, David Holtzman, Russ Hornbeck, Siri Houeland DiBari, Takeshi Ikeuchi, Snezana Ikonomovic, Gina Jerome, Mathias Jucker, Celeste Karch, Kensaku Kasuga, Takeshi Kawarabayashi, William Bill Klunk, Robert Koeppe, Elke Kuder-Buletta, Christoph Laske, Jae-Hong Lee, Johannes Levin, Ralph Martins, Neal Scott Mason, Colin Masters, Denise Maue-Dreyfus, Eric McDade, Hiroshi Mori, John Morris, Akem Nagamatsu, Katie Neimeyer, James Noble, Joanne Norton, Richard Perrin, Marc Raichle, Alan Renton, John Ringman, Jee Hoon Roh, Stephen Salloway, Peter Schofield, Hiroyuki Shimada, Wendy Sigurdson, Hamid Sohrabi, Paige Sparks, Kazushi Suzuki, Kevin Taddei, Peter Wang, Chengjie Xiong, Xiong Xu, Technische Universität München [München] (TUM)-Ludwig-Maximilians-Universität München (LMU), BioCampus (BCM), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), and Michel-Avella, Amandine

Subjects
0301 basic medicine, Male, [SDV]Life Sciences [q-bio], Inheritance Patterns, genetics [Alzheimer Disease], Plaque, Amyloid, Disease, 0302 clinical medicine, Cerebrospinal fluid, Cognition, pathology [Brain], Phosphorylation, biology, Neurodegeneration, Brain, General Medicine, Middle Aged, Magnetic Resonance Imaging, 3. Good health, [SDV] Life Sciences [q-bio], cerebrospinal fluid [Alzheimer Disease], 030220 oncology & carcinogenesis, Disease Progression, Female, Alzheimer's disease, metabolism [Alzheimer Disease], Adult, Amyloid, genetics [Inheritance Patterns], Tau protein, Neuroimaging, tau Proteins, General Biochemistry, Genetics and Molecular Biology, Article, 03 medical and health sciences, Atrophy, Alzheimer Disease, Fluorodeoxyglucose F18, mental disorders, medicine, Humans, ddc:610, pathology [Plaque, Amyloid], chemistry [Fluorodeoxyglucose F18], metabolism [Amyloid], Aged, medicine.disease, metabolism [tau Proteins], 030104 developmental biology, cerebrospinal fluid [tau Proteins], Solubility, biology.protein, diagnostic imaging [Alzheimer Disease], Neuroscience
Abstract

International audience; Development of tau-based therapies for Alzheimer's disease requires an understanding of the timing of disease-related changes in tau. We quantified the phosphorylation state at multiple sites of the tau protein in cerebrospinal fluid markers across four decades of disease progression in dominantly inherited Alzheimer's disease. We identified a pattern of tau staging where site-specific phosphorylation changes occur at different periods of disease progression and follow distinct trajectories over time. These tau phosphorylation state changes are uniquely associated with structural, metabolic, neurodegenerative and clinical markers of disease, and some (p-tau217 and p-tau181) begin with the initial increases in aggregate amyloid-β as early as two decades before the development of aggregated tau pathology. Others (p-tau205 and t-tau) increase with atrophy and hypometabolism closer to symptom onset. These findings provide insights into the pathways linking tau, amyloid-β and neurodegeneration, and may facilitate clinical trials of tau-based treatments.

Published
2020

43. Single-subject grey matter network trajectories over the disease course of autosomal dominant Alzheimer's disease

Author

Vermunt, Lisa, Dicks, Ellen, Wang, Guoqiao, Dincer, Aylin, Flores, Shaney, Keefe, Sarah J., Berman, Sarah B., Cash, David M., Chhatwal, Jasmeer P., Cruchaga, Carlos, Fox, Nick C., Ghetti, Bernardino, Graff-Radford, Neill R., Hassenstab, Jason, Karch, Celeste M., Laske, Christoph, Levin, Johannes, Masters, Colin L., McDade, Eric, Mori, Hiroshi, Morris, John C., Noble, James M., Perrin, Richard J., Schofield, Peter R., Xiong, Chengjie, Scheltens, Philip, Visser, Pieter Jelle, Bateman, Randall J., Benzinger, Tammie L. S., Tijms, Betty M., Gordon, Brian A., Allegri, Ricardo, Amtashar, Fatima, Berman, Sarah, Bodge, Courtney, Brandon, Susan, Brooks, William, Buck, Jill, Buckles, Virginia, Chea, Sochenda, Chrem, Patricio, Chui, Helena, Cinco, Jake, Jack, Clifford, D'Mello, Mirelle, Donahue, Tamara, Douglas, Jane, Edigo, Noelia, Erekin-Taner, Nilufer, Fagan, Anne, Farlow, Marty, Farrar, Angela, Feldman, Howard, Flynn, Gigi, Fox, Nick, Franklin, Erin, Fujii, Hisako, Gant, Cortaiga, Gardener, Samantha, Goate, Alison, Goldman, Jill, Gordon, Brian, Gray, Julia, Gurney, Jenny, Hirohara, Mie, Holtzman, David, Hornbeck, Russ, Dibari, Siri Houeland, Ikeuchi, Takeshi, Ikonomovic, Snezana, Jerome, Gina, Jucker, Mathias, Kasuga, Kensaku, Kawarabayashi, Takeshi, Klunk, William, Koeppe, Robert, Kuder-Buletta, Elke, Marcus, Daniel, Martins, Ralph, Mason, Neal Scott, Maue-Dreyfus, Denise, Montoya, Lucy, Nagamatsu, Akem, Neimeyer, Katie, Noble, James, Norton, Joanne, Perrin, Richard, Raichle, Marc, Ringman, John, Roh, Jee Hoon, Schofield, Peter, Shimada, Hiroyuki, Shiroto, Tomoyo, Shoji, Mikio, Sigurdson, Wendy, Sohrabi, Hamid, Sparks, Paige, Suzuki, Kazushi, Swisher, Laura, Taddei, Kevin, Wang, Jen, Wang, Peter, Weiner, Mike, Wolfsberger, Mary, Xu, Xiong, Clinical chemistry, Neurology, Amsterdam Neuroscience - Neurodegeneration, Amsterdam Neuroscience - Brain Imaging, RS: MHeNs - R1 - Cognitive Neuropsychiatry and Clinical Neuroscience, and Psychiatrie & Neuropsychologie

Subjects
structural covariance, 0301 basic medicine, medicine.medical_specialty, Amyloid beta, subject-level networks, Precuneus, PROGRESSION, ORGANIZATION, Disease, Grey matter, disruptions, 03 medical and health sciences, disease progression, 0302 clinical medicine, CEREBRAL-CORTEX, Internal medicine, autosomal dominant, medicine, Dementia, patterns, ddc:610, Cognitive decline, BIOMARKER CHANGES, biology, AcademicSubjects/SCI01870, General Engineering, Cognition, Alzheimer's disease, cognitive decline, AMYLOID-BETA, medicine.disease, Scientific Commentary, INDIVIDUALS, 030104 developmental biology, medicine.anatomical_structure, network, Cardiology, biology.protein, Original Article, AcademicSubjects/MED00310, Alzheimer’s disease, 030217 neurology & neurosurgery
Abstract

Structural grey matter covariance networks provide an individual quantification of morphological patterns in the brain. The network integrity is disrupted in sporadic Alzheimer’s disease, and network properties show associations with the level of amyloid pathology and cognitive decline. Therefore, these network properties might be disease progression markers. However, it remains unclear when and how grey matter network integrity changes with disease progression. We investigated these questions in autosomal dominant Alzheimer’s disease mutation carriers, whose conserved age at dementia onset allows individual staging based upon their estimated years to symptom onset. From the Dominantly Inherited Alzheimer Network observational cohort, we selected T1-weighted MRI scans from 269 mutation carriers and 170 non-carriers (mean age 38 ± 15 years, mean estimated years to symptom onset −9 ± 11), of whom 237 had longitudinal scans with a mean follow-up of 3.0 years. Single-subject grey matter networks were extracted, and we calculated for each individual the network properties which describe the network topology, including the size, clustering, path length and small worldness. We determined at which time point mutation carriers and non-carriers diverged for global and regional grey matter network metrics, both cross-sectionally and for rate of change over time. Based on cross-sectional data, the earliest difference was observed in normalized path length, which was decreased for mutation carriers in the precuneus area at 13 years and on a global level 12 years before estimated symptom onset. Based on longitudinal data, we found the earliest difference between groups on a global level 6 years before symptom onset, with a greater rate of decline of network size for mutation carriers. We further compared grey matter network small worldness with established biomarkers for Alzheimer disease (i.e. amyloid accumulation, cortical thickness, brain metabolism and cognitive function). We found that greater amyloid accumulation at baseline was associated with faster decline of small worldness over time, and decline in grey matter network measures over time was accompanied by decline in brain metabolism, cortical thinning and cognitive decline. In summary, network measures decline in autosomal dominant Alzheimer’s disease, which is alike sporadic Alzheimer’s disease, and the properties show decline over time prior to estimated symptom onset. These data suggest that single-subject networks properties obtained from structural MRI scans form an additional non-invasive tool for understanding the substrate of cognitive decline and measuring progression from preclinical to severe clinical stages of Alzheimer’s disease., Grey matter covariance networks are extracted from structural MRI. In the DIAN autosomal dominant Alzheimer’s disease family cohort, we demonstrate for the first time the trajectory of network properties in Alzheimer’s disease. These network properties related to other eurodegeneration markers and can form a non-invasive tool for studying Alzheimer’s disease progression., Graphical Abstract Graphical Abstract

Published
2020

44. Pathological manifestation of the induced pluripotent stem cell‐derived cortical neurons from an early‐onset Alzheimer's disease patient carrying a presenilin‐1 mutation (S170F)

Author

Li, Ling, primary, Kim, Hee Jin, additional, Roh, Jee Hoon, additional, Kim, Minchul, additional, Koh, Wonyoung, additional, Kim, Younghoon, additional, Heo, Hyohoon, additional, Chung, Jaehoon, additional, Nakanishi, Mahito, additional, Yoon, Taeyoung, additional, Hong, Chang Pyo, additional, Seo, Sang Won, additional, Na, Duk L., additional, and Song, Jihwan, additional

Published
2020
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45. Intra-individual correlations between quantitative THK-5351 PET and MRI-derived cortical volume in Alzheimer’s disease differ according to disease severity and amyloid positivity

Author

Park, Ji Eun, primary, Yun, Jessica, additional, Kim, Sang Joon, additional, Shim, Woo Hyun, additional, Oh, Jungsu S., additional, Oh, Minyoung, additional, Roh, Jee Hoon, additional, Seo, Sang Won, additional, Oh, Seung Jun, additional, and Kim, Jae Seung, additional

Published
2019
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50. An atlas of cortical circular RNA expression in Alzheimer disease brains demonstrates clinical and pathological associations

Author

Dube, Umber, Del-Aguila, Jorge L, Gentsch, Jen, Wang, Peter, Weiner, Mike, Wolfsberger, Mary, Xiong, Chengjie, Xu, Xiong, Wang, Fengxian, Network, Dominantly Inherited Alzheimer, Salloway, Stephen, Masters, Colin L, Lee, Jae-Hong, Graff-Radford, Neill R, Chhatwal, Jasmeer P, Bateman, Randall J, Morris, John C, Li, Zeran, Karch, Celeste M, Harari, Oscar, Cruchaga, Carlos, Allegri, Ricardo, Amtashar, Fatima, Benzinger, Tammie, Berman, Sarah, Bodge, Courtney, Brandon, Susan, Brooks, William, Budde, John P, Buck, Jill, Buckles, Virginia, Chea, Sochenda, Chrem, Patricio, Chui, Helena, Cinco, Jake, Clifford, Jack, D'Mello, Mirelle, Donahue, Tamara, Douglas, Jane, Jiang, Shan, Edigo, Noelia, Erekin-Taner, Nilufer, Fagan, Anne, Farlow, Marty, Farrar, Angela, Feldman, Howard, Flynn, Gigi, Fox, Nick, Franklin, Erin, Fujii, Hisako, Hsu, Simon, Gant, Cortaiga, Gardener, Samantha, Ghetti, Bernardino, Goate, Alison, Goldman, Jill, Gordon, Brian, Gray, Julia, Gurney, Jenny, Hassenstab, Jason, Hirohara, Mie, Ibanez, Laura, Holtzman, David, Hornbeck, Russ, DiBari, Siri Houeland, Ikeuchi, Takeshi, Ikonomovic, Snezana, Jerome, Gina, Jucker, Mathias, Kasuga, Kensaku, Kawarabayashi, Takeshi, Klunk, William, Fernandez, Maria Victoria, Koeppe, Robert, Kuder-Buletta, Elke, Laske, Christoph, Levin, Johannes, Marcus, Daniel, Martins, Ralph, Mason, Neal Scott, Maue-Dreyfus, Denise, McDade, Eric, Montoya, Lucy, Farias, Fabiana, Mori, Hiroshi, Nagamatsu, Akem, Neimeyer, Katie, Noble, James, Norton, Joanne, Perrin, Richard, Raichle, Marc, Ringman, John, Roh, Jee Hoon, Schofield, Peter, Shimada, Hiroyuki, Shiroto, Tomoyo, Shoji, Mikio, Sigurdson, Wendy, Sohrabi, Hamid, Sparks, Paige, Suzuki, Kazushi, Swisher, Laura, Taddei, Kevin, and Wang, Jen

Subjects
0301 basic medicine, metabolism [Parietal Lobe], Posterior parietal cortex, Biology, Severity of Illness Index, Article, Pathogenesis, 03 medical and health sciences, pathology [Alzheimer Disease], 0302 clinical medicine, Atlases as Topic, Alzheimer Disease, Circular RNA, metabolism [MicroRNAs], Parietal Lobe, ddc:570, microRNA, medicine, Dementia, Humans, RNA, Messenger, Gene, Messenger RNA, biosynthesis [RNA, Messenger], Sequence Analysis, RNA, General Neuroscience, Gene Expression Profiling, diagnosis [Alzheimer Disease], RNA, Circular, medicine.disease, biosynthesis [RNA, Circular], MicroRNAs, 030104 developmental biology, Case-Control Studies, Alzheimer's disease, Neuroscience, 030217 neurology & neurosurgery, metabolism [Alzheimer Disease]
Abstract

Parietal cortex RNA-sequencing (RNA-seq) data were generated from individuals with and without Alzheimer disease (AD; ncontrol = 13; nAD = 83) from the Knight Alzheimer Disease Research Center (Knight ADRC). Using this and an independent (Mount Sinai Brain Bank (MSBB)) AD RNA-seq dataset, cortical circular RNA (circRNA) expression was quantified in the context of AD. Significant associations were identified between circRNA expression and AD diagnosis, clinical dementia severity and neuropathological severity. It was demonstrated that most circRNA-AD associations are independent of changes in cognate linear messenger RNA expression or estimated brain cell-type proportions. Evidence was provided for circRNA expression changes occurring early in presymptomatic AD and in autosomal dominant AD. It was also observed that AD-associated circRNAs co-expressed with known AD genes. Finally, potential microRNA-binding sites were identified in AD-associated circRNAs for miRNAs predicted to target AD genes. Together, these results highlight the importance of analyzing non-linear RNAs and support future studies exploring the potential roles of circRNAs in AD pathogenesis.

Published
2019

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