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1. Dynamic proportional loss of functional connectivity revealed change of left superior frontal gyrus in subjective cognitive decline: an explanatory study based on Chinese and Western cohorts

Author

Wang, Luyao, Hu, Wenjing, Dong, Fan, Sheng, Can, Wu, Jinglong, Han, Ying, Jiang, Jiehui, Weiner, Michael W., Aisen, Paul, Petersen, Ronald, Jack, Clifford R., Jagust, William, Trojanowski, John Q., Toga, Arthur W., Beckett, Laurel, Green, Robert C., Saykin, Andrew J., Morris, John, Shaw, Leslie M., Khachaturian, Zaven, Sorensen, Greg, Kuller, Lew, Raichle, Marcus, Paul, Steven, Davies, Peter, Fillit, Howard, Hefti, Franz, Holtzman, David, Mesulam, Marek M., Potter, William, Snyder, Peter, Schwartz, Adam, Montine, Tom, Thomas, Ronald G., Donohue, Michael, Walter, Sarah, Gessert, Devon, Sather, Tamie, Jiminez, Gus, Harvey, Danielle, Bernstein, Matthew, Thompson, Paul, Schuff, Norbert, Borowski, Bret, Gunter, Jeff, Senjem, Matt, Vemuri, Prashanthi, Jones, David, Kantarci, Kejal, Ward, Chad, Koeppe, Robert A., Foster, Norm, Reiman, Eric M., Chen, Kewei, Mathis, Chet, Landau, Susan, Cairns, Nigel J., Householder, Erin, Taylor-Reinwald, Lisa, Lee, Virginia, Korecka, Magdalena, Figurski, Michal, Crawford, Karen, Neu, Scott, Foroud, Tatiana M., Potkin, Steven G., Shen, Li, Faber, Kelley, Kim, Sungeun, Nho, Kwangsik, Thal, Leon, Buckholtz, Neil, Albert, Marylyn, Frank, Richard, Hsiao, John, Kaye, Jeffrey, Quinn, Joseph, Lind, Betty, Carter, Raina, Dolen, Sara, Schneider, Lon S., Pawluczyk, Sonia, Beccera, Mauricio, Teodoro, Liberty, Spann, Bryan M., Brewer, James, Vanderswag, Helen, Fleisher, Adam, Heidebrink, Judith L., Lord, Joanne L., Mason, Sara S., Albers, Colleen S., Knopman, David, Johnson, Kris, Doody, Rachelle S., Villanueva-Meyer, Javier, Chowdhury, Munir, Rountree, Susan, Dang, Mimi, Stern, Yaakov, Honig, Lawrence S., Bell, Karen L., Ances, Beau, Carroll, Maria, Leon, Sue, Mintun, Mark A., Schneider, Stacy, Oliver, Angela, Marson, Daniel, Griffith, Randall, Clark, David, Geldmacher, David, Brockington, John, Roberson, Erik, Grossman, Hillel, Mitsis, Effie, de Toledo-Morrell, Leyla, Shah, Raj C., Duara, Ranjan, Varon, Daniel, Greig, Maria T., Roberts, Peggy, Onyike, Chiadi, D’Agostino, Daniel, Kielb, Stephanie, Galvin, James E., Cerbone, Brittany, Michel, Christina A., Rusinek, Henry, de Leon, Mony J., Glodzik, Lidia, De Santi, Susan, Doraiswamy, PMurali, Petrella, Jeffrey R., Wong, Terence Z., Arnold, Steven E., Karlawish, Jason H., Wolk, David, Smith, Charles D., Jicha, Greg, Hardy, Peter, Sinha, Partha, Oates, Elizabeth, Conrad, Gary, Lopez, Oscar L., Oakley, MaryAnn, Simpson, Donna M., Porsteinsson, Anton P., Goldstein, Bonnie S., Martin, Kim, Makino, Kelly M., Ismail, MSaleem, Brand, Connie, Mulnard, Ruth A., Thai, Gaby, McAdams-Ortiz, Catherine, Womack, Kyle, Mathews, Dana, Quiceno, Mary, Diaz-Arrastia, Ramon, King, Richard, Weiner, Myron, Martin-Cook, Kristen, DeVous, Michael, Levey, Allan I., Lah, James J., Cellar, Janet S., Burns, Jeffrey M., Anderson, Heather S., Swerdlow, Russell H., Apostolova, Liana, Tingus, Kathleen, Woo, Ellen, Silverman, Daniel H. S., Lu, Po H., Bartzokis, George, Graff-Radford, Neill R., Parfitt, Francine, Kendall, Tracy, Johnson, Heather, Farlow, Martin R., Hake, Ann Marie, Matthews, Brandy R., Herring, Scott, Hunt, Cynthia, van Dyck, Christopher H., Carson, Richard E., MacAvoy, Martha G., Chertkow, Howard, Bergman, Howard, Hosein, Chris, Hsiung, Ging-Yuek Robin, Feldman, Howard, Mudge, Benita, Assaly, Michele, Bernick, Charles, Munic, Donna, Kertesz, Andrew, Rogers, John, Trost, Dick, Kerwin, Diana, Lipowski, Kristine, Wu, Chuang-Kuo, Johnson, Nancy, Sadowsky, Carl, Martinez, Walter, Villena, Teresa, Turner, Raymond Scott, Johnson, Kathleen, Reynolds, Brigid, Sperling, Reisa A., Johnson, Keith A., Marshall, Gad, Frey, Meghan, Lane, Barton, Rosen, Allyson, Tinklenberg, Jared, Sabbagh, Marwan N., Belden, Christine M., Jacobson, Sandra A., Sirrel, Sherye A., Kowall, Neil, Killiany, Ronald, Budson, Andrew E., Norbash, Alexander, Johnson, Patricia Lynn, Allard, Joanne, Lerner, Alan, Ogrocki, Paula, Hudson, Leon, Fletcher, Evan, Carmichae, Owen, Olichney, John, DeCarli, Charles, Kittur, Smita, Borrie, Michael, Lee, T.-Y., Bartha, Rob, Johnson, Sterling, Asthana, Sanjay, Carlsson, Cynthia M., Preda, Adrian, Nguyen, Dana, Tariot, Pierre, Reeder, Stephanie, Bates, Vernice, Capote, Horacio, Rainka, Michelle, Scharre, Douglas W., Kataki, Maria, Adeli, Anahita, Zimmerman, Earl A., Celmins, Dzintra, Brown, Alice D., Pearlson, Godfrey D., Blank, Karen, Anderson, Karen, Santulli, Robert B., Kitzmiller, Tamar J., Schwartz, Eben S., Sink, Kaycee M., Williamson, Jeff D., Garg, Pradeep, Watkins, Franklin, Ott, Brian R., Querfurth, Henry, Tremont, Geoffrey, Salloway, Stephen, Malloy, Paul, Correia, Stephen, Rosen, Howard J., Miller, Bruce L., Mintzer, Jacobo, Spicer, Kenneth, Bachman, David, Pasternak, Stephen, Rachinsky, Irina, Drost, Dick, Pomara, Nunzio, Hernando, Raymundo, Sarrael, Antero, Schultz, Susan K., Ponto, Laura L. Boles, Shim, Hyungsub, Smith, Karen Elizabeth, Relkin, Norman, Chaing, Gloria, Raudin, Lisa, Smith, Amanda, Fargher, Kristin, Raj, Balebail Ashok, Neylan, Thomas, Grafman, Jordan, Davis, Melissa, Morrison, Rosemary, Hayes, Jacqueline, Finley, Shannon, Friedl, Karl, Fleischman, Debra, Arfanakis, Konstantinos, James, Olga, Massoglia, Dino, Fruehling, JJay, Harding, Sandra, Peskind, Elaine R., Petrie, Eric C., Li, Gail, Yesavage, Jerome A., Taylor, Joy L., and Furst, Ansgar J.

Published
2025
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2. Robust, fully-automated assessment of cerebral perivascular spaces and white matter lesions: a multicentre MRI longitudinal study of their evolution and association with risk of dementia and accelerated brain atrophy

Author

Weiner, Michael, Aisen, Paul, Petersen, Ronald, Jack, Clifford R., Jagust, William, Trojanowki, John Q., Toga, Arthur W., Beckett, Laurel, Green, Robert C., Saykin, Andrew J., Morris, John, Shaw, Leslie M., Liu, Enchi, Montine, Tom, Thomas, Ronald G., Donohue, Michael, Walter, Sarah, Gessert, Devon, Sather, Tamie, Jiminez, Gus, Harvey, Danielle, Bernstein, Matthew, Fox, Nick, Thompson, Paul, Schuff, Norbert, DeCarli, Charles, Borowski, Bret, Gunter, Jeff, Senjem, Matt, Vemuri, Prashanthi, Jones, David, Kantarci, Kejal, Ward, Chad, Koeppe, Robert A., Foster, Norm, Reiman, Eric M., Chen, Kewei, Mathis, Chet, Landau, Susan, Cairns, Nigel J., Householder, Erin, Reinwald, Lisa Taylor, Lee, Virginia, Korecka, Magdalena, Figurski, Michal, Crawford, Karen, Neu, Scott, Foroud, Tatiana M., Potkin, Steven, Shen, Li, Kelley, Faber, Kim, Sungeun, Nho, Kwangsik, Kachaturian, Zaven, Frank, Richard, Snyder, Peter J., Molchan, Susan, Kaye, Jeffrey, Quinn, Joseph, Lind, Betty, Carter, Raina, Dolen, Sara, Schneider, Lon S., Pawluczyk, Sonia, Beccera, Mauricio, Teodoro, Liberty, Spann, Bryan M., Brewer, James, Vanderswag, Helen, Fleisher, Adam, Heidebrink, Judith L., Lord, Joanne L., Mason, Sara S., Albers, Colleen S., Knopman, David, Johnson, Kris, Doody, Rachelle S., Meyer, Javier Villanueva, Chowdhury, Munir, Rountree, Susan, Dang, Mimi, Stern, Yaakov, Honig, Lawrence S., Bell, Karen L., Ances, Beau, Morris, John C., Carroll, Maria, Leon, Sue, Mintun, Mark A., Schneider, Stacy, Oliver, Angela, Marson, Daniel, Griffith, Randall, Clark, David, Geld-macher, David, Brockington, John, Roberson, Erik, Grossman, Hillel, Mitsis, Effie, Leyla deToledo-Morrell, Shah, Raj C., Duara, Ranjan, Varon, Daniel, Greig, Maria T., Roberts, Peggy, Albert, Marilyn, Onyike, Chiadi, D’Agostino, Daniel, Kielb, Stephanie, Galvin, James E., Pogorelec, Dana M., Cerbone, Brittany, Michel, Christina A., Rusinek, Henry, de Leon, Mony J., Glodzik, Lidia, De Santi, Susan, Doraiswamy, P. Murali, Petrella, Jeffrey R., Wong, Terence Z., Arnold, Steven E., Karlawish, Jason H., Wolk, David, Smith, Charles D., Jicha, Greg, Hardy, Peter, Sinha, Partha, Oates, Elizabeth, Conrad, Gary, Lopez, Oscar L., Oakley, MaryAnn, Simpson, Donna M., Porsteinsson, Anton P., Goldstein, Bonnie S., Martin, Kim, Makino, Kelly M., Ismail, M. Saleem, Brand, Connie, Mulnard, Ruth A., Thai, Gaby, Adams Ortiz, Catherine Mc, Womack, Kyle, Mathews, Dana, Quiceno, Mary, Arrastia, Ramon Diaz, King, Richard, Weiner, Myron, Cook, Kristen Martin, DeVous, Michael, Levey, Allan I., Lah, James J., Cellar, Janet S., Burns, Jeffrey M., Anderson, Heather S., Swerdlow, Russell H., Apostolova, Liana, Tingus, Kathleen, Woo, Ellen, Silverman, Daniel H.S., Lu, Po H., Bartzokis, George, Graff Radford, Neill R., Parfitt, Francine, Kendall, Tracy, Johnson, Heather, Farlow, Martin R., Hake, AnnMarie, Matthews, Brandy R., Herring, Scott, Hunt, Cynthia, van Dyck, Christopher H., Carson, Richard E., MacAvoy, Martha G., Chertkow, Howard, Bergman, Howard, Hosein, Chris, Black, Sandra, Stefanovic, Bojana, Caldwell, Curtis, Robin Hsiung, Ging-Yuek, Feldman, Howard, Mudge, Benita, Assaly, Michele, Kertesz, Andrew, Rogers, John, Trost, Dick, Bernick, Charles, Munic, Donna, Kerwin, Diana, Mesulam, Marek Marsel, Lipowski, Kristine, Wu, Chuang Kuo, Johnson, Nancy, Sadowsky, Carl, Martinez, Walter, Villena, Teresa, Turner, Raymond Scott, Johnson, Kathleen, Reynolds, Brigid, Sperling, Reisa A., Johnson, Keith A., Marshall, Gad, Frey, Meghan, Yesavage, Jerome, Taylor, Joy L., Lane, Barton, Rosen, Allyson, Tinklenberg, Jared, Sabbagh, Marwan N., Belden, Christine M., Jacobson, Sandra A., Sirrel, Sherye A., Kowall, Neil, Killiany, Ronald, Budson, Andrew E., Norbash, Alexander, Johnson, Patricia Lynn, Obisesan, Thomas O., Wolday, Saba, Allard, Joanne, Lerner, Alan, Ogrocki, Paula, Hudson, Leon, Fletcher, Evan, Carmichael, Owen, Olichney, John, Kittur, Smita, Borrie, Michael, Lee, T.Y., Bartha, Rob, Johnson, Sterling, Asthana, Sanjay, Carlsson, Cynthia M., Potkin, Steven G., Preda, Adrian, Nguyen, Dana, Tariot, Pierre, Reeder, Stephanie, Bates, Vernice, Capote, Horacio, Rainka, Michelle, Scharre, Douglas W., Kataki, Maria, Adeli, Anahita, Zimmerman, Earl A., Celmins, Dzintra, Brown, Alice D., Pearlson, Godfrey D., Blank, Karen, Anderson, Karen, Santulli, Robert B., Kitzmiller, Tamar J., Schwartz, Eben S., Sink, Kaycee M., Williamson, Jeff D., Garg, Pradeep, Watkins, Franklin, Ott, Brian R., Querfurth, Henry, Tremont, Geoffrey, Salloway, Stephen, Malloy, Paul, Correia, Stephen, Rosen, Howard J., Miller, Bruce L., Mintzer, Jacobo, Spicer, Kenneth, Bachman, David, Finger, Elizabeth, Pasternak, Stephen, Rachinsky, Irina, Drost, Dick, Pomara, Nunzio, Hernando, Raymundo, Sarrael, Antero, Schultz, Susan K., Boles Ponto, Laura L., Shim, Hyungsub, Smith, Karen Elizabeth, Relkin, Norman, Chaing, Gloria, Raudin, Lisa, Smith, Amanda, Fargher, Kristin, Raj, Balebail Ashok, Barisano, Giuseppe, Iv, Michael, Choupan, Jeiran, and Hayden-Gephart, Melanie

Published
2025
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3. Accuracy of Tau Positron Emission Tomography as a Prognostic Marker in Preclinical and Prodromal Alzheimer Disease

Author

Ossenkoppele, Rik, Smith, Ruben, Mattsson-Carlgren, Niklas, Groot, Colin, Leuzy, Antoine, Strandberg, Olof, Palmqvist, Sebastian, Olsson, Tomas, Jögi, Jonas, Stormrud, Erik, Cho, Hanna, Ryu, Young Hoon, Choi, Jae Yong, Boxer, Adam L, Gorno-Tempini, Maria L, Miller, Bruce L, Soleimani-Meigooni, David, Iaccarino, Leonardo, La Joie, Renaud, Baker, Suzanne, Borroni, Edilio, Klein, Gregory, Pontecorvo, Michael J, Devous, Michael D, Jagust, William J, Lyoo, Chul Hyoung, Rabinovici, Gil D, and Hansson, Oskar

Subjects
Biomedical and Clinical Sciences, Neurosciences, Clinical Sciences, Aging, Alzheimer's Disease, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Clinical Research, Prevention, Brain Disorders, Dementia, Neurodegenerative, Acquired Cognitive Impairment, Biomedical Imaging, Behavioral and Social Science, 4.1 Discovery and preclinical testing of markers and technologies, 2.1 Biological and endogenous factors, 4.2 Evaluation of markers and technologies, Neurological, Aged, Alzheimer Disease, Amyloid beta-Peptides, Apolipoproteins E, Carbolines, Cerebral Cortex, Female, Follow-Up Studies, Humans, Longitudinal Studies, Magnetic Resonance Imaging, Male, Mental Status and Dementia Tests, Middle Aged, Neuroimaging, Positron-Emission Tomography, Predictive Value of Tests, Prodromal Symptoms, Prognosis, Radiopharmaceuticals, Treatment Outcome, tau Proteins
Abstract

ImportanceTau positron emission tomography (PET) tracers have proven useful for the differential diagnosis of dementia, but their utility for predicting cognitive change is unclear.ObjectiveTo examine the prognostic accuracy of baseline fluorine 18 (18F)-flortaucipir and [18F]RO948 (tau) PET in individuals across the Alzheimer disease (AD) clinical spectrum and to perform a head-to-head comparison against established magnetic resonance imaging (MRI) and amyloid PET markers.Design, setting, and participantsThis prognostic study collected data from 8 cohorts in South Korea, Sweden, and the US from June 1, 2014, to February 28, 2021, with a mean (SD) follow-up of 1.9 (0.8) years. A total of 1431 participants were recruited from memory clinics, clinical trials, or cohort studies; 673 were cognitively unimpaired (CU group; 253 [37.6%] positive for amyloid-β [Aβ]), 443 had mild cognitive impairment (MCI group; 271 [61.2%] positive for Aβ), and 315 had a clinical diagnosis of AD dementia (315 [100%] positive for Aβ).Exposures[18F]Flortaucipir PET in the discovery cohort (n = 1135) or [18F]RO948 PET in the replication cohort (n = 296), T1-weighted MRI (n = 1431), and amyloid PET (n = 1329) at baseline and repeated Mini-Mental State Examination (MMSE) evaluation.Main outcomes and measuresBaseline [18F]flortaucipir/[18F]RO948 PET retention within a temporal region of interest, MRI-based AD-signature cortical thickness, and amyloid PET Centiloids were used to predict changes in MMSE using linear mixed-effects models adjusted for age, sex, education, and cohort. Mediation/interaction analyses tested whether associations between baseline tau PET and cognitive change were mediated by baseline MRI measures and whether age, sex, and APOE genotype modified these associations.ResultsAmong 1431 participants, the mean (SD) age was 71.2 (8.8) years; 751 (52.5%) were male. Findings for [18F]flortaucipir PET predicted longitudinal changes in MMSE, and effect sizes were stronger than for AD-signature cortical thickness and amyloid PET across all participants (R2, 0.35 [tau PET] vs 0.24 [MRI] vs 0.17 [amyloid PET]; P < .001, bootstrapped for difference) in the Aβ-positive MCI group (R2, 0.25 [tau PET] vs 0.15 [MRI] vs 0.07 [amyloid PET]; P

Published
2021

4. The impact of demographic, clinical, genetic, and imaging variables on tau PET status

Author

Ossenkoppele, Rik, Leuzy, Antoine, Cho, Hanna, Sudre, Carole H, Strandberg, Olof, Smith, Ruben, Palmqvist, Sebastian, Mattsson-Carlgren, Niklas, Olsson, Tomas, Jögi, Jonas, Stormrud, Erik, Ryu, Young Hoon, Choi, Jae Yong, Boxer, Adam L, Gorno-Tempini, Maria L, Miller, Bruce L, Soleimani-Meigooni, David, Iaccarino, Leonardo, La Joie, Renaud, Borroni, Edilio, Klein, Gregory, Pontecorvo, Michael J, Devous, Michael D, Villeneuve, Sylvia, Lyoo, Chul Hyoung, Rabinovici, Gil D, and Hansson, Oskar

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Neurodegenerative, Dementia, Acquired Cognitive Impairment, Clinical Research, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Biomedical Imaging, Cerebrovascular, Neurosciences, Aging, Brain Disorders, Alzheimer's Disease, 2.1 Biological and endogenous factors, Neurological, Alzheimer Disease, Amyloid beta-Peptides, Cognitive Dysfunction, Demography, Humans, Positron-Emission Tomography, tau Proteins, PET, Tau, A&#946, Alzheimer&#8217, s disease, MCI, Alzheimer’s Disease Neuroimaging Initiative, PREVENT-AD research group, Alzheimer’s disease, Aβ, Other Physical Sciences, Nuclear Medicine & Medical Imaging, Clinical sciences
Abstract

PurposeA substantial proportion of amyloid-β (Aβ)+ patients with clinically diagnosed Alzheimer's disease (AD) dementia and mild cognitive impairment (MCI) are tau PET-negative, while some clinically diagnosed non-AD neurodegenerative disorder (non-AD) patients or cognitively unimpaired (CU) subjects are tau PET-positive. We investigated which demographic, clinical, genetic, and imaging variables contributed to tau PET status.MethodsWe included 2338 participants (430 Aβ+ AD dementia, 381 Aβ+ MCI, 370 non-AD, and 1157 CU) who underwent [18F]flortaucipir (n = 1944) or [18F]RO948 (n = 719) PET. Tau PET positivity was determined in the entorhinal cortex, temporal meta-ROI, and Braak V-VI regions using previously established cutoffs. We performed bivariate binary logistic regression models with tau PET status (positive/negative) as dependent variable and age, sex, APOEε4, Aβ status (only in CU and non-AD analyses), MMSE, global white matter hyperintensities (WMH), and AD-signature cortical thickness as predictors. Additionally, we performed multivariable binary logistic regression models to account for all other predictors in the same model.ResultsTau PET positivity in the temporal meta-ROI was 88.6% for AD dementia, 46.5% for MCI, 9.5% for non-AD, and 6.1% for CU. Among Aβ+ participants with AD dementia and MCI, lower age, MMSE score, and AD-signature cortical thickness showed the strongest associations with tau PET positivity. In non-AD and CU participants, presence of Aβ was the strongest predictor of a positive tau PET scan.ConclusionWe identified several demographic, clinical, and neurobiological factors that are important to explain the variance in tau PET retention observed across the AD pathological continuum, non-AD neurodegenerative disorders, and cognitively unimpaired persons.

Published
2021

5. Four distinct trajectories of tau deposition identified in Alzheimer’s disease

Author

Vogel, Jacob W, Young, Alexandra L, Oxtoby, Neil P, Smith, Ruben, Ossenkoppele, Rik, Strandberg, Olof T, La Joie, Renaud, Aksman, Leon M, Grothe, Michel J, Iturria-Medina, Yasser, Pontecorvo, Michael J, Devous, Michael D, Rabinovici, Gil D, Alexander, Daniel C, Lyoo, Chul Hyoung, Evans, Alan C, and Hansson, Oskar

Subjects
Biomedical and Clinical Sciences, Health Sciences, Neurodegenerative, Dementia, Acquired Cognitive Impairment, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Neurosciences, Aging, Brain Disorders, Alzheimer's Disease, 2.1 Biological and endogenous factors, 4.1 Discovery and preclinical testing of markers and technologies, Neurological, Aged, Alzheimer Disease, Carbolines, Cerebral Cortex, Cognitive Dysfunction, Female, Humans, Male, Neuroimaging, Phenotype, Positron-Emission Tomography, Radiopharmaceuticals, Spatio-Temporal Analysis, tau Proteins, Alzheimer’s Disease Neuroimaging Initiative, Medical and Health Sciences, Immunology, Biomedical and clinical sciences, Health sciences
Abstract

Alzheimer's disease (AD) is characterized by the spread of tau pathology throughout the cerebral cortex. This spreading pattern was thought to be fairly consistent across individuals, although recent work has demonstrated substantial variability in the population with AD. Using tau-positron emission tomography scans from 1,612 individuals, we identified 4 distinct spatiotemporal trajectories of tau pathology, ranging in prevalence from 18 to 33%. We replicated previously described limbic-predominant and medial temporal lobe-sparing patterns, while also discovering posterior and lateral temporal patterns resembling atypical clinical variants of AD. These 'subtypes' were stable during longitudinal follow-up and were replicated in a separate sample using a different radiotracer. The subtypes presented with distinct demographic and cognitive profiles and differing longitudinal outcomes. Additionally, network diffusion models implied that pathology originates and spreads through distinct corticolimbic networks in the different subtypes. Together, our results suggest that variation in tau pathology is common and systematic, perhaps warranting a re-examination of the notion of 'typical AD' and a revisiting of tau pathological staging.

Published
2021

6. 18F‐flortaucipir tau positron emission tomography distinguishes established progressive supranuclear palsy from controls and Parkinson disease: A multicenter study

Author

Schonhaut, Daniel R, McMillan, Corey T, Spina, Salvatore, Dickerson, Bradford C, Siderowf, Andrew, Devous, Michael D, Tsai, Richard, Winer, Joseph, Russell, David S, Litvan, Irene, Roberson, Erik D, Seeley, William W, Grinberg, Lea T, Kramer, Joel H, Miller, Bruce L, Pressman, Peter, Nasrallah, Ilya, Baker, Suzanne L, Gomperts, Stephen N, Johnson, Keith A, Grossman, Murray, Jagust, William J, Boxer, Adam L, and Rabinovici, Gil D

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Neurosciences, Parkinson's Disease, Frontotemporal Dementia (FTD), Alzheimer's Disease Related Dementias (ADRD), Brain Disorders, Rare Diseases, Dementia, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Aging, Acquired Cognitive Impairment, Biomedical Imaging, Neurodegenerative, Clinical Research, 2.1 Biological and endogenous factors, 4.2 Evaluation of markers and technologies, Neurological, Good Health and Well Being, Aged, Aniline Compounds, Brain, Brain Mapping, Carbolines, Case-Control Studies, Cognition Disorders, Diagnosis, Female, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Neuropsychological Tests, Parkinson Disease, Positron-Emission Tomography, Severity of Illness Index, Supranuclear Palsy, Progressive, Thiazoles, tau Proteins, Neurology & Neurosurgery, Clinical sciences
Abstract

Objective18 F-flortaucipir (formerly 18 F-AV1451 or 18 F-T807) binds to neurofibrillary tangles in Alzheimer disease, but tissue studies assessing binding to tau aggregates in progressive supranuclear palsy (PSP) have yielded mixed results. We compared in vivo 18 F-flortaucipir uptake in patients meeting clinical research criteria for PSP (n = 33) to normal controls (n = 46) and patients meeting criteria for Parkinson disease (PD; n = 26).MethodsParticipants underwent magnetic resonance imaging and positron emission tomography for amyloid-β (11 C-PiB or 18 F-florbetapir) and tau (18 F-flortaucipir). 18 F-flortaucipir standardized uptake value ratios were calculated (t = 80-100 minutes, cerebellum gray matter reference). Voxelwise and region-of-interest group comparisons were performed in template space, with receiver operating characteristic curve analyses to assess single-subject discrimination. Qualitative comparisons with postmortem tau are reported in 1 patient who died 9 months after 18 F-flortaucipir.ResultsClinical PSP patients showed bilaterally elevated 18 F-flortaucipir uptake in globus pallidus, putamen, subthalamic nucleus, midbrain, and dentate nucleus relative to controls and PD patients (voxelwise p

Published
2017

7. 18 F-flortaucipir tau positron emission tomography distinguishes established progressive supranuclear palsy from controls and Parkinson disease: A multicenter study.

Author

Schonhaut, Daniel R, McMillan, Corey T, Spina, Salvatore, Dickerson, Bradford C, Siderowf, Andrew, Devous, Michael D, Tsai, Richard, Winer, Joseph, Russell, David S, Litvan, Irene, Roberson, Erik D, Seeley, William W, Grinberg, Lea T, Kramer, Joel H, Miller, Bruce L, Pressman, Peter, Nasrallah, Ilya, Baker, Suzanne L, Gomperts, Stephen N, Johnson, Keith A, Grossman, Murray, Jagust, William J, Boxer, Adam L, and Rabinovici, Gil D

Subjects
Brain, Humans, Parkinson Disease, Supranuclear Palsy, Progressive, Aniline Compounds, Carbolines, Thiazoles, tau Proteins, Diagnosis, Positron-Emission Tomography, Magnetic Resonance Imaging, Brain Mapping, Severity of Illness Index, Case-Control Studies, Cognition Disorders, Neuropsychological Tests, Aged, Middle Aged, Female, Male, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Neurodegenerative, Rare Diseases, Neurosciences, Dementia, Brain Disorders, Aging, Biomedical Imaging, Parkinson's Disease, Acquired Cognitive Impairment, Alzheimer's Disease, 2.1 Biological and endogenous factors, Neurological, Neurology & Neurosurgery, Clinical Sciences
Abstract

Objective18 F-flortaucipir (formerly 18 F-AV1451 or 18 F-T807) binds to neurofibrillary tangles in Alzheimer disease, but tissue studies assessing binding to tau aggregates in progressive supranuclear palsy (PSP) have yielded mixed results. We compared in vivo 18 F-flortaucipir uptake in patients meeting clinical research criteria for PSP (n = 33) to normal controls (n = 46) and patients meeting criteria for Parkinson disease (PD; n = 26).MethodsParticipants underwent magnetic resonance imaging and positron emission tomography for amyloid-β (11 C-PiB or 18 F-florbetapir) and tau (18 F-flortaucipir). 18 F-flortaucipir standardized uptake value ratios were calculated (t = 80-100 minutes, cerebellum gray matter reference). Voxelwise and region-of-interest group comparisons were performed in template space, with receiver operating characteristic curve analyses to assess single-subject discrimination. Qualitative comparisons with postmortem tau are reported in 1 patient who died 9 months after 18 F-flortaucipir.ResultsClinical PSP patients showed bilaterally elevated 18 F-flortaucipir uptake in globus pallidus, putamen, subthalamic nucleus, midbrain, and dentate nucleus relative to controls and PD patients (voxelwise p

Published
2017

8. Trauma, stress and alcoholism

Author

Yang, Hongyu, Spence, Jeffrey S, Briggs, Richard W, Rao, Uma, North, Carol, Devous, Michael D, Xiao, Hong, and Adinoff, Bryon

Subjects
Biological Psychology, Pharmacology and Pharmaceutical Sciences, Biomedical and Clinical Sciences, Psychology, Mental Health, Behavioral and Social Science, Clinical Research, Alcoholism, Alcohol Use and Health, Brain Disorders, Basic Behavioral and Social Science, Neurosciences, Substance Misuse, Mental health, Good Health and Well Being, Alcohol Abstinence, Alcoholism, Amygdala, Anticipation, Psychological, Anxiety, Case-Control Studies, Cerebral Cortex, Frontal Lobe, Humans, Magnetic Resonance Imaging, Male, Oxygen, Pain, Psychological Tests, Putamen, Stress, Psychological, brain imaging, childhood adversity, functional magnetic resonance imaging, maltreatment, striatum, Medical and Health Sciences, Psychology and Cognitive Sciences, Substance Abuse, Biomedical and clinical sciences, Health sciences
Abstract

Stress response biologic systems are altered in alcohol-dependent individuals. Early life stress (ELS) is associated with a heightened risk of alcohol dependence, presumably because of stress-induced neuroplastic changes. This study was designed to assess the contribution of ELS to a stress-induced neural response in alcohol-dependent participants. Fifteen alcohol-dependent men abstinent for 3-5 weeks and 15 age- and race-matched healthy controls were studied. Anticipatory anxiety was induced by a conditioned stimulus paired with an uncertain physically painful unconditioned stressor. Neural response was assessed with functional magnetic resonance imaging. ELS was assessed with the Childhood Adversity Interview. There was a significant interaction between ELS and group on blood-oxygen-level-dependent (BOLD) amplitude during anticipatory anxiety in the right amygdala and bilateral orbitofrontal cortex, posterior putamen and insula. Higher ELS scores were associated with decreased BOLD amplitude during anticipatory anxiety in alcohol-dependent, but not control, participants. These findings suggest that ELS interacts with alcohol dependence to induce a muted cortico-striatal response to high threat stimuli. Allostatic changes due to both ELS and excessive alcohol use may jointly induce persistent changes in the neural response to acute stressors.

Published
2015

9. Interaction between early life stress and alcohol dependence on neural stress reactivity.

Author

Yang, Hongyu, Spence, Jeffrey S, Briggs, Richard W, Rao, Uma, North, Carol, Devous, Michael D, Xiao, Hong, and Adinoff, Bryon

Subjects
Amygdala, Putamen, Cerebral Cortex, Frontal Lobe, Humans, Pain, Alcoholism, Oxygen, Magnetic Resonance Imaging, Case-Control Studies, Stress, Psychological, Anxiety, Psychological Tests, Male, Anticipation, Psychological, Alcohol Abstinence, brain imaging, childhood adversity, functional magnetic resonance imaging, maltreatment, striatum, Substance Abuse, Medical and Health Sciences, Psychology and Cognitive Sciences
Abstract

Stress response biologic systems are altered in alcohol-dependent individuals. Early life stress (ELS) is associated with a heightened risk of alcohol dependence, presumably because of stress-induced neuroplastic changes. This study was designed to assess the contribution of ELS to a stress-induced neural response in alcohol-dependent participants. Fifteen alcohol-dependent men abstinent for 3-5 weeks and 15 age- and race-matched healthy controls were studied. Anticipatory anxiety was induced by a conditioned stimulus paired with an uncertain physically painful unconditioned stressor. Neural response was assessed with functional magnetic resonance imaging. ELS was assessed with the Childhood Adversity Interview. There was a significant interaction between ELS and group on blood-oxygen-level-dependent (BOLD) amplitude during anticipatory anxiety in the right amygdala and bilateral orbitofrontal cortex, posterior putamen and insula. Higher ELS scores were associated with decreased BOLD amplitude during anticipatory anxiety in alcohol-dependent, but not control, participants. These findings suggest that ELS interacts with alcohol dependence to induce a muted cortico-striatal response to high threat stimuli. Allostatic changes due to both ELS and excessive alcohol use may jointly induce persistent changes in the neural response to acute stressors.

Published
2015

10. The Centiloid Project: Standardizing quantitative amyloid plaque estimation by PET

Author

Klunk, William E, Koeppe, Robert A, Price, Julie C, Benzinger, Tammie L, Devous, Michael D, Jagust, William J, Johnson, Keith A, Mathis, Chester A, Minhas, Davneet, Pontecorvo, Michael J, Rowe, Christopher C, Skovronsky, Daniel M, and Mintun, Mark A

Subjects
Biological Psychology, Psychology, Neurosciences, Dementia, Bioengineering, Neurodegenerative, Brain Disorders, Alzheimer's Disease, Biomedical Imaging, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Acquired Cognitive Impairment, Aging, Aged, Aged, 80 and over, Alzheimer Disease, Amyloid, Aniline Compounds, Brain, Calibration, Fluorodeoxyglucose F18, Humans, Image Interpretation, Computer-Assisted, Middle Aged, Plaque, Amyloid, Positron-Emission Tomography, Radiopharmaceuticals, Thiazoles, Amyloid imaging, Positron emission tomography, Pittsburgh compound B, Centiloid scale, Standardize, Clinical Sciences, Geriatrics, Clinical sciences, Biological psychology
Abstract

Although amyloid imaging with PiB-PET ([C-11]Pittsburgh Compound-B positron emission tomography), and now with F-18-labeled tracers, has produced remarkably consistent qualitative findings across a large number of centers, there has been considerable variability in the exact numbers reported as quantitative outcome measures of tracer retention. In some cases this is as trivial as the choice of units, in some cases it is scanner dependent, and of course, different tracers yield different numbers. Our working group was formed to standardize quantitative amyloid imaging measures by scaling the outcome of each particular analysis method or tracer to a 0 to 100 scale, anchored by young controls (≤ 45 years) and typical Alzheimer's disease patients. The units of this scale have been named "Centiloids." Basically, we describe a "standard" method of analyzing PiB PET data and then a method for scaling any "nonstandard" method of PiB PET analysis (or any other tracer) to the Centiloid scale.

Published
2015

11. CONCORDANCE BETWEEN VISUAL INTERPRETATION AND QUANTITATIVE ANALYSIS OF [18F]FLORTAUCIPIR PET IMAGES

Author

Moscoso, Alexis, primary, Heeman, Fiona, additional, Raghavan, Sheelakumari, additional, Sparrman, Kohl Johnson, additional, Costoya‐Sánchez, Alejandro, additional, Camacho, Valle, additional, van Essen, Martijn, additional, Grothe, Michel J., additional, Mainta, Isminni, additional, Ribaldi, Federica, additional, Devous, Michael D, additional, Pontecorvo, Michael J., additional, Frisoni, Giovanni B, additional, Garibotto, Valentina, additional, Petersen, Ronald C., additional, Jack, Clifford R., additional, Vemuri, Prashanthi, additional, and Schöll, Michael, additional

Published
2023
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13. Amyloid-&bgr; assessed by florbetapir F 18 PET and 18-month cognitive decline

Author

Doraiswamy, P Murali, Sperling, Reisa A, Coleman, R Edward, Johnson, Keith A, Reiman, Eric M, Davis, Mat D, Grundman, Michael, Sabbagh, Marwan N, Sadowsky, Carl H, Fleisher, Adam S, Carpenter, Alan, Clark, Christopher M, Joshi, Abhinay D, Mintun, Mark A, Skovronsky, Daniel M, Pontecorvo, Michael J, Duara, Ranjan, Sabbagh, Marwan, Ahern, Geoffrey Lawrence, Holub, Richard F, Farmer, Mildred V, Safirstein, Beth Emmie, Alva, Gustavo, Longmire, Crystal F, Jewell, George, Korn, Ron, Wendt, Jeanette K, Wong, Dean, Devous, Michael, Jennings, Danna, Weiner, Michael W, Murphy, Cynthia A, Kovnat, Karel D, and Williamson, Jeff D

Subjects
Acquired Cognitive Impairment, Neurosciences, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Brain Disorders, Clinical Research, Dementia, Aging, Alzheimer's Disease, Biomedical Imaging, Neurodegenerative, 4.2 Evaluation of markers and technologies, Detection, screening and diagnosis, Neurological, Aged, Alzheimer Disease, Amyloid beta-Peptides, Aniline Compounds, Brain, Cognition Disorders, Cognitive Dysfunction, Ethylene Glycols, Female, Follow-Up Studies, Humans, Longitudinal Studies, Male, Neuropsychological Tests, Positron-Emission Tomography, Predictive Value of Tests, Psychiatric Status Rating Scales, Psychomotor Performance, Radiopharmaceuticals, Risk, AV45-A11 Study Group, Clinical Sciences, Cognitive Sciences, Neurology & Neurosurgery
Abstract

ObjectivesFlorbetapir F 18 PET can image amyloid-β (Aβ) aggregates in the brains of living subjects. We prospectively evaluated the prognostic utility of detecting Aβ pathology using florbetapir PET in subjects at risk for progressive cognitive decline.MethodsA total of 151 subjects who previously participated in a multicenter florbetapir PET imaging study were recruited for longitudinal assessment. Subjects included 51 with recently diagnosed mild cognitive impairment (MCI), 69 cognitively normal controls (CN), and 31 with clinically diagnosed Alzheimer disease dementia (AD). PET images were visually scored as positive (Aβ+) or negative (Aβ-) for pathologic levels of β-amyloid aggregation, blind to diagnostic classification. Cerebral to cerebellar standardized uptake value ratios (SUVr) were determined from the baseline PET images. Subjects were followed for 18 months to evaluate changes in cognition and diagnostic status. Analysis of covariance and correlation analyses were conducted to evaluate the association between baseline PET amyloid status and subsequent cognitive decline.ResultsIn both MCI and CN, baseline Aβ+ scans were associated with greater clinical worsening on the Alzheimer's Disease Assessment Scale-Cognitive subscale (ADAS-Cog (p < 0.01) and Clinical Dementia Rating-sum of boxes (CDR-SB) (p < 0.02). In MCI Aβ+ scans were also associated with greater decline in memory, Digit Symbol Substitution (DSS), and Mini-Mental State Examination (MMSE) (p < 0.05). In MCI, higher baseline SUVr similarly correlated with greater subsequent decline on the ADAS-Cog (p < 0.01), CDR-SB (p < 0.03), a memory measure, DSS, and MMSE (p < 0.05). Aβ+ MCI tended to convert to AD dementia at a higher rate than Aβ- subjects (p < 0.10).ConclusionsFlorbetapir PET may help identify individuals at increased risk for progressive cognitive decline.

Published
2012

14. Predicting missing biomarker data in a longitudinal study of Alzheimer disease

Author

Lo, Raymond Y., Jagust, William J., Aisen, Paul, Jack, Clifford R., Toga, Arthur W., Beckett, Laurel, Gamst, Anthony, Soares, Holly, C. Green, Robert, Montine, Tom, Thomas, Ronald G., Donohue, Michael, Walter, Sarah, Dale, Anders, Bernstein, Matthew, Felmlee, Joel, Fox, Nick, Thompson, Paul, Schuff, Norbert, Alexander, Gene, DeCarli, Charles, Bandy, Dan, Chen, Kewei, Morris, John, Lee, Virginia M.-Y., Korecka, Magdalena, Crawford, Karen, Neu, Scott, Harvey, Danielle, Kornak, John, Saykin, Andrew J., Foroud, Tatiana M., Potkin, Steven, Shen, Li, Buckholtz, Neil, Kaye, Jeffrey, Dolen, Sara, Quinn, Joseph, Schneider, Lon, Pawluczyk, Sonia, Spann, Bryan M., Brewer, James, Vanderswag, Helen, Heidebrink, Judith L., Lord, Joanne L., Petersen, Ronald, Johnson, Kris, Doody, Rachelle S., Villanueva-Meyer, Javier, Chowdhury, Munir, Stern, Yaakov, Honig, Lawrence S., Bell, Karen L., Morris, John C., Mintun, Mark A., Schneider, Stacy, Marson, Daniel, Griffith, Randall, Clark, David, Grossman, Hillel, Tang, Cheuk, Marzloff, George, Toledo-Morrell, Leylade, Shah, Raj C., Duara, Ranjan, Varon, Daniel, Roberts, Peggy, Albert, Marilyn S., Pedroso, Julia, Toroney, Jaimie, Rusinek, Henry, de Leon, Mony J, De Santi, Susan M, Doraiswamy, P. Murali, Petrella, Jeffrey R., Aiello, Marilyn, Clark, Christopher M., Pham, Cassie, Nunez, Jessica, Smith, Charles D., Given, Curtis A., Hardy, Peter, Lopez, Oscar L., Oakley, MaryAnn, Simpson, Donna M., Ismail, M. Saleem, Brand, Connie, Richard, Jennifer, Mulnard, Ruth A., Thai, Gaby, Mc-Adams-Ortiz, Catherine, Diaz-Arrastia, Ramon, Martin-Cook, Kristen, DeVous, Michael, Levey, Allan I., Lah, James J., Cellar, Janet S., Burns, Jeffrey M., Anderson, Heather S., and Laubinger, Mary M.

Abstract

Objective:To investigate predictors of missing data in a longitudinal study of Alzheimer disease (AD).Methods:The Alzheimer's Disease Neuroimaging Initiative (ADNI) is a clinic-based, multicenter, longitudinal study with blood, CSF, PET, and MRI scans repeatedly measured in 229 participants with normal cognition (NC), 397 with mild cognitive impairment (MCI), and 193 with mild AD during 2005–2007. We used univariate and multivariable logistic regression models to examine the associations between baseline demographic/clinical features and loss of biomarker follow-ups in ADNI.Results:CSF studies tended to recruit and retain patients with MCI with more AD-like features, including lower levels of baseline CSF Aβ42. Depression was the major predictor for MCI dropouts, while family history of AD kept more patients with AD enrolled in PET and MRI studies. Poor cognitive performance was associated with loss of follow-up in most biomarker studies, even among NC participants. The presence of vascular risk factors seemed more critical than cognitive function for predicting dropouts in AD.Conclusion:The missing data are not missing completely at random in ADNI and likely conditional on certain features in addition to cognitive function. Missing data predictors vary across biomarkers and even MCI and AD groups do not share the same missing data pattern. Understanding the missing data structure may help in the design of future longitudinal studies and clinical trials in AD.

Published
2012

20. CONCORDANCE BETWEEN VISUAL INTERPRETATION AND QUANTITATIVE ANALYSIS OF [18F]FLORTAUCIPIR PET IMAGES.

Author

Moscoso, Alexis, Heeman, Fiona, Raghavan, Sheelakumari, Sparrman, Kohl Johnson, Costoya‐Sánchez, Alejandro, Camacho, Valle, van Essen, Martijn, Grothe, Michel J., Mainta, Isminni, Ribaldi, Federica, Devous, Michael D, Pontecorvo, Michael J., Frisoni, Giovanni B, Garibotto, Valentina, Petersen, Ronald C., Jack, Clifford R., Vemuri, Prashanthi, and Schöll, Michael

Abstract

Background: Positron emission tomography (PET) imaging with [18F]flortaucipir allows for in‐vivo visualization of aggregated tau in Alzheimer's disease (AD). The FDA‐approved label for [18F]flortaucipir PET provides a standardized, clinically applicable definition of tau‐PET positivity by visual interpretation. Here, we studied the concordance between this visual interpretation and quantitative approaches employed in research. Method: We included 2692 participants (cognitively unimpaired [CU] and impaired [CI, MCI or AD dementia]) from four cohorts (Mayo Clinic Study of Aging and ADRC, ADNI, A4, and A05) with available [18F]flortaucipir PET (mean age: 70.2 y, 50.0% females). Three trained readers assessed each [18F]flortaucipir PET scan according to the FDA‐approved method. Visual reads were compared to an established approach for defining tau‐PET positivity based on SUVR values in a temporal meta‐ROI (Jack, et al. Alzheimers Dement. 2017). Previously defined "lenient" (SUVR = 1.22) and "conservative" (SUVR = 1.30) cut‐points were explored. In addition, visual reads were compared to tau‐PET positivity as defined by a scheme based on the expected spatial progression of tau pathology from the medial temporal lobe (MTL) to the temporal neocortex (NEO) (Ossenkoppele, et al. Nat Med. 2022; cut‐points: SUVRMTL = 1.30, SUVRNEO = 1.37). Result: Concordance between visual and quantitative approaches was limited (Figure 1): the "lenient" and MTL‐NEO methods yielded high rates of quantitative‐positive, visual‐negative scans (73‐52% and 26‐18% for CU and CI, respectively), while the "conservative" cut‐point failed to detect 45% and 13% of the CU and CI visual‐positive scans, respectively. The prevalence of tau‐PET positivity in Aβ‐negative individuals was highest with the "lenient" cut‐point (∼24%) and lowest with visual interpretation (∼3%) (Figure 2). Visual‐positive, quantitative‐negative individuals were more frequently Aβ‐positive than visual‐negative, quantitative‐positive individuals ("lenient": 86% vs 50%, p<0.001; "conservative": 87% vs 58%, p<0.001; MTL‐NEO: 85% vs 70%, p = 0.005). Among visually‐positive participants, 164 (28%) showed a tau deposition pattern that deviated from the expected MTL to NEO progression (Figure 3). Conclusion: Visual and quantitative methods for [18F]flortaucipir PET are non‐exchangeable. Tau‐PET positivity based on visual interpretation aligns better with Aβ‐pathology. A significant number of visually‐positive participants showed a pattern of tau accumulation that deviated from the expected stereotypical spatial progression and was not detected by standard quantitative methods. [ABSTRACT FROM AUTHOR]

Published
2023
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22. Quantification of Tau Load Using [18F]AV1451 PET

Author

Golla, Sandeep S. V., Timmers, Tessa, Ossenkoppele, Rik, Groot, Colin, Verfaillie, Sander, Scheltens, Philip, van der Flier, Wiesje M., Schwarte, Lothar, Mintun, Mark A., Devous, Michael, Schuit, Robert C., Windhorst, Albert D., Lammertsma, Adriaan A., Boellaard, Ronald, van Berckel, Bart N. M., and Yaqub, Maqsood

Published
2017
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23. Early tau detection in flortaucipir images: validation in autopsy-confirmed data and implications for disease progression

Author

Kotari, Vikas, primary, Southekal, Sudeepti, additional, Navitsky, Michael, additional, Kennedy, Ian A., additional, Lu, Ming, additional, Morris, Amanda, additional, Zimmer, Jennifer Ann, additional, Fleisher, Adam S., additional, Mintun, Mark A., additional, Devous, Michael D., additional, and Pontecorvo, Michael J., additional

Published
2023
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25. Relationship between [ 18 F]flortaucipir PET visual patterns and neurodegeneration

Author

Heeman, Fiona, primary, Moscoso, Alexis, additional, Camacho, Valle, additional, van Essen, Martijn, additional, Grothe, Michel J., additional, Lin, Li, additional, Mainta, Isminni, additional, Ribaldi, Federica, additional, Devous, Michael D., additional, Pontecorvo, Michael J., additional, Frisoni, Giovanni B, additional, Garibotto, Valentina, additional, and Schöll, Michael, additional

Published
2022
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26. Prevalence and longitudinal clinical outcomes of negative, moderate, and advanced [18F]flortaucipir PET visual patterns across the Alzheimer's disease spectrum

Author

Moscoso, Alexis, primary, Heeman, Fiona, additional, Camacho, Valle, additional, van Essen, Martijn, additional, Grothe, Michel J., additional, Lin, Li, additional, Mainta, Isminni, additional, Ribaldi, Federica, additional, Devous, Michael D., additional, Pontecorvo, Michael J., additional, Frisoni, Giovanni B, additional, Garibotto, Valentina, additional, and Schöll, Michael, additional

Published
2022
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27. Prevalence and longitudinal clinical outcomes of negative, moderate, and advanced 18F‐flortaucipir PET visual patterns in aging and Alzheimer’s disease

Author

Moscoso, Alexis, primary, Heeman, Fiona, additional, Camacho, Valle, additional, van Essen, Martijn, additional, Grothe, Michel J., additional, Lin, Li, additional, Mainta, Isminni, additional, Ribaldi, Federica, additional, Devous, Michael D., additional, Pontecorvo, Michael J., additional, Frisoni, Giovanni B, additional, Garibotto, Valentina, additional, and Schöll, Michael, additional

Published
2022
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28. Type 2 diabetes mellitus, brain atrophy, and cognitive decline

Author

Moran, Chris, Beare, Richard, Wang, Wei, Callisaya, Michele, Srikanth, Velandai, Weiner, Michael, Aisen, Paul, Weiner, Michael, Aisen, Paul, Petersen, Ronald, Jack, Clifford R., Jr., Jagust, William, Trojanowki, John Q., Toga, Arthur W., Beckett, Laurel, Green, Robert C., Saykin, Andrew J., Morris, John, Liu, Enchi, Green, Robert C., Montine, Tom, Petersen, Ronald, Aisen, Paul, Gamst, Anthony, Thomas, Ronald G., Donohue, Michael, Walter, Sarah, Gessert, Devon, Sather, Tamie, Beckett, Laurel, Harvey, Danielle, Gamst, Anthony, Donohue, Michael, Kornak, John, Jack, Clifford R., Jr., Dale, Anders, Bernstein, Matthew, Felmlee, Joel, Fox, Nick, Thompson, Paul, Schuff, Norbert, Alexander, Gene, DeCarli, Charles, Jagust, William, Bandy, Dan, Koeppe, Robert A., Foster, Norm, Reiman, Eric M., Chen, Kewei, Mathis, Chet, Morris, John, Cairns, Nigel J., Taylor-Reinwald, Lisa, Trojanowki, J.Q., Shaw, Les, Lee, Virginia M.Y., Korecka, Magdalena, Toga, Arthur W., Crawford, Karen, Neu, Scott, Saykin, Andrew J., Foroud, Tatiana M., Potkin, Steven, Shen, Li, Kachaturian, Zaven, Frank, Richard, Snyder, Peter J., Molchan, Susan, Kaye, Jeffrey, Quinn, Joseph, Lind, Betty, Dolen, Sara, Schneider, Lon S., Pawluczyk, Sonia, Spann, Bryan M., Brewer, James, Vanderswag, Helen, Heidebrink, Judith L., Lord, Joanne L., Petersen, Ronald, Johnson, Kris, Doody, Rachelle S., Villanueva-Meyer, Javier, Chowdhury, Munir, Stern, Yaakov, Honig, Lawrence S., Bell, Karen L., Morris, John C., Ances, Beau, Carroll, Maria, Leon, Sue, Mintun, Mark A., Schneider, Stacy, Marson, Daniel, Griffith, Randall, Clark, David, Grossman, Hillel, Mitsis, Effie, Romirowsky, Aliza, deToledo-Morrell, Leyla, Shah, Raj C., Duara, Ranjan, Varon, Daniel, Roberts, Peggy, Albert, Marilyn, Onyike, Chiadi, Kielb, Stephanie, Rusinek, Henry, de Leon, Mony J, Glodzik, Lidia, De Santi, Susan, Doraiswamy, P. Murali, Petrella, Jeffrey R., Coleman, R. Edward, Arnold, Steven E., Karlawish, Jason H., Wolk, David, Smith, Charles D., Jicha, Greg, Hardy, Peter, Lopez, Oscar L., Oakley, MaryAnn, Simpson, Donna M., Porsteinsson, Anton P., Goldstein, Bonnie S., Martin, Kim, Makino, Kelly M., Ismail, M. Saleem, Brand, Connie, Mulnard, Ruth A., Thai, Gaby, McAdams-Ortiz, Catherine, Womack, Kyle, Mathews, Dana, Quiceno, Mary, Diaz-Arrastia, Ramon, King, Richard, Weiner, Myron, Martin-Cook, Kristen, DeVous, Michael, Levey, Allan I., Lah, James J., Cellar, Janet S., Burns, Jeffrey M., Anderson, Heather S., Swerdlow, Russell H., Apostolova, Liana, Lu, Po H., Bartzokis, George, Silverman, Daniel H.S., Graff-Radford, Neill R, Parfitt, Francine, Johnson, Heather, Farlow, Martin R., Hake, Ann Marie, Matthews, Brandy R., Herring, Scott, van Dyck, Christopher H., Carson, Richard E., MacAvoy, Martha G., Chertkow, Howard, Bergman, Howard, Hosein, Chris, Black, Sandra, Stefanovic, Bojana, Caldwell, Curtis, Robin Hsiung, Ging-Yuek, Feldman, Howard, Mudge, Benita, Assaly, Michele, Kertesz, Andrew, Rogers, John, Trost, Dick, Bernick, Charles, Munic, Donna, Kerwin, Diana, Mesulam, Marek-Marsel, Lipowski, Kristina, Wu, Chuang-Kuo, Johnson, Nancy, Sadowsky, Carl, Martinez, Walter, Villena, Teresa, Turner, Raymond Scott, Johnson, Kathleen, Reynolds, Brigid, Sperling, Reisa A., Johnson, Keith A., Marshall, Gad, Frey, Meghan, Yesavage, Jerome, Taylor, Joy L., Lane, Barton, Rosen, Allyson, Tinklenberg, Jared, Sabbagh, Marwan, Belden, Christine, Jacobson, Sandra, Kowall, Neil, Killiany, Ronald, Budson, Andrew E., Norbash, Alexander, Johnson, Patricia Lynn, Obisesan, Thomas O., Wolday, Saba, Bwayo, Salome K., Lerner, Alan, Hudson, Leon, Ogrocki, Paula, Fletcher, Evan, Carmichael, Owen, Olichney, John, DeCarli, Charles, Kittur, Smita, Borrie, Michael, Lee, T-Y, Bartha, Dr Rob, Johnson, Sterling, Asthana, Sanjay, Carlsson, Cynthia M., Potkin, Steven G., Preda, Adrian, Nguyen, Dana, Tariot, Pierre, Fleisher, Adam, Reeder, Stephanie, Bates, Vernice, Capote, Horacio, Rainka, Michelle, Scharre, Douglas W., Kataki, Maria, Zimmerman, Earl A., Celmins, Dzintra, Brown, Alice D., Pearlson, Godfrey D., Blank, Karen, Anderson, Karen, Saykin, Andrew J., Santulli, Robert B., Schwartz, Eben S., Sink, Kaycee M., Williamson, Jeff D., Garg, Pradeep, Watkins, Franklin, Ott, Brian R., Querfurth, Henry, Tremont, Geoffrey, Salloway, Stephen, Malloy, Paul, Correia, Stephen, Rosen, Howard J., Miller, Bruce L., Mintzer, Jacobo, Longmire, Crystal Flynn, Spicer, Kenneth, Finger, Elizabether, Rachinsky, Irina, Rogers, John, Kertesz, Andrew, Drost, Dick, Pomara, Nunzio, Hernando, Raymundo, Sarrael, Antero, Schultz, Susan K., Boles Ponto, Laura L., Shim, Hyungsub, Smith, Karen Elizabeth, Relkin, Norman, Chaing, Gloria, Raudin, Lisa, Smith, Amanda, Fargher, Kristin, and Raj, Balebail Ashok

Published
2019
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30. Maturation of Speech and Language Functional Neuroanatomy in Pediatric Normal Controls

Author

Devous, Michael D.,, Altuna, Dianne, and Furl, Nicholas, Cooper, William

Abstract

Purpose: This study explores the relationship between age and resting-state regional cerebral blood flow (rCBF) in regions associated with higher order language skills using a population of normal children, adolescents, and young adults. Method: rCBF was measured in 33 normal participants between the ages of 7 and 19 years using single photon emission computed tomography. Participants' ages were regressed on rCBF values (normalized to whole-brain CBF) in 2 ways: (a) within anatomically defined, language-related regions of interest (ROIs) including Wernicke's area, Broca's area, angular gyrus, planum temporale, and Heschl's gyrus and (b) within clusters of voxels found to be significantly related to age in voxel-wise analyses. Results: rCBF in all anatomically defined ROIs except Heschl's gyrus declined as a function of age. Additionally, voxel-wise analyses revealed clusters where rCBF declined with age in left inferior parietal, left superior temporal, and right middle temporal regions--areas often implicated in higher order language functions. Conclusions: These data suggest that ongoing maturation (e.g., dendritic pruning) in higher order cognitive areas (e.g., angular gyrus) continues into adolescence, as reflected by declining rCBF, while the primary auditory area (Heschl's gyrus) has become a stable neuronal population by age 7 years.

Published
2006

34. Glucose metabolism patterns: A potential index to characterize brain ageing and predict high conversion risk into cognitive impairment

Author

Jiang, Jiehui, Sheng, Can, Aisen, Paul, Dang, Mimi, Stern, Yaakov, Honig, Lawrence S, Bell, Karen L, Ances, Beau, Carroll, Maria, Leon, Sue, Mintun, Mark A, Schneider, Stacy, Oliver, Angela, Petersen, Ronald, Marson, Daniel, Griffith, Randall, Clark, David, Geldmacher, David, Brockington, John, Roberson, Erik, Grossman, Hillel, Mitsis, Effie, de Toledo-Morrell, Leyla, Shah, Raj C, Jack, Clifford R, Duara, Ranjan, Varon, Daniel, Greig, Maria T, Roberts, Peggy, Onyike, Chiadi, D'Agostino, Daniel, Kielb, Stephanie, Galvin, James E, Cerbone, Brittany, Michel, Christina A, Jagust, William, Rusinek, Henry, de Leon, Mony J, Glodzik, Lidia, De Santi, Susan, Murali Doraiswamy, P., Petrella, Jeffrey R, Wong, Terence Z, Arnold, Steven E, Karlawish, Jason H, Wolk, David, Trojanowski, John Q, Smith, Charles D, Jicha, Greg, Hardy, Peter, Sinha, Partha, Oates, Elizabeth, Conrad, Gary, Lopez, Oscar L, Oakley, MaryAnn, Simpson, Donna M, Porsteinsson, Anton P, Toga, Arthur W, Goldstein, Bonnie S, Martin, Kim, Makino, Kelly M, Saleem Ismail, M., Brand, Connie, Mulnard, Ruth A, Thai, Gaby, McAdams-Ortiz, Catherine, Womack, Kyle, Mathews, Dana, Beckett, Laurel, Quiceno, Mary, Diaz-Arrastia, Ramon, King, Richard, Weiner, Myron, Martin-Cook, Kristen, DeVous, Michael, I Levey, Allan, Lah, James J, Cellar, Janet S, Burns, Jeffrey M, Green, Robert C, Anderson, Heather S, Swerdlow, Russell H, Apostolova, Liana, Tingus, Kathleen, Woo, Ellen, Silverman, Daniel H S, Lu, Po H, Bartzokis, George, Graff-Radford, Neill R, Parfitt, Francine, Saykin, Andrew J, Kendall, Tracy, Johnson, Heather, Farlow, Martin R, Hake, Ann Marie, Matthews, Brandy R, Herring, Scott, Hunt, Cynthia, van Dyck, Christopher H, Carson, Richard E, MacAvoy, Martha G, Morris, John, Chertkow, Howard, Bergman, Howard, Hosein, Chris, Robin Hsiung, Ging-Yuek, Feldman, Howard, Mudge, Benita, Assaly, Michele, Bernick, Charles, Munic, Donna, Kertesz, Andrew, Chen, Guanqun, Shaw, Leslie, Rogers, John, Trost, Dick, Kerwin, Diana, Lipowski, Kristine, Wu, Chuang-Kuo, Johnson, Nancy, Sadowsky, Carl, Martinez, Walter, Villena, Teresa, Turner, Raymond Scott, Khachaturian, Zaven, Johnson, Kathleen, Reynolds, Brigid, Sperling, Reisa A, Johnson, Keith A, Marshall, Gad, Frey, Meghan, Lane, Barton, Rosen, Allyson, Tinklenberg, Jared, Sabbagh, Marwan N, Sorensen, Greg, Belden, Christine M, Jacobson, Sandra A, Sirrel, Sherye A, Kowall, Neil, Killiany, Ronald, Budson, Andrew E, Norbash, Alexander, Johnson, Patricia Lynn, Allard, Joanne, Lerner, Alan, Kuller, Lew, Ogrocki, Paula, Hudson, Leon, Fletcher, Evan, Carmichae, Owen, Olichney, John, DeCarli, Charles, Kittur, Smita, Borrie, Michael, Lee, T-Y, Bartha, Rob, Raichle, Marcus, Johnson, Sterling, Asthana, Sanjay, Carlsson, Cynthia M, Preda, Adrian, Nguyen, Dana, Tariot, Pierre, Reeder, Stephanie, Bates, Vernice, Capote, Horacio, Rainka, Michelle, Paul, Steven, Scharre, Douglas W, Kataki, Maria, Adeli, Anahita, Zimmerman, Earl A, Celmins, Dzintra, Brown, Alice D, Pearlson, Godfrey D, Blank, Karen, Anderson, Karen, Santulli, Robert B, Davies, Peter, Kitzmiller, Tamar J, Schwartz, Eben S, Sink, Kaycee M, Williamson, Jeff D, Garg, Pradeep, Watkins, Franklin, Ott, Brian R, Querfurth, Henry, Tremont, Geoffrey, Salloway, Stephen, Fillit, Howard, Malloy, Paul, Correia, Stephen, Rosen, Howard J, Miller, Bruce L, Mintzer, Jacobo, Spicer, Kenneth, Bachman, David, Pasternak, Stephen, Rachinsky, Irina, Drost, Dick, Hefti, Franz, Pomara, Nunzio, Hernando, Raymundo, Sarrael, Antero, Schultz, Susan K, Ponto, Laura L Boles, Shim, Hyungsub, Elizabeth Smith, Karen, Relkin, Norman, Chaing, Gloria, Raudin, Lisa, Holtzman, David, Smith, Amanda, Fargher, Kristin, Raj, Balebail Ashok, Neylan, Thomas, Grafman, Jordan, Davis, Melissa, Morrison, Rosemary, Hayes, Jacqueline, Finley, Shannon, Friedl, Karl, Liu, Chunhua, Mesulam, Marek M, Fleischman, Debra, Arfanakis, Konstantinos, James, Olga, Massoglia, Dino, Jay Fruehling, J., Harding, Sandra, Peskind, Elaine R, Petrie, Eric C, Li, Gail, Yesavage, Jerome A, Potter, William, Taylor, Joy L, Furst, Ansgar J, Snyder, Peter, Schwartz, Adam, Montine, Tom, Thomas, Ronald G, Donohue, Michael, Walter, Sarah, Gessert, Devon, Sather, Tamie, Jin, Shichen, Jiminez, Gus, Harvey, Danielle, Bernstein, Matthew, Thompson, Paul, Schuff, Norbert, Borowski, Bret, Gunter, Jeff, Senjem, Matt, Vemuri, Prashanthi, Jones, David, Li, Lanlan, Kantarci, Kejal, Ward, Chad, Koeppe, Robert A, Foster, Norm, Reiman, Eric M, Chen, Kewei, Mathis, Chet, Landau, Susan, Cairns, Nigel J, Householder, Erin, Jiang, Xueyan, Taylor-Reinwald, Lisa, Lee, Virginia, Korecka, Magdalena, Figurski, Michal, Crawford, Karen, Neu, Scott, Foroud, Tatiana M, Potkin, Steven G, Shen, Li, Faber, Kelley, Han, Ying, Kim, Sungeun, Nho, Kwangsik, Thal, Leon, Buckholtz, Neil, Albert, Marylyn, Frank, Richard, Hsiao, John, Kaye, Jeffrey, Quinn, Joseph, Lind, Betty, Initiative, Alzheimer’s Disease Neuroimaging, Carter, Raina, Dolen, Sara, Schneider, Lon S, Pawluczyk, Sonia, Beccera, Mauricio, Teodoro, Liberty, Spann, Bryan M, Brewer, James, Vanderswag, Helen, Fleisher, Adam, Weiner, Michael W, Heidebrink, Judith L, Lord, Joanne L, Mason, Sara S, Albers, Colleen S, Knopman, David S, Johnson, Kris, Doody, Rachelle S, Villanueva-Meyer, Javier, Chowdhury, Munir, and Rountree, Susan

Subjects
Glucose metabolism, Positron emission tomography, Aging, Pattern, Brain, Glucose, Brain ageing, Alzheimer Disease, Fluorodeoxyglucose F18, Positron-Emission Tomography, Humans, Original Article, Cognitive Dysfunction, ddc:610, Geriatrics and Gerontology, Aged
Abstract

Exploring individual hallmarks of brain ageing is important. Here, we propose the age-related glucose metabolism pattern (ARGMP) as a potential index to characterize brain ageing in cognitively normal (CN) elderly people. We collected (18)F-fluorodeoxyglucose ((18)F-FDG) PET brain images from two independent cohorts: the Alzheimer’s Disease Neuroimaging Initiative (ADNI, N = 127) and the Xuanwu Hospital of Capital Medical University, Beijing, China (N = 84). During follow-up (mean 80.60 months), 23 participants in the ADNI cohort converted to cognitive impairment. ARGMPs were identified using the scaled subprofile model/principal component analysis method, and cross-validations were conducted in both independent cohorts. A survival analysis was further conducted to calculate the predictive effect of conversion risk by using ARGMPs. The results showed that ARGMPs were characterized by hypometabolism with increasing age primarily in the bilateral medial superior frontal gyrus, anterior cingulate and paracingulate gyri, caudate nucleus, and left supplementary motor area and hypermetabolism in part of the left inferior cerebellum. The expression network scores of ARGMPs were significantly associated with chronological age (R = 0.808, p

Published
2022
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35. Increased Medial Temporal Tau Positron Emission Tomography Uptake in the Absence of Amyloid-β Positivity

Author

Costoya-Sánchez, Alejandro, Moscoso, Alexis, Silva-Rodríguez, Jesús, Pontecorvo, Michael J., Devous, Michael D., Aguiar, Pablo, Schöll, Michael, and Grothe, Michel J.

Abstract

IMPORTANCE: An increased tau positron emission tomography (PET) signal in the medial temporal lobe (MTL) has been observed in older individuals in the absence of amyloid-β (Aβ) pathology. Little is known about the longitudinal course of this condition, and its association with Alzheimer disease (AD) remains unclear. OBJECTIVE: To study the pathologic and clinical course of older individuals with PET-evidenced MTL tau deposition (TMTL+) in the absence of Aβ pathology (A−), and the association of this condition with the AD continuum. DESIGN, SETTING, AND PARTICIPANTS: A multicentric, observational, longitudinal cohort study was conducted using pooled data from the Alzheimer’s Disease Neuroimaging Initiative (ADNI), Harvard Aging Brain Study (HABS), and the AVID-A05 study, collected between July 2, 2015, and August 23, 2021. Participants in the ADNI, HABS, and AVID-A05 studies (N = 1093) with varying degrees of cognitive performance were deemed eligible if they had available tau PET, Aβ PET, and magnetic resonance imaging scans at baseline. Of these, 128 participants did not meet inclusion criteria based on Aβ PET and tau PET biomarker profiles (A+ TMTL−). EXPOSURES: Tau and Aβ PET, magnetic resonance imaging, cerebrospinal fluid biomarkers, and cognitive assessments. MAIN OUTCOMES AND MEASURES: Cross-sectional and longitudinal measures for tau and Aβ PET, cortical atrophy, cognitive scores, and core AD cerebrospinal fluid biomarkers (Aβ42/40 and tau phosphorylated at threonine 181 p-tau181 available in a subset). RESULTS: Among the 965 individuals included in the study, 503 were women (52.1%) and the mean (SD) age was 73.9 (8.1) years. A total of 51% of A− individuals and 78% of A+ participants had increased tau PET signal in the entorhinal cortex (TMTL+) compared with healthy younger (aged &lt;39 years) controls. Compared with A− TMTL−, A− TMTL+ participants showed statistically significant, albeit moderate, longitudinal (mean [SD], 1.83 [0.84] years) tau PET increases that were largely limited to the temporal lobe, whereas those with A+ TMTL+ showed faster and more cortically widespread tau PET increases. In contrast to participants with A+ TMTL+, those with A− TMTL+ did not show any noticeable Aβ accumulation over follow-up (mean [SD], 2.36 [0.76] years). Complementary cerebrospinal fluid analysis confirmed longitudinal p-tau181 increases in A− TMTL+ in the absence of increased Aβ accumulation. Participants with A− TMTL+ had accelerated MTL atrophy, whereas those with A+ TMTL+ showed accelerated atrophy in widespread temporoparietal brain regions. Increased MTL tau PET uptake in A− individuals was associated with cognitive decline, but at a significantly slower rate compared with A+ TMTL+. CONCLUSIONS AND RELEVANCE: In this study, individuals with A− TMTL+ exhibited progressive tau accumulation and neurodegeneration, but these processes were comparably slow, remained largely restricted to the MTL, were associated with only subtle changes in global cognitive performance, and were not accompanied by detectable accumulation of Aβ biomarkers. These data suggest that individuals with A− TMTL+ are not on a pathologic trajectory toward AD.

Published
2023
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39. Tau PET as a prognostic marker in preclinical and prodromal Alzheimer’s disease

Author

Ossenkoppele, Rik, primary, Mattsson, Niklas, additional, Smith, Ruben, additional, Groot, Colin, additional, Cho, Hanna, additional, La Joie, Renaud, additional, Baker, Suzanne L., additional, Borroni, Edilio, additional, Klein, Gregory, additional, Pontecorvo, Michael J., additional, Devous, Michael D., additional, Jagust, William J., additional, Lyoo, Chul Hyoung, additional, Rabinovici, Gil D., additional, and Hansson, Oskar, additional

Published
2021
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43. KL-VS heterozygosity is associated with lower amyloid-dependent tau accumulation and memory impairment in Alzheimer’s disease

Author

Neitzel, Julia, Franzmeier, Nicolai, Petersen, Ronald, Clark, David, Geldmacher, David, Brockington, John, Roberson, Erik, Grossman, Hillel, Mitsis, Effie, deToledo-Morrell, Leyla, Shah, Raj C, Duara, Ranjan, Varon, Daniel, Jack, Clifford R, Greig, Maria T, Roberts, Peggy, Albert, Marilyn, Onyike, Chiadi, D'Agostino, Daniel, Kielb, Stephanie, Galvin, James E, Pogorelec, Dana M, Cerbone, Brittany, Michel, Christina A, Jagust, William, Rusinek, Henry, de Leon, Mony J, Glodzik, Lidia, De Santi, Susan, Doraiswamy, P Murali, Petrella, Jeffrey R, Wong, Terence Z, Arnold, Steven E, Karlawish, Jason H, Wolk, David, Trojanowki, John Q, Smith, Charles D, Jicha, Greg, Hardy, Peter, Sinha, Partha, Oates, Elizabeth, Conrad, Gary, Lopez, Oscar L, Oakley, MaryAnn, Simpson, Donna M, Porsteinsson, Anton P, Toga, Arthur W, Goldstein, Bonnie S, Martin, Kim, Makino, Kelly M, Ismail, Muhammad, Brand, Connie, Mulnard, Ruth A, Thai, Gaby, Mc Adams Ortiz, Catherine, Womack, Kyle, Mathews, Dana, Beckett, Laurel, Quiceno, Mary, Arrastia, Ramon Diaz, King, Richard, Weiner, Myron, Cook, Kristen Martin, DeVous, Michael, Levey, Allan I, Lah, James J, Cellar, Janet S, Burns, Jeffrey M, Green, Robert C, Anderson, Heather S, Swerdlow, Russell H, Apostolova, Liana, Tingus, Kathleen, Woo, Ellen, Silverman, Daniel H S, Lu, Po H, Bartzokis, George, Radford, Neill R Graff, ParfittH, Francine, Saykin, Andrew J, Kendall, Tracy, Johnson, Heather, Farlow, Martin R, Hake, Ann Marie, Matthews, Brandy R, Herring, Scott, Hunt, Cynthia, van Dyck, Christopher H, Carson, Richard E, MacAvoy, Martha G, Morris, John, Chertkow, Howard, Bergman, Howard, Hosein, Chris, Black, Sandra, Stefanovic, Bojana, Caldwell, Curtis, Hsiung, Ging Yuek Robin, Feldman, Howard, Mudge, Benita, Past, Michele Assaly, Shaw, Leslie, Kertesz, Andrew, Rogers, John, Trost, Dick, Bernick, Charles, Munic, Donna, Kerwin, Diana, Mesulam, Marek Marsel, Lipowski, Kristine, Wu, Chuang Kuo, Johnson, Nancy, Rubinski, Anna, Liu, Enchi, Sadowsky, Carl, Martinez, Walter, Villena, Teresa, Turner, Raymond Scott, Johnson, Kathleen, Reynolds, Brigid, Sperling, Reisa A, Johnson, Keith A, Marshall, Gad, Frey, Meghan, Montine, Tom, Yesavage, Jerome, Taylor, Joy L, Lane, Barton, Rosen, Allyson, Tinklenberg, Jared, Sabbagh, Marwan N, Belden, Christine M, Jacobson, Sandra A, Sirrel, Sherye A, Kowall, Neil, Thomas, Ronald G, Killiany, Ronald, Budson, Andrew E, Norbash, Alexander, Johnson, Patricia Lynn, Obisesan, Thomas O, Wolday, Saba, Allard, Joanne, Lerner, Alan, Ogrocki, Paula, Hudson, Leon, Donohue, Michael, Fletcher, Evan, Carmichael, Owen, Olichney, John, DeCarli, Charles, Kittur, Smita, Borrie, Michael, Lee, T. Y., Bartha, Rob, Johnson, Sterling, Asthana, Sanjay, Walter, Sarah, Carlsson, Cynthia M, Potkin, Steven G, Preda, Adrian, Nguyen, Dana, Tariot, Pierre, Reeder, Stephanie, Bates, Vernice, Capote, Horacio, Rainka, Michelle, Scharre, Douglas W, Gessert, Devon, Kataki, Maria, Adeli, Anahita, Zimmerman, Earl A, Celmins, Dzintra, Brown, Alice D, Pearlson, Godfrey D, Blank, Karen, Anderson, Karen, Santulli, Robert B, Kitzmiller, Tamar J, Sather, Tamie, Schwartz, Eben S, SinkS, Kaycee M, Williamson, Jeff D, Garg, Pradeep, Watkins, Franklin, Ott, Brian R, Querfurth, Henry, Tremont, Geoffrey, Salloway, Stephen, Malloy, Paul, Jiminez, Gus, Correia, Stephen, Rosen, Howard J, Miller, Bruce L, Mintzer, Jacobo, Spicer, Kenneth, Bachman, David, Finger, Elizabether, Pasternak, Stephen, Rachinsky, Irina, Drost, Dick, Harvey, Danielle, Pomara, Nunzio, Hernando, Raymundo, Sarrael, Antero, Schultz, Susan K, Ponto, Laura L Boles, Shim, Hyungsub, Smith, Karen Elizabeth, Relkin, Norman, Chaing, Gloria, Raudin, Lisa, Bernstein, Matthew, Smith, Amanda, Fargher, Kristin, Raj, Balebail Ashok, Dichgans, Martin, Fox, Nick, Thompson, Paul, Schuff, Norbert, DeCArli, Charles, Borowski, Bret, Gunter, Jeff, Senjem, Matt, Vemuri, Prashanthi, Jones, David, Kantarci, Kejal, Brendel, Matthias, Ward, Chad, Koeppe, Robert A, Foster, Norm, Reiman, Eric M, Chen, Kewei, Mathis, Chet, Landau, Susan, Cairns, Nigel J, Householder, Erin, Reinwald, Lisa Taylor, Initiative, Alzheimer’s Disease Neuroimaging, Lee, Virginia, Korecka, Magdalena, Figurski, Michal, Crawford, Karen, Neu, Scott, Foroud, Tatiana M, Potkin, Steven, Shen, Li, Kelley, Faber, Kim, Sungeun, Malik, Rainer, Nho, Kwangsik, Kachaturian, Zaven, Frank, Richard, Snyder, Peter J, Molchan, Susan, Kaye, Jeffrey, Quinn, Joseph, Lind, Betty, Carter, Raina, Dolen, Sara, Ewers, Michael, Schneider, Lon S, Pawluczyk, Sonia, Beccera, Mauricio, Teodoro, Liberty, Spann, Bryan M, Brewer, James, Vanderswag, Helen, Fleisher, Adam, Heidebrink, Judith L, Lord, Joanne L, Weiner, Michael, Mason, Sara S, Albers, Colleen S, Knopman, David S, Johnson, Kris, Doody, Rachelle S, Meyer, Javier Villanueva, Chowdhury, Munir, Rountree, Susan, Dang, Mimi, Stern, Yaakov, Aisen, Paul, Honig, Lawrence S, Bell, Karen L, Ances, Beau, Morris, John C, Carroll, Maria, Leon, Sue, Mintun, Mark A, Schneider, Stacy, OliverNG, Angela, Griffith, Randall, Radiology & Nuclear Medicine, and Epidemiology

Subjects
Male, Heterozygote, metabolism [Amyloid beta-Peptides], Molecular imaging, Gene Expression, genetics [Alzheimer Disease], klotho protein, tau Proteins, Polymorphism, Single Nucleotide, Article, metabolism [Apolipoproteins E], Apolipoproteins E, genetics [Memory Disorders], Alzheimer Disease, mental disorders, Humans, metabolism [Glucuronidase], diagnostic imaging [Brain], Klotho Proteins, Aged, Glucuronidase, Memory Disorders, Amyloid beta-Peptides, genetics [Glucuronidase], methods [Positron-Emission Tomography], metabolism [Memory Disorders], Brain, Alzheimer's disease, Middle Aged, metabolism [tau Proteins], Haplotypes, metabolism [Brain], Positron-Emission Tomography, genetics [Apolipoproteins E], Dementia, Female, ddc:500, metabolism [Alzheimer Disease], Protein Binding
Abstract

Klotho-VS heterozygosity (KL-VShet) is associated with reduced risk of Alzheimer’s disease (AD). However, whether KL-VShet is associated with lower levels of pathologic tau, i.e., the key AD pathology driving neurodegeneration and cognitive decline, is unknown. Here, we assessed the interaction between KL-VShet and levels of beta-amyloid, a key driver of tau pathology, on the levels of PET-assessed neurofibrillary tau in 551 controls and patients across the AD continuum. KL-VShet showed lower cross-sectional and longitudinal increase in tau-PET per unit increase in amyloid-PET when compared to that of non-carriers. This association of KL-VShet on tau-PET was stronger in Klotho mRNA-expressing brain regions mapped onto a gene expression atlas. KL-VShet was related to better memory functions in amyloid-positive participants and this association was mediated by lower tau-PET. Amyloid-PET levels did not differ between KL-VShet carriers versus non-carriers. Together, our findings provide evidence to suggest a protective role of KL-VShet against amyloid-related tau pathology and tau-related memory impairments in elderly humans at risk of AD dementia., The KL-VS haplotype of the Klotho gene has been associated with reduced risk of Alzheimer’s disease and dementia. Here the authors show an association between the KL-VS haplotype and amyloid-dependent tau accumulation using PET data.

Published
2021
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45. Four distinct trajectories of tau deposition identified in Alzheimer’s disease

Author

National Institutes of Health (US), Government of Canada, Medical Research Council (UK), UK Research and Innovation, National Institute for Health Research (UK), Engineering and Physical Sciences Research Council (UK), Instituto de Salud Carlos III, European Commission, Swedish Research Council, Knut and Alice Wallenberg Foundation, Marianne and Marcus Wallenberg Foundation, Lund University, Swedish Alzheimer Foundation, Swedish Brain Foundation, Swedish Parkinson Foundation, Skåne University Hospital, Government of Sweden, National Research Foundation of Korea, Ministry of Education (South Korea), Ministry of Health and Welfare (South Korea), National Institute on Aging (US), GE Healthcare, Roche, Radiopharmaceuticals, Alzheimer's Disease Neuroimaging Initiative, National Institute of Biomedical Imaging and Bioengineering (US), Northern California Institute for Research and Education, Vogel, Jacob W., Young, Alexandra L., Oxtoby, Neil P., Smith, Ruben, Ossenkoppele, Rik, Strandberg, Olof T., La Joie, Renaud, Aksman, Leon M., Grothe, Michel J., Iturria-Medina, Yasser, Pontecorvo, Michael J., Devous, Michael D., Rabinovici, Gil D., Alexander, Daniel C., Lyoo, Chul Hyoung, Evans, Alan C., Hansson, Oskar, National Institutes of Health (US), Government of Canada, Medical Research Council (UK), UK Research and Innovation, National Institute for Health Research (UK), Engineering and Physical Sciences Research Council (UK), Instituto de Salud Carlos III, European Commission, Swedish Research Council, Knut and Alice Wallenberg Foundation, Marianne and Marcus Wallenberg Foundation, Lund University, Swedish Alzheimer Foundation, Swedish Brain Foundation, Swedish Parkinson Foundation, Skåne University Hospital, Government of Sweden, National Research Foundation of Korea, Ministry of Education (South Korea), Ministry of Health and Welfare (South Korea), National Institute on Aging (US), GE Healthcare, Roche, Radiopharmaceuticals, Alzheimer's Disease Neuroimaging Initiative, National Institute of Biomedical Imaging and Bioengineering (US), Northern California Institute for Research and Education, Vogel, Jacob W., Young, Alexandra L., Oxtoby, Neil P., Smith, Ruben, Ossenkoppele, Rik, Strandberg, Olof T., La Joie, Renaud, Aksman, Leon M., Grothe, Michel J., Iturria-Medina, Yasser, Pontecorvo, Michael J., Devous, Michael D., Rabinovici, Gil D., Alexander, Daniel C., Lyoo, Chul Hyoung, Evans, Alan C., and Hansson, Oskar

Abstract

Alzheimer’s disease (AD) is characterized by the spread of tau pathology throughout the cerebral cortex. This spreading pattern was thought to be fairly consistent across individuals, although recent work has demonstrated substantial variability in the population with AD. Using tau-positron emission tomography scans from 1,612 individuals, we identified 4 distinct spatiotemporal trajectories of tau pathology, ranging in prevalence from 18 to 33%. We replicated previously described limbic-predominant and medial temporal lobe-sparing patterns, while also discovering posterior and lateral temporal patterns resembling atypical clinical variants of AD. These ‘subtypes’ were stable during longitudinal follow-up and were replicated in a separate sample using a different radiotracer. The subtypes presented with distinct demographic and cognitive profiles and differing longitudinal outcomes. Additionally, network diffusion models implied that pathology originates and spreads through distinct corticolimbic networks in the different subtypes. Together, our results suggest that variation in tau pathology is common and systematic, perhaps warranting a re-examination of the notion of ‘typical AD’ and a revisiting of tau pathological staging.

Published
2021

46. Brain functional localization: a survey of image registration techniques

Author

Gholipour, Ali, Kehtarnavaz, Nasser, Briggs, Richard, Devous, Michael, and Gopinath, Kaundinya

Subjects
Brain mapping -- Methods, Image processing -- Equipment and supplies, Image processing -- Usage, Image processing -- Health aspects, Image processor, Business, Electronics, Electronics and electrical industries, Health care industry
Abstract

Functional localization is a concept which involves the application of a sequence of geometrical and statistical image processing operations in order to define the location of brain activity or to produce functional/parametric maps with respect to the brain structure or anatomy. Considering that functional brain images do not normally convey detailed structural information and, thus, do not present an anatomically specific localization of functional activity, various image registration techniques are introduced in the literature for the purpose of mapping functional activity into an anatomical image or a brain atlas. The problems addressed by these techniques differ depending on the application and the type of analysis, i.e., single-subject versus group analysis. Functional to anatomical brain image registration is the core part of functional localization in most applications and is accompanied by intersubject and subject-to-atlas registration for group analysis studies. Cortical surface registration and automatic brain labeling are some of the other tools towards establishing a fully automatic functional localization procedure. While several previous survey papers have reviewed and classified general-purpose medical image registration techniques, this paper provides an overview of brain functional localization along with a survey and classification of the image registration techniques related to this problem. Index Terms--Brain functional localization, fMRI image processing, functional imaging, survey of image registration techniques.

Published
2007

49. Relationships Between Cognition and Neuropathological Tau in Alzheimer's Disease Assessed by 18F Flortaucipir PET.

Author

Devous Sr., Michael D., Fleisher, Adam S., Pontecorvo, Michael J., Lu, Ming, Siderowf, Andrew, Navitsky, Michael, Kennedy, Ian, Southekal, Sudeepti, Harris, Thomas S., Mintun, Mark A., Devous, Michael D, and Devous, Michael D Sr

Subjects
ALZHEIMER'S disease, TAU proteins, POSITRON emission tomography, TRAIL Making Test, COGNITION disorders, PYRIDINE, RESEARCH, NEURONS, NERVE tissue proteins, CLINICAL trials, WECHSLER Memory Scale, RESEARCH methodology, COGNITION, MEDICAL cooperation, EVALUATION research, COMPARATIVE studies, QUESTIONNAIRES
Abstract

Background: Tau neurofibrillary tangle burden increases with Alzheimer's disease (AD) stage and correlates with degree of cognitive impairment. Tau PET imaging could facilitate understanding the relationship between tau pathology and cognitive impairment.Objective: Evaluate the relationship between 18F flortaucipir uptake patterns and cognition across multiple cognitive domains.Methods: We acquired flortaucipir PET scans in 84 amyloid-positive control, mild cognitive impairment (MCI), and AD subjects. Flortaucipir standardized uptake value ratio (SUVr) values were obtained from a neocortical volume of interest (VOI), a precuneus VOI, and VOIs defined by the correlation between flortaucipir SUVr images and domain-specific cognitive tests. Cognitive assessments included Mini-Mental State Exam (MMSE), Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-cog), and a neuropsychological test battery (i.e., Wechsler Memory Scale-Revised Logical Memory (WMS-R), Trail Making Test, Boston Naming Test, Digit Symbol Substitution Test, Animal List Generation, WMS-R Digit Span, American National Adult Reading Test, Clock Drawing Test, Judgment of Line Orientation, and WMS-R Logical Memory II (Delayed Recall)) and the Functional Activities Questionnaire (FAQ). Correlation analyses compared regional and voxel-wise VOIs to cognitive scores.Results: Subjects included 5 controls, 47 MCI, and 32 AD subjects. Significant correlations were seen between both flortaucipir and florbetapir SUVrs and MMSE, ADAS-Cog, and FAQ. Cognitive impairment was associated with increased flortaucipir uptake in regionally specific patterns consistent with the neuroanatomy underlying specific cognitive tests.Conclusion: Flortaucipir SUVr values demonstrated significant inverse correlations with cognitive scores in domain-specific patterns. Findings support the hypothesis that PET imaging of neuropathologic tau deposits may reflect underlying neurodegeneration in AD. [ABSTRACT FROM AUTHOR]

Published
2021
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