Search

Your search keyword '"Koeppe, Robert A"' showing total 1,563 results
Start Over Author "Koeppe, Robert A"
1,563 results on '"Koeppe, Robert A"'

1. Genetic associations with dementia‐related proteinopathy: Application of item response theory

Author

Katsumata, Yuriko, Fardo, David W, Shade, Lincoln MP, Wu, Xian, Karanth, Shama D, Hohman, Timothy J, Schneider, Julie A, Bennett, David A, Farfel, Jose M, Gauthreaux, Kathryn, Mock, Charles, Kukull, Walter A, Abner, Erin L, Nelson, Peter T, Carrillo, Maria, Reiman, Eric M, Chen, Kewei, Masterman, Donna, Green, Robert C, Ho, Carole, Fleisher, Adam, Saykin, Andrew J, Nho, Kwangsik, Apostolova, Liana G, Risacher, Shannon L, Jackson, Jonathan, Forghanian-Arani, Arvin, Borowski, Bret, Ward, Chad, Schwarz, Christopher, Jack, Clifford R, Jones, David, Gunter, Jeff, Kantarci, Kejal, Senjem, Matthew, Vemuri, Prashanthi, Reid, Robert, Petersen, Ronald, Hsiao, John K, Potter, William, Masliah, Eliezer, Ryan, Laurie, Bernard, Marie, Silverberg, Nina, Kormos, Adrienne, Conti, Cat, Veitch, Dallas, Flenniken, Derek, Sacrey, Diana Truran, Choe, Mark, Ashford, Miriam, Chen, Stephanie Rossi, Faber, Kelley, Nudelman, Kelly, Wilme, Kristi, Foroud, Tatiana M, Trojanowki, John Q, Shaw, Leslie M, Korecka, Magdalena, Figurski, Michal, Khachaturian, Zaven, Barnes, Lisa, Malone, Ian, Fox, Nick C, Beckett, Laurel, Weiner, Michael W, Jagust, William, Landau, Susan, Knaack, Alexander, DeCarli, Charles, Harvey, Danielle, Fletcher, Evan, González, Hector, Jin, Chengshi, Tosun‐Turgut, Duygu, Neuhaus, John, Fockler, Juliet, Nosheny, Rachel, Koeppe, Robert A, Yushkevich, Paul A, Das, Sandhitsu, Mathis, Chet, Toga, Arthur W, Zimmerman, Caileigh, Gessert, Devon, Shcrer, Elizabeth, Miller, Garrett, Coker, Godfrey, Jimenez, Gustavo, Salazar, Jennifer, Pizzola, Jeremy, Crawford, Karen, Hergesheimer, Lindsey, Donohue, Michael, and Rafii, Michael

Subjects
Biomedical and Clinical Sciences, Biological Psychology, Clinical Sciences, Neurosciences, Psychology, Acquired Cognitive Impairment, Neurodegenerative, Brain Disorders, Dementia, Genetics, Prevention, Aging, 2.1 Biological and endogenous factors, Aetiology, Neurological, Humans, alpha-Synuclein, TDP-43 Proteinopathies, Proteostasis Deficiencies, DNA-Binding Proteins, Biological Products, Alzheimer Disease, Membrane Proteins, Nerve Tissue Proteins, Alzheimer's Disease Neuroimaging Initiative, National Alzheimer's Coordinating Center, ARHGEF28, Alzheimer's Coordinating Center, Alzheimer's Disease Sequencing Project, Alzheimer's disease neuropathologic changes, Item response theory, Lewy, RGNEF, Religious Orders Study, Rush Memory and Aging Project, SDHAF1, TMEM68, neuropathology, Geriatrics, Clinical sciences, Biological psychology
Abstract

IntroductionAlthough dementia-related proteinopathy has a strong negative impact on public health, and is highly heritable, understanding of the related genetic architecture is incomplete.MethodsWe applied multidimensional generalized partial credit modeling (GPCM) to test genetic associations with dementia-related proteinopathies. Data were analyzed to identify candidate single nucleotide variants for the following proteinopathies: Aβ, tau, α-synuclein, and TDP-43.ResultsFinal included data comprised 966 participants with neuropathologic and WGS data. Three continuous latent outcomes were constructed, corresponding to TDP-43-, Aβ/Tau-, and α-synuclein-related neuropathology endophenotype scores. This approach helped validate known genotype/phenotype associations: for example, TMEM106B and GRN were risk alleles for TDP-43 pathology; and GBA for α-synuclein/Lewy bodies. Novel suggestive proteinopathy-linked alleles were also discovered, including several (SDHAF1, TMEM68, and ARHGEF28) with colocalization analyses and/or high degrees of biologic credibility.DiscussionA novel methodology using GPCM enabled insights into gene candidates for driving misfolded proteinopathies.HighlightsLatent factor scores for proteinopathies were estimated using a generalized partial credit model. The three latent continuous scores corresponded well with proteinopathy severity. Novel genes associated with proteinopathies were identified. Several genes had high degrees of biologic credibility for dementia risk factors.

Published
2024

2. Individuals with Alzheimer's disease and low tau burden: Characteristics and implications

Author

Landau, Susan M, Lee, JiaQie, Murphy, Alice, Ward, Tyler J, Harrison, Theresa M, Baker, Suzanne L, DeCarli, Charles, Harvey, Danielle, Tosun, Duygu, Weiner, Michael W, Koeppe, Robert A, Jagust, William J, and Initiative, for the Alzheimer's Disease Neuroimaging

Subjects
Biomedical and Clinical Sciences, Biological Psychology, Clinical Sciences, Neurosciences, Psychology, Aging, Alzheimer's Disease, Acquired Cognitive Impairment, Brain Disorders, Dementia, Neurodegenerative, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), 2.1 Biological and endogenous factors, Aetiology, Neurological, Humans, Male, Alzheimer Disease, Amyloid beta-Peptides, Cognition, Cognitive Dysfunction, Positron-Emission Tomography, tau Proteins, Female, Alzheimer's disease, A beta PET, florbetaben, florbetapir, flortaucipir, tau PET, Alzheimer's Disease Neuroimaging Initiative, Aβ PET, Geriatrics, Clinical sciences, Biological psychology
Abstract

IntroductionAbnormal amyloid-beta (Aβ) and tau deposition define Alzheimer's Disease (AD), but non-elevated tau is relatively frequent in patients on the AD pathway.MethodsWe examined characteristics and regional patterns of 397 Aβ+ unimpaired and impaired individuals with low tau (A+T-) in relation to their higher tau counterparts (A+T+).ResultsSeventy-one percent of Aβ+ unimpaired and 42% of impaired Aβ+ individuals were categorized as A+T- based on global tau. In impaired individuals only, A+T- status was associated with older age, male sex, and greater cardiovascular risk. α-synuclein was linked to poorer cognition, particularly when tau was low. Tau burden was most frequently elevated in a common set of temporal regions regardless of T+/T- status.DiscussionLow tau is relatively common in patients on the AD pathway and is linked to comorbidities that contribute to impairment. These findings have implications for the selection of individuals for Aβ- and tau-modifying therapies.

Published
2024

3. Biomarker clustering in autosomal dominant Alzheimers disease.

Author

Luckett, Patrick, Chen, Charlie, Gordon, Brian, Wisch, Julie, Berman, Sarah, Chhatwal, Jasmeer, Cruchaga, Carlos, Fagan, Anne, Farlow, Martin, Fox, Nick, Jucker, Mathias, Levin, Johannes, Masters, Colin, Mori, Hiroshi, Noble, James, Salloway, Stephen, Schofield, Peter, Brickman, Adam, Brooks, William, Cash, David, Fulham, Michael, Ghetti, Bernardino, Jack, Clifford, Vöglein, Jonathan, Klunk, William, Koeppe, Robert, Su, Yi, Weiner, Michael, Wang, Qing, Marcus, Daniel, Koudelis, Deborah, Joseph-Mathurin, Nelly, Cash, Lisa, Hornbeck, Russ, Xiong, Chengjie, Perrin, Richard, Karch, Celeste, Hassenstab, Jason, McDade, Eric, Morris, John, Benzinger, Tammie, Bateman, Randall, and Ances, Beau

Subjects
Autosomal dominant Alzheimers disease, biomarkers, machine learning, Humans, Alzheimer Disease, Amyloid beta-Peptides, Amyloidogenic Proteins, Biomarkers, Cross-Sectional Studies, Inflammation, tau Proteins
Abstract

INTRODUCTION: As the number of biomarkers used to study Alzheimers disease (AD) continues to increase, it is important to understand the utility of any given biomarker, as well as what additional information a biomarker provides when compared to others. METHODS: We used hierarchical clustering to group 19 cross-sectional biomarkers in autosomal dominant AD. Feature selection identified biomarkers that were the strongest predictors of mutation status and estimated years from symptom onset (EYO). Biomarkers identified included clinical assessments, neuroimaging, cerebrospinal fluid amyloid, and tau, and emerging biomarkers of neuronal integrity and inflammation. RESULTS: Three primary clusters were identified: neurodegeneration, amyloid/tau, and emerging biomarkers. Feature selection identified amyloid and tau measures as the primary predictors of mutation status and EYO. Emerging biomarkers of neuronal integrity and inflammation were relatively weak predictors. DISCUSSION: These results provide novel insight into our understanding of the relationships among biomarkers and the staging of biomarkers based on disease progression.

Published
2023

4. Optimizing quantification of MK6240 tau PET in unimpaired older adults

Author

Harrison, Theresa M, Ward, Tyler J, Murphy, Alice, Baker, Suzanne L, Dominguez, Pablo A, Koeppe, Robert, Vemuri, Prashanthi, Lockhart, Samuel N, Jung, Youngkyoo, Harvey, Danielle J, Lovato, Laura, Toga, Arthur W, Masdeu, Joseph, Oh, Hwamee, Gitelman, Darren R, Aggarwal, Neelum, Snyder, Heather M, Baker, Laura D, DeCarli, Charles, Jagust, William J, Landau, Susan M, and Group, US POINTER Study

Subjects
Health Sciences, Dementia, Biomedical Imaging, Aging, Acquired Cognitive Impairment, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Behavioral and Social Science, Alzheimer's Disease, Neurodegenerative, Clinical Research, Prevention, Brain Disorders, Clinical Trials and Supportive Activities, Neurosciences, 2.1 Biological and endogenous factors, Neurological, Aged, Humans, Alzheimer Disease, Amyloid beta-Peptides, Brain, Cognitive Dysfunction, Positron-Emission Tomography, tau Proteins, Middle Aged, PET, Tau, Amyloid, Alzheimer's disease, off-target signal, meninges, U.S. POINTER Study Group, Medical and Health Sciences, Psychology and Cognitive Sciences, Neurology & Neurosurgery, Biomedical and clinical sciences, Health sciences
Abstract

Accurate measurement of Alzheimer's disease (AD) pathology in older adults without significant clinical impairment is critical to assessing intervention strategies aimed at slowing AD-related cognitive decline. The U.S. Study to Protect Brain Health Through Lifestyle Intervention to Reduce Risk (POINTER) is a 2-year randomized controlled trial to evaluate the effect of multicomponent risk reduction strategies in older adults (60-79 years) who are cognitively unimpaired but at increased risk for cognitive decline/dementia due to factors such as cardiovascular disease and family history. The POINTER Imaging ancillary study is collecting tau-PET ([18F]MK6240), beta-amyloid (Aβ)-PET ([18F]florbetaben [FBB]) and MRI data to evaluate neuroimaging biomarkers of AD and cerebrovascular pathophysiology in this at-risk sample. Here 481 participants (70.0±5.0; 66% F) with baseline MK6240, FBB and structural MRI scans were included. PET scans were coregistered to the structural MRI which was used to create FreeSurfer-defined reference regions and target regions of interest (ROIs). We also created off-target signal (OTS) ROIs to examine the magnitude and distribution of MK6240 OTS across the brain as well as relationships between OTS and age, sex, and race. OTS was unimodally distributed, highly correlated across OTS ROIs and related to younger age and sex but not race. Aiming to identify an optimal processing approach for MK6240 that would reduce the influence of OTS, we compared our previously validated MRI-guided standard PET processing and 6 alternative approaches. The alternate approaches included combinations of reference region erosion and meningeal OTS masking before spatial smoothing as well as partial volume correction. To compare processing approaches we examined relationships between target ROIs (entorhinal cortex (ERC), hippocampus or a temporal meta-ROI (MetaROI)) SUVR and age, sex, race, Aβ and a general cognitive status measure, the Modified Telephone Interview for Cognitive Status (TICSm). Overall, the processing approaches performed similarly, and none showed a meaningful improvement over standard processing. Across processing approaches we observed previously reported relationships with MK6240 target ROIs including positive associations with age, an Aβ+> Aβ- effect and negative associations with cognition. In sum, we demonstrated that different methods for minimizing effects of OTS, which is highly correlated across the brain within subject, produced no substantive change in our performance metrics. This is likely because OTS contaminates both reference and target regions and this contamination largely cancels out in SUVR data. Caution should be used when efforts to reduce OTS focus on target or reference regions in isolation as this may exacerbate OTS contamination in SUVR data.

Published
2023

5. A data‐driven examination of apathy and depressive symptoms in dementia with independent replication

Author

Da Silva, Miguel Vasconcelos, Melendez‐Torres, Gerardo Javier, Ismail, Zahinoor, Testad, Ingelin, Ballard, Clive, Creese, Byron, 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, Van der Swag, 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, and Oliver, Angela

Subjects
Clinical and Health Psychology, Biomedical and Clinical Sciences, Psychology, Brain Disorders, Mental Health, Depression, Mental Illness, Mental health, Alzheimer's Disease Neuroimaging Initiative, apathy, dementia, depression, latent class analysis, Genetics, Neurosciences, Biological psychology
Abstract

Apathy is one of the most common neuropsychiatric symptoms (NPS) and is associated with poor clinical outcomes. Research that helps define the apathy phenotype is urgently needed, particularly for clinical and biomarker studies. We used latent class analysis (LCA) with two independent cohorts to understand how apathy and depression symptoms co-occur statistically. We further explored the relationship between latent class membership, demographics, and the presence of other NPS. The LCA identified a four-class solution (no symptoms, apathy, depression, and combined apathy/depression), reproducible over both cohorts, providing robust support for an apathy syndrome distinct from depression and confirming that an apathy/depression syndrome exists, supported by the model fit test with the four-class solution scores evidencing better fitting (Bayesian information criterion adjusted and entropy R 2). Using a data-driven method, we show distinct and statistically meaningful co-occurrence of apathy and depressive symptoms. There was evidence that these classes have different clinical associations, which may help inform diagnostic categories for research studies and clinical practice.HighlightsWe found four classes: no symptoms, apathy, depression and apathy/depression.Apathy conferred a higher probability for agitation.Apathy diagnostic criteria should include accompanying neuropsychiatric symptoms.

Published
2023

6. Positron emission tomography and magnetic resonance imaging methods and datasets within the Dominantly Inherited Alzheimer Network (DIAN)

Author

McKay, Nicole S., Gordon, Brian A., Hornbeck, Russ C., Dincer, Aylin, Flores, Shaney, Keefe, Sarah J., Joseph-Mathurin, Nelly, Jack, Clifford R., Koeppe, Robert, Millar, Peter R., Ances, Beau M., Chen, Charles D., Daniels, Alisha, Hobbs, Diana A., Jackson, Kelley, Koudelis, Deborah, Massoumzadeh, Parinaz, McCullough, Austin, Nickels, Michael L., Rahmani, Farzaneh, Swisher, Laura, Wang, Qing, Allegri, Ricardo F., Berman, Sarah B., Brickman, Adam M., Brooks, William S., Cash, David M., Chhatwal, Jasmeer P., Day, Gregory S., Farlow, Martin R., la Fougère, Christian, Fox, Nick C., Fulham, Michael, Ghetti, Bernardino, Graff-Radford, Neill, Ikeuchi, Takeshi, Klunk, William, Lee, Jae-Hong, Levin, Johannes, Martins, Ralph, Masters, Colin L., McConathy, Jonathan, Mori, Hiroshi, Noble, James M., Reischl, Gerald, Rowe, Christopher, Salloway, Stephen, Sanchez-Valle, Raquel, Schofield, Peter R., Shimada, Hiroyuki, Shoji, Mikio, Su, Yi, Suzuki, Kazushi, Vöglein, Jonathan, Yakushev, Igor, Cruchaga, Carlos, Hassenstab, Jason, Karch, Celeste, McDade, Eric, Perrin, Richard J., Xiong, Chengjie, Morris, John C., Bateman, Randall J., and Benzinger, Tammie L. S.

Published
2023
Full Text
View/download PDF

7. Longitudinal head-to-head comparison of 11C-PiB and 18F-florbetapir PET in a Phase 2/3 clinical trial of anti-amyloid-β monoclonal antibodies in dominantly inherited Alzheimer’s disease

Author

Chen, Charles D., McCullough, Austin, Gordon, Brian, Joseph-Mathurin, Nelly, Flores, Shaney, McKay, Nicole S., Hobbs, Diana A., Hornbeck, Russ, Fagan, Anne M., Cruchaga, Carlos, Goate, Alison M., Perrin, Richard J., Wang, Guoqiao, Li, Yan, Shi, Xinyu, Xiong, Chengjie, Pontecorvo, Michael J., Klein, Gregory, Su, Yi, Klunk, William E., Jack, Clifford, Koeppe, Robert, Snider, B. Joy, Berman, Sarah B., Roberson, Erik D., Brosch, Jared, Surti, Ghulam, Jiménez-Velázquez, Ivonne Z., Galasko, Douglas, Honig, Lawrence S., Brooks, William S., Clarnette, Roger, Wallon, David, Dubois, Bruno, Pariente, Jérémie, Pasquier, Florence, Sanchez-Valle, Raquel, Shcherbinin, Sergey, Higgins, Ixavier, Tunali, Ilke, Masters, Colin L., van Dyck, Christopher H., Masellis, Mario, Hsiung, Robin, Gauthier, Serge, Salloway, Steve, Clifford, David B., Mills, Susan, Supnet-Bell, Charlene, McDade, Eric, Bateman, Randall J., and Benzinger, Tammie L. S.

Published
2023
Full Text
View/download PDF

9. The Longitudinal Early‐onset Alzheimer's Disease Study (LEADS): Framework and methodology

Author

Apostolova, Liana G, Aisen, Paul, Eloyan, Ani, Fagan, Anne, Fargo, Keith N, Foroud, Tatiana, Gatsonis, Constantine, Grinberg, Lea T, Jack, Clifford R, Kramer, Joel, Koeppe, Robert, Kukull, Walter A, Murray, Melissa E, Nudelman, Kelly, Rumbaugh, Malia, Toga, Arthur, Vemuri, Prashanthi, Trullinger, Amy, Iaccarino, Leonardo, Day, Gregory S, Graff‐Radford, Neill R, Honig, Lawrence S, Jones, David T, Masdeu, Joseph, Mendez, Mario, Musiek, Erik, Onyike, Chiadi U, Rogalski, Emily, Salloway, Steve, Wolk, David A, Wingo, Thomas S, Carrillo, Maria C, Dickerson, Bradford C, Rabinovici, Gil D, and Consortium, the LEADS

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Brain Disorders, Alzheimer's Disease, Clinical Research, Neurosciences, Dementia, Neurodegenerative, Acquired Cognitive Impairment, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Aging, Biomedical Imaging, 4.1 Discovery and preclinical testing of markers and technologies, 2.1 Biological and endogenous factors, 4.2 Evaluation of markers and technologies, Detection, screening and diagnosis, Aetiology, Neurological, Alzheimer Disease, Aniline Compounds, Autopsy, Biomarkers, Brain, Cognitive Dysfunction, Early Diagnosis, Female, Humans, Longitudinal Studies, Magnetic Resonance Imaging, Male, Middle Aged, National Institute on Aging (U.S.), Positron-Emission Tomography, Stilbenes, United States, Alzheimer&apos, s disease, early&#8208, onset, EOAD, LEADS, YOAD, young onset, LEADS Consortium, Alzheimer's disease, early-onset, Geriatrics, Clinical sciences, Biological psychology
Abstract

Patients with early-onset Alzheimer's disease (EOAD) are commonly excluded from large-scale observational and therapeutic studies due to their young age, atypical presentation, or absence of pathogenic mutations. The goals of the Longitudinal EOAD Study (LEADS) are to (1) define the clinical, imaging, and fluid biomarker characteristics of EOAD; (2) develop sensitive cognitive and biomarker measures for future clinical and research use; and (3) establish a trial-ready network. LEADS will follow 400 amyloid beta (Aβ)-positive EOAD, 200 Aβ-negative EOnonAD that meet National Institute on Aging-Alzheimer's Association (NIA-AA) criteria for mild cognitive impairment (MCI) or AD dementia, and 100 age-matched controls. Participants will undergo clinical and cognitive assessments, magnetic resonance imaging (MRI), [18 F]Florbetaben and [18 F]Flortaucipir positron emission tomography (PET), lumbar puncture, and blood draw for DNA, RNA, plasma, serum and peripheral blood mononuclear cells, and post-mortem assessment. To develop more effective AD treatments, scientists need to understand the genetic, biological, and clinical processes involved in EOAD. LEADS will develop a public resource that will enable future planning and implementation of EOAD clinical trials.

Published
2021

10. Late-Life Depression Is Associated With Reduced Cortical Amyloid Burden: Findings From the Alzheimer’s Disease Neuroimaging Initiative Depression Project

Author

Mackin, R Scott, Insel, Philip S, Landau, Susan, Bickford, David, Morin, Ruth, Rhodes, Emma, Tosun, Duygu, Rosen, Howie J, Butters, Meryl, Aisen, Paul, Raman, Rema, Saykin, Andrew, Toga, Arthur, Jack, Clifford, Koeppe, Robert, Weiner, Michael W, Nelson, Craig, and Project, Alzheimer’s Disease Neuroimaging Initiative and the ADNI Depression

Subjects
Biological Psychology, Biomedical and Clinical Sciences, Clinical Sciences, Psychology, Depression, Genetics, Aging, Neurodegenerative, Brain Disorders, Acquired Cognitive Impairment, Neurosciences, Mental Health, Dementia, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Major Depressive Disorder, Alzheimer's Disease, 2.1 Biological and endogenous factors, Aetiology, Neurological, Mental health, Aged, Alzheimer Disease, Amyloid beta-Peptides, Cognitive Dysfunction, Humans, Neuroimaging, Positron-Emission Tomography, Alzheimer's disease, Amyloid, Cognition, Depressive symptoms, Late-life depression, Mild cognitive impairment, Alzheimer’s Disease Neuroimaging Initiative and the ADNI Depression Project, Alzheimer’s disease, Biological Sciences, Medical and Health Sciences, Psychology and Cognitive Sciences, Psychiatry, Biological sciences, Biomedical and clinical sciences
Abstract

BackgroundWe evaluated the role of cortical amyloid deposition as a factor contributing to memory dysfunction and increased risk of dementia associated with late-life depression (LLD).MethodsA total of 119 older adult participants with a current diagnosis of major depression (LLD) from the Alzheimer's Disease Neuroimaging Initiative (ADNI) Depression Project study and 119 nondepressed (ND) cognitively unimpaired participants matched on age, sex, and APOE genotype were obtained from the ADNI database.ResultsThirty-three percent of LLD participants met ADNI criteria for mild cognitive impairment. Compared with ND individuals, the LLD group exhibited less global amyloid beta (Aβ) accumulation (p = .05). The proportion of amyloid positivity in the LLD group was 19.3% compared with 31.1% for the ND participants (p = .02). Among LLD participants, global Aβ was not associated with lifetime number of depressive episodes, lifetime length of depression, length of lifetime selective serotonin reuptake inhibitor use, or lifetime length of untreated depression (p > .21 for all). Global Aβ was associated with worse memory performance (p = .05). Similar results were found in secondary analyses restricting comparisons to the cognitively unimpaired LLD participants as well as when comparing the LLD group with an ND group that included participants with mild cognitive impairment.ConclusionsContrary to expectation, the LLD group showed less Aβ deposition than the ND group and Aβ deposition was not associated with depression history characteristics. Aβ was associated with memory, but this relationship did not differ between LLD and ND. Our results suggest that memory deficits and accelerated cognitive decline reported in previous studies of LLD are not due to greater cortical Aβ accumulation.

Published
2021

11. Circular-SWAT for deep learning based diagnostic classification of Alzheimer's disease: application to metabolome data

Author

Kaddurah-Daouk, Rima, Kueider-Paisley, Alexandra, Doraiswamy, P. Murali, Blach, Colette, Moseley, Arthur, Thompson, Will, St John-Williams, Lisa, Mahmoudiandehkhordi, Siamak, Tenenbaum, Jessica, Welsh-Balmer, Kathleen, Plassman, Brenda, Saykin, Andrew J., Nho, Kwangsik, Risacher, Shannon L., Kastenmüller, Gabi, Arnold, Matthias, Han, Xianlin, Baillie, Rebecca, Knight, Rob, Dorrestein, Pieter, Brewer, James, Mayer, Emeran, Labus, Jennifer, Baldi, Pierre, Gupta, Arpana, Fiehn, Oliver, Barupal, Dinesh, Meikle, Peter, Mazmanian, Sarkis, Rader, Dan, Kling, Mitchel, Shaw, Leslie, Trojanowski, John, van Duijin, Cornelia, Nevado-Holgado, Alejo, Bennett, David, Krishnan, Ranga, Keshavarzian, Ali, Vogt, Robin, Ikram, Arfan, Hankemeier, Thomas, Thiele, Ines, Price, Nathan, Funk, Cory, Baloni, Priyanka, Jia, Wei, Wishart, David, Brinton, Roberta, Chang, Rui, Farrer, Lindsay, Au, Rhoda, Qiu, Wendy, Würtz, Peter, Koal, Therese, Mangravite, Lara, Krumsiek, Jan, Suhre, Karsten, Newman, John, Moreno, Herman, Foroud, Tatania, Sacks, Frank, Jansson, Janet, Weiner, Michael W., Aisen, Paul, Petersen, Ronald, Jack, Clifford R., Jr., Jagust, William, Trojanowki, John Q., Toga, Arthur W., Beckett, Laurel, Green, Robert C., Morris, John C., Perrin, Richard J., Shaw, Leslie M., Khachaturian, Zaven, Carrillo, Maria, Potter, William, Barnes, Lisa, Bernard, Marie, Gonzalez, Hector, Ho, Carole, Hsiao, John K., Jackson, Jonathan, Masliah, Eliezer, Masterman, Donna, Okonkwo, Ozioma, Perrin, Richard, Ryan, Laurie, Silverberg, Nina, Fleisher, Adam, Sacrey, Diana Truran, Fockler, Juliet, Conti, Cat, Veitch, Dallas, Neuhaus, John, Jin, Chengshi, Nosheny, Rachel, Ashford, Miriam, Flenniken, Derek, Kormos, Adrienne, Montine, Tom, Rafii, Michael, Raman, Rema, Jimenez, Gustavo, Donohue, Michael, Gessert, Devon, Salazar, Jennifer, Zimmerman, Caileigh, Cabrera, Yuliana, Walter, Sarah, Miller, Garrett, Coker, Godfrey, Clanton, Taylor, Hergesheimer, Lindsey, Smith, Stephanie, Adegoke, Olusegun, Mahboubi, Payam, Moore, Shelley, Pizzola, Jeremy, Shaffer, Elizabeth, Sloan, Brittany, Harvey, Danielle, Forghanian-Arani, Arvin, Borowski, Bret, Ward, Chad, Schwarz, Christopher, Jones, David, Gunter, Jeff, Kantarci, Kejal, Senjem, Matthew, Vemuri, Prashanthi, Reid, Robert, Fox, Nick C., Malone, Ian, Thompson, Paul, Thomopoulos, Sophia I., Nir, Talia M., Jahanshad, Neda, DeCarli, Charles, Knaack, Alexander, Fletcher, Evan, Tosun-Turgut, Duygu, Chen, Stephanie Rossi, Choe, Mark, Crawford, Karen, Yushkevich, Paul A., Das, Sandhitsu, Koeppe, Robert A., Reiman, Eric M., Chen, Kewei, Mathis, Chet, Landau, Susan, Cairns, Nigel J., Householder, Erin, Franklin, Erin, Bernhardt, Haley, Taylor-Reinwald, Lisa, Korecka, Magdalena, Figurski, Michal, Neu, Scott, Apostolova, Liana G., Shen, Li, Foroud, Tatiana M., Nudelman, Kelly, Faber, Kelley, Wilmes, Kristi, Thal, Leon, Silbert, Lisa C., Lind, Betty, Crissey, Rachel, Kaye, Jeffrey A., Carter, Raina, Dolen, Sara, Quinn, Joseph, Schneider, Lon S., Pawluczyk, Sonia, Becerra, Mauricio, Teodoro, Liberty, Dagerman, Karen, Spann, Bryan M., Vanderswag, Helen, Ziolkowski, Jaimie, Heidebrink, Judith L., Zbizek-Nulph, Lisa, Lord, Joanne L., Mason, Sara S., Albers, Colleen S., Knopman, David, Johnson, Kris, Villanueva-Meyer, Javier, Pavlik, Valory, Pacini, Nathaniel, Lamb, Ashley, Kass, Joseph S., Doody, Rachelle S., Shibley, Victoria, Chowdhury, Munir, Rountree, Susan, Dang, Mimi, Stern, Yaakov, Honig, Lawrence S., Mintz, Akiva, Ances, Beau, Winkfield, David, Carroll, Maria, Stobbs-Cucchi, Georgia, Oliver, Angela, Creech, Mary L., Mintun, Mark A., Schneider, Stacy, Geldmacher, David, Love, Marissa Natelson, Griffith, Randall, Clark, David, Brockington, John, Marson, Daniel, Grossman, Hillel, Goldstein, Martin A., Greenberg, Jonathan, Mitsis, Effie, Shah, Raj C., Lamar, Melissa, Samuels, Patricia, Duara, Ranjan, Greig-Custo, Maria T., Rodriguez, Rosemarie, Albert, Marilyn, Onyike, Chiadi, Farrington, Leonie, Rudow, Scott, Brichko, Rottislav, Kielb, Stephanie, Smith, Amanda, Raj, Balebail Ashok, Fargher, Kristin, Sadowski, Martin, Wisniewski, Thomas, Shulman, Melanie, Faustin, Arline, Rao, Julia, Castro, Karen M., Ulysse, Anaztasia, Chen, Shannon, Sheikh, Mohammed O., Singleton-Garvin, Jamika, Petrella, JeffreyR., James, Olga, Wong, Terence Z., Borges-Neto, Salvador, Karlawish, Jason H., Wolk, David A., Vaishnavi, Sanjeev, Clark, Christopher M., Arnold, Steven E., Smith, Charles D., Jicha, Gregory A., Raslau, Flavius D., Lopez, Oscar L., Oakley, MaryAnn, Simpson, Donna M., Porsteinsson, Anton P., Martin, Kim, Kowalski, Nancy, Keltz, Melanie, Goldstein, Bonnie S., Makino, Kelly M., Ismail, M. Saleem, Brand, Connie, Thai, Gaby, Pierce, Aimee, Yanez, Beatriz, Sosa, Elizabeth, Witbracht, Megan, Kelley, Brendan, Nguyen, Trung, Womack, Kyle, Mathews, Dana, Quiceno, Mary, Levey, Allan I., Lah, James J., Hajjar, Ihab, Cellar, Janet S., Burns, Jeffrey M., Swerdlow, Russell H., Brooks, William M., Silverman, Daniel H.S., Kremen, Sarah, Apostolova, Liana, Tingus, Kathleen, Lu, Po H., Bartzokis, George, Woo, Ellen, Teng, Edmond, Graff-Radford, Neill R., Parfitt, Francine, Poki-Walker, Kim, Farlow, Martin R., Hake, Ann Marie, Matthews, Brandy R., Brosch, Jared R., Herring, Scott, van, Christopher H., Mecca, Adam P., Good, Susan P., MacAvoy, Martha G., Carson, Richard E., Varma, Pradeep, Chertkow, Howard, Vaitekunis, Susan, Hosein, Chris, Black, Sandra, Stefanovic, Bojana, Heyn, Chris (Chinthaka), Robin Hsiung, Ging-Yuek, Kim, Ellen, Mudge, Benita, Sossi, Vesna, Feldman, Howard, Assaly, Michele, Finger, Elizabeth, Pasternak, Stephen, Rachinsky, Irina, Kertesz, Andrew, Drost, Dick, Rogers, John, Grant, Ian, Muse, Brittanie, Rogalski, Emily, Robson, Jordan, Mesulam, M.-Marsel, Kerwin, Diana, Wu, Chuang-Kuo, Johnson, Nancy, Lipowski, Kristine, Weintraub, Sandra, Bonakdarpour, Borna, Pomara, Nunzio, Hernando, Raymundo, Sarrael, Antero, Rosen, Howard J., Miller, Bruce L., Perry, David, Turner, Raymond Scott, Johnson, Kathleen, Reynolds, Brigid, MCCann, Kelly, Poe, Jessica, Sperling, Reisa A., Johnson, Keith A., Marshall, Gad A., Yesavage, Jerome, Taylor, Joy L., Chao, Steven, Coleman, Jaila, White, Jessica D., Lane, Barton, Rosen, Allyson, Tinklenberg, Jared, Belden, Christine M., Atri, Alireza, Clark, Kelly A., Zamrini, Edward, Sabbagh, Marwan, Killiany, Ronald, Stern, Robert, Mez, Jesse, Kowall, Neil, Budson, Andrew E., Obisesan, Thomas O., Ntekim, Oyonumo E., Wolday, Saba, Khan, Javed I., Nwulia, Evaristus, Nadarajah, Sheeba, Lerner, Alan, Ogrocki, Paula, Tatsuoka, Curtis, Fatica, Parianne, Maillard, Pauline, Olichney, John, Carmichael, Owen, Bates, Vernice, Capote, Horacio, Rainka, Michelle, Borrie, Michael, Lee, T.-Y., Bartha, Dr Rob, Johnson, Sterling, Asthana, Sanjay, Carlsson, Cynthia M., Perrin, Allison, Burke, Anna, Scharre, Douglas W., Kataki, Maria, Tarawneh, Rawan, Hart, David, Zimmerman, Earl A., Celmins, Dzintra, Miller, Delwyn D., BolesPonto, Laura L., Smith, Karen Ekstam, Koleva, Hristina, Shim, Hyungsub, Nam, Ki Won, Schultz, Susan K., Williamson, Jeff D., Craft, Suzanne, Cleveland, Jo, Yang, Mia, Sink, Kaycee M., Ott, Brian R., Drake, Jonathan, Tremont, Geoffrey, Daiello, Lori A., Drake, Jonathan D., Ritter, Aaron, Bernick, Charles, Munic, Donna, O'Connelll, Abigail, Mintzer, Jacobo, Wiliams, Arthur, Masdeu, Joseph, Shi, Jiong, Garcia, Angelica, Newhouse, Paul, Potkin, Steven, Salloway, Stephen, Malloy, Paul, Correia, Stephen, Kittur, Smita, Pearlson, Godfrey D., Blank, Karen, Anderson, Karen, Flashman, Laura A., Seltzer, Marc, Hynes, Mary L., Santulli, Robert B., Relkin, Norman, Chiang, Gloria, Lee, Athena, Lin, Michael, Ravdin, Lisa, Petersen, Ron, Neylan, Thomas, Grafman, Jordan, Danowski, Sarah, Nguyen-Barrera, Catherine, Hayes, Jacqueline, Finley, Shannon, Bernstein, Matthew, Senjem, Matt, Foster, Norm, Kim, Sungeun, Sood, Ajay, Blanchard, Kimberly S., Fleischman, Debra, Arfanakis, Konstantinos, Varon, Daniel, Greig, Maria T., Petrella, Jeffrey R., Goldstein, Bonnie, Martin, Kimberly S., Reist, Christopher, Sadowsky, Carl, Martinez, Walter, Villena, Teresa, Rosen, Howard, Marshall, Gad, Peskind, Elaine R., Petrie, Eric C., Li, Gail, Mackin, Scott, Jimenez-Maggiora, Gustavo, Drake, Erin, Donohue, Mike, Nelson, Craig, Bickford, David, Butters, Meryl, Zmuda, Michelle, Reyes, Denise, Faber, Kelley M., Nudelman, Kelly N., Au, Yiu Ho, Scherer, Kelly, Catalinotto, Daniel, Stark, Samuel, Ong, Elise, Fernandez, Dariella, Jo, Taeho, Kim, Junpyo, Bice, Paula, Huynh, Kevin, Wang, Tingting, Meikle, Peter J., and Giles, Corey

Published
2023
Full Text
View/download PDF

13. Women can bear a bigger burden: ante- and post-mortem evidence for reserve in the face of tau

Author

Digma, Leonardino A, Madsen, John R, Rissman, Robert A, Jacobs, Diane M, Brewer, James B, Banks, Sarah J, 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, and Oliver, Angela

Subjects
Biological Psychology, Psychology, Brain Disorders, Neurodegenerative, Alzheimer's Disease, Neurosciences, Acquired Cognitive Impairment, Women's Health, Aging, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Dementia, Clinical Research, tau, verbal memory, sex differences, Alzheimer's disease, Alzheimer’s Disease Neuroimaging Initiative, Alzheimer’s disease, Clinical sciences, Biological psychology
Abstract

In this study, we aimed to assess whether women are able to withstand more tau before exhibiting verbal memory impairment. Using data from 121 amyloid-β-positive Alzheimer's Disease Neuroimaging Initiative participants, we fit a linear model with Rey Auditory Verbal Learning Test score as the response variable and tau-PET standard uptake value ratio as the predictor and took the residuals as an estimate of verbal memory reserve for each subject. Women demonstrated higher reserve (i.e. residuals), whether the Learning (t = 2.78, P = 0.006) or Delay (t = 2.14, P = 0.03) score from the Rey Auditory Verbal Learning Test was used as a measure of verbal memory ability. To validate these findings, we examined 662 National Alzheimer's Coordinating Center participants with a C2/C3 score (Consortium to Establish a Registry for Alzheimer's Disease) at autopsy. We stratified our National Alzheimer's Coordinating Center sample into Braak 1/2, Braak 3/4 and Braak 5/6 subgroups. Within each subgroup, we compared Logical Memory scores between men and women. Men had worse verbal memory scores within the Braak 1/2 (Logical Memory Immediate: β = -5.960 ± 1.517, P

Published
2020

14. Comparison of Pittsburgh compound B and florbetapir in cross‐sectional and longitudinal studies

Author

Su, Yi, Flores, Shaney, Wang, Guoqiao, Hornbeck, Russ C, Speidel, Benjamin, Joseph‐Mathurin, Nelly, Vlassenko, Andrei G, Gordon, Brian A, Koeppe, Robert A, Klunk, William E, Jack, Clifford R, Farlow, Martin R, Salloway, Stephen, Snider, Barbara J, Berman, Sarah B, Roberson, Erik D, Brosch, Jared, Jimenez‐Velazques, Ivonne, Dyck, Christopher H, Galasko, Douglas, Yuan, Shauna H, Jayadev, Suman, Honig, Lawrence S, Gauthier, Serge, Hsiung, Ging‐Yuek R, Masellis, Mario, Brooks, William S, Fulham, Michael, Clarnette, Roger, Masters, Colin L, Wallon, David, Hannequin, Didier, Dubois, Bruno, Pariente, Jeremie, Sanchez‐Valle, Raquel, Mummery, Catherine, Ringman, John M, Bottlaender, Michel, Klein, Gregory, Milosavljevic‐Ristic, Smiljana, McDade, Eric, Xiong, Chengjie, Morris, John C, Bateman, Randall J, and Benzinger, Tammie LS

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Bioengineering, Aging, Alzheimer's Disease, Clinical Research, Brain Disorders, Neurodegenerative, Dementia, Acquired Cognitive Impairment, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Biomedical Imaging, Neurosciences, Detection, screening and diagnosis, 4.1 Discovery and preclinical testing of markers and technologies, PiB, Florbetapir, Amyloid imaging, Centiloid, Positron emission tomography, Genetics, Biological psychology
Abstract

IntroductionQuantitative in vivo measurement of brain amyloid burden is important for both research and clinical purposes. However, the existence of multiple imaging tracers presents challenges to the interpretation of such measurements. This study presents a direct comparison of Pittsburgh compound B-based and florbetapir-based amyloid imaging in the same participants from two independent cohorts using a crossover design.MethodsPittsburgh compound B and florbetapir amyloid PET imaging data from three different cohorts were analyzed using previously established pipelines to obtain global amyloid burden measurements. These measurements were converted to the Centiloid scale to allow fair comparison between the two tracers. The mean and inter-individual variability of the two tracers were compared using multivariate linear models both cross-sectionally and longitudinally.ResultsGlobal amyloid burden measured using the two tracers were strongly correlated in both cohorts. However, higher variability was observed when florbetapir was used as the imaging tracer. The variability may be partially caused by white matter signal as partial volume correction reduces the variability and improves the correlations between the two tracers. Amyloid burden measured using both tracers was found to be in association with clinical and psychometric measurements. Longitudinal comparison of the two tracers was also performed in similar but separate cohorts whose baseline amyloid load was considered elevated (i.e., amyloid positive). No significant difference was detected in the average annualized rate of change measurements made with these two tracers.DiscussionAlthough the amyloid burden measurements were quite similar using these two tracers as expected, difference was observable even after conversion into the Centiloid scale. Further investigation is warranted to identify optimal strategies to harmonize amyloid imaging data acquired using different tracers.

Published
2019

15. Optimizing quantification of MK6240 tau PET in unimpaired older adults

Author

Harrison, Theresa M., Ward, Tyler J., Murphy, Alice, Baker, Suzanne L., Dominguez, Pablo A., Koeppe, Robert, Vemuri, Prashanthi, Lockhart, Samuel N., Jung, Youngkyoo, Harvey, Danielle J., Lovato, Laura, Toga, Arthur W., Masdeu, Joseph, Oh, Hwamee, Gitelman, Darren R., Aggarwal, Neelum, Snyder, Heather M., Baker, Laura D., DeCarli, Charles, Jagust, William J., and Landau, Susan M.

Published
2023
Full Text
View/download PDF

18. Comparison of amyloid burden in individuals 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 MD, 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, Adams, Sarah, Allegri, Ricardo, Araki, Aki, Barthelemy, Nicolas, Bechara, Jacob, Berman, Sarah, Bodge, Courtney, Brandon, Susan, Brooks, William, Brosch, Jared, Buck, Jill, Buckles, Virginia, Carter, Kathleen, Cash, Lisa, Mendez, Patricio C, Chua, Jasmin, Chui, Helena, Courtney, Laura, Day, Gregory, DeLaCruz, Chrismary, Denner, Darcy, Diffenbacher, Anna, Dincer, Aylin, Donahue, Tamara, Douglas, Jane, Duong, Duc, Egido, Noelia, Esposito, Bianca, Farlow, Marty, Feldman, Becca, Fitzpatrick, Colleen, Fox, Nick, Franklin, Erin, Joseph-Mathurin, Nelly, Fujii, Hisako, Gardener, Samantha, Ghetti, Bernardino, Goate, Alison, Goldberg, Sarah, Goldman, Jill, Gonzalez, Alyssa, Gräber-Sultan, Susanne, Graff-Radford, Neill, Graham, Morgan, Gray, Julia, Gremminger, Emily, Grilo, Miguel, Groves, Alex, Haass, Christian, Häslerc, Lisa, Hellm, Cortaiga, Herries, Elizabeth, Hoechst-Swisher, Laura, Hofmann, Anna, Holtzman, David, Hornbeck, Russ, Igor, Yakushev, Ihara, Ryoko, Ikeuchi, Takeshi, Ikonomovic, Snezana, Ishii, Kenji, Jack, Clifford, Jerome, Gina, Johnson, Erik, Jucker, Mathias, Karch, Celeste, Käser, Stephan, Kasuga, Kensaku, Keefe, Sarah, Klunk, William, Koeppe, Robert, Koudelis, Deb, Kuder-Buletta, Elke, Laske, Christoph, Levey, Allan, Levin, Johannes, Li, Yan, Lopez, Oscar, Marsh, Jacob, Martins, Ralph, Mason, Neal S, Masters, Colin, Mawuenyega, Kwasi, McCullough, Austin, Mejia, Arlene, Morenas-Rodriguez, Estrella, Morris, John C, Mountz, James, Mummery, Catherine, Nagamatsu, Akemi, Neimeyer, Katie, Niimi, Yoshiki, Noble, James, Norton, Joanne, Nuscher, Brigitte, Obermüller, Ulricke, O'Connor, Antoinette, Patira, Riddhi, Ping, Lingyan, Preische, Oliver, Renton, Alan, Ringman, John, Salloway, Stephen, Schofield, Peter, Senda, Michio, Seyfried, Nicholas T, Shady, Kristine, Shimada, Hiroyuki, Sigurdson, Wendy, Smith, Jennifer, Smith, Lori, Snitz, Beth, Sohrabi, Hamid, Stephens, Sochenda, Taddei, Kevin, Thompson, Sarah, Vöglein, Jonathan, Wang, Peter, Wang, Qing, Weamer, Elise, Xu, Jinbin, Xu, Xiong, Boerwinkle, Anna H, Gordon, Brian A, Wisch, Julie, Flores, Shaney, Henson, Rachel L, Butt, Omar H, McKay, Nicole, Chen, Charles D, Benzinger, Tammie L S, Fagan, Anne M, Handen, Benjamin L, Christian, Bradley T, Head, Elizabeth, Mapstone, Mark, Rafii, Michael S, O'Bryant, Sid, Lai, Florence, Rosas, H Diana, Lee, Joseph H, Silverman, Wayne, Brickman, Adam M, Chhatwal, Jasmeer P, Cruchaga, Carlos, Perrin, Richard J, Xiong, Chengjie, Hassenstab, Jason, McDade, Eric, Bateman, Randall J, and Ances, Beau M

Published
2023
Full Text
View/download PDF

21. Predicting brain age from functional connectivity in symptomatic and preclinical Alzheimer disease

Author

Adams, Sarah, Allegri, Ricardo, Araki, Aki, Barthelemy, Nicolas, Bateman, Randall, Bechara, Jacob, Benzinger, Tammie, Berman, Sarah, Bodge, Courtney, Brandon, Susan, Brooks, William (Bill), Brosch, Jared, Buck, Jill, Buckles, Virginia, Carter, Kathleen, Cash, Lisa, Chen, Charlie, Chhatwal, Jasmeer, Mendez, Patricio Chrem, Chua, Jasmin, Chui, Helena, Courtney, Laura, Cruchaga, Carlos, Day, Gregory S, DeLaCruz, Chrismary, Denner, Darcy, Diffenbacher, Anna, Dincer, Aylin, Donahue, Tamara, Douglas, Jane, Duong, Duc, Egido, Noelia, Esposito, Bianca, Fagan, Anne, Farlow, Marty, Feldman, Becca, Fitzpatrick, Colleen, Flores, Shaney, Fox, Nick, Franklin, Erin, Joseph-Mathurin, Nelly, Fujii, Hisako, Gardener, Samantha, Ghetti, Bernardino, Goate, Alison, Goldberg, Sarah, Goldman, Jill, Gonzalez, Alyssa, Gordon, Brian, Gräber-Sultan, Susanne, Graff-Radford, Neill, Graham, Morgan, Gray, Julia, Gremminger, Emily, Grilo, Miguel, Groves, Alex, Haass, Christian, Häsler, Lisa, Hassenstab, Jason, Hellm, Cortaiga, Herries, Elizabeth, Hoechst-Swisher, Laura, Hofmann, Anna, Holtzman, David, Hornbeck, Russ, Igor, Yakushev, Ihara, Ryoko, Ikeuchi, Takeshi, Ikonomovic, Snezana, Ishii, Kenji, Jack, Clifford, Jerome, Gina, Johnson, Erik, Jucker, Mathias, Karch, Celeste, Käser, Stephan, Kasuga, Kensaku, Keefe, Sarah, Klunk, William, Koeppe, Robert, Koudelis, Deb, Kuder-Buletta, Elke, Laske, Christoph, Levey, Allan, Levin, Johannes, Li, Yan, Lopez, Oscar, Marsh, Jacob, Martins, Ralph, Mason, Neal Scott, Masters, Colin, Mawuenyega, Kwasi, McCullough, Austin, McDade, Eric, Mejia, Arlene, Morenas-Rodriguez, Estrella, Morris, John, Mountz, James, Mummery, Cath, Nadkarni, N eelesh, Nagamatsu, Akemi, Neimeyer, Katie, Niimi, Yoshiki, Noble, James, Norton, Joanne, Nuscher, Brigitte, Obermüller, Ulricke, O'Connor, Antoinette, Patira, Riddhi, Perrin, Richard, Ping, Lingyan, Preische, Oliver, Renton, Alan, Ringman, John, Salloway, Stephen, Schofield, Peter, Senda, Michio, Seyfried, Nicholas T, Shady, Kristine, Shimada, Hiroyuki, Sigurdson, Wendy, Smith, Jennifer, Smith, Lori, Snitz, Beth, Sohrabi, Hamid, Stephens, Sochenda, Taddei, Kevin, Thompson, Sarah, Vöglein, Jonathan, Wang, Peter, Wang, Qing, Weamer, Elise, Xiong, Chengjie, Xu, Jinbin, Xu, Xiong, Millar, Peter R., Luckett, Patrick H., Gordon, Brian A., Benzinger, Tammie L.S., Schindler, Suzanne E., Fagan, Anne M., Bateman, Randall J., Lee, Jae-Hong, Mori, Hiroshi, Salloway, Stephen P, Yakushev, Igor, Morris, John C., and Ances, Beau M.

Published
2022
Full Text
View/download PDF

22. Soluble TREM2 in CSF and its association with other biomarkers and cognition in autosomal-dominant Alzheimer's disease: a longitudinal observational study

Author

Adams, Sarah, Allegri, Ricardo, Araki, Aki, Barthelemy, Nicolas, Bechara, Jacob, Berman, Sarah, Bodge, Courtney, Brandon, Susan, Brooks, William (Bill), Brosch, Jared, Buck, Jill, Buckles, Virginia, Carter, Kathleen, Cash, Lisa, Chen, Charlie, Chhatwal, Jasmeer, Chrem, Patricio, Chua, Jasmin, Chui, Helena, Cruchaga, Carlos, Day, Gregory S, De La Cruz, Chrismary, Denner, Darcy, Diffenbacher, Anna, Dincer, Aylin, Donahue, Tamara, Douglas, Jane, Duong, Duc, Egido, Noelia, Esposito, Bianca, Farlow, Marty, Feldman, Becca, Fitzpatrick, Colleen, Flores, Shaney, Fox, Nick, Franklin, Erin, Friedrichsen, Nelly, Fujii, Hisako, Gardener, Samantha, Ghetti, Bernardino, Goate, Alison, Goldberg, Sarah, Goldman, Jill, Gonzalez, Alyssa, Gräber-Sultan, Susanne, Graff-Radford, Neill, Graham, Morgan, Gray, Julia, Gremminger, Emily, Grilo, Miguel, Groves, Alex, Häsler, Lisa, Hellm, Cortaiga, Herries, Elizabeth, Hoechst-Swisher, Laura, Hofmann, Anna, Holtzman, David, Hornbeck, Russ, Igor, Yakushev, Ihara, Ryoko, Ikeuchi, Takeshi, Ikonomovic, Snezana, Ishii, Kenji, Jack, Clifford, Jerome, Gina, Johnson, Erik, Käser, Stephan, Kasuga, Kensaku, Keefe, Sarah, Klunk, William (Bill), Koeppe, Robert, Koudelis, Deb, Kuder-Buletta, Elke, Laske, Christoph, Levey, Allan, Lopez, Oscar, Marsh, Jacob, Martinez, Rita, Martins, Ralph, Mason, Neal Scott, Masters, Colin, Mawuenyega, Kwasi, McCullough, Austin, Mejia, Arlene, MountzMD, James, Mummery, Cath, Nadkarni, Neelesh, Nagamatsu, Akemi, Neimeyer, Katie, Niimi, Yoshiki, Noble, James, Norton, Joanne, Nuscher, Brigitte, O'Connor, Antoinette, Obermüller, Ulricke, Patira, Riddhi, Perrin, Richard, Ping, Lingyan, Preische, Oliver, Renton, Alan, Ringman, John, Salloway, Stephen, Schofield, Peter, Senda, Michio, Seyfried, Nick, Shady, Kristine, Shimada, Hiroyuki, Sigurdson, Wendy, Smith, Jennifer, Smith, Lori, Snitz, Beth, Sohrabi, Hamid, Stephens, Sochenda, Taddei, Kevin, Thompson, Sarah, Wang, Peter, Wang, Qing, Weamer, Elise, Xu, Jinbin, Xu, Xiong, Morenas-Rodríguez, Estrella, Li, Yan, Franzmeier, Nicolai, Xiong, Chengjie, Suárez-Calvet, Marc, Fagan, Anne M, Schultz, Stephanie, Gordon, Brian A, Benzinger, Tammie L S, Hassenstab, Jason, McDade, Eric, Feederle, Regina, Karch, Celeste M, Schlepckow, Kai, Morris, John C, Kleinberger, Gernot, Nellgard, Bengt, Vöglein, Jonathan, Blennow, Kaj, Zetterberg, Henrik, Ewers, Michael, Jucker, Mathias, Levin, Johannes, Bateman, Randall J, and Haass, Christian

Published
2022
Full Text
View/download PDF

26. Comparing amyloid-β plaque burden with antemortem PiB PET in autosomal dominant and late-onset Alzheimer disease

Author

Chen, Charles D., Joseph-Mathurin, Nelly, Sinha, Namita, Zhou, Aihong, Li, Yan, Friedrichsen, Karl, McCullough, Austin, Franklin, Erin E., Hornbeck, Russ, Gordon, Brian, Sharma, Vijay, Cruchaga, Carlos, Goate, Alison, Karch, Celeste, McDade, Eric, Xiong, Chengjie, Bateman, Randall J., Ghetti, Bernardino, Ringman, John M., Chhatwal, Jasmeer, Masters, Colin L., McLean, Catriona, Lashley, Tammaryn, Su, Yi, Koeppe, Robert, Jack, Clifford, Klunk, William E., Morris, John C., Perrin, Richard J., Cairns, Nigel J., and Benzinger, Tammie L. S.

Published
2021
Full Text
View/download PDF

27. 18F-florbetapir Positron Emission Tomography–determined Cerebral &bgr;-Amyloid Deposition and Neurocognitive Performance after Cardiac Surgery

Author

Klinger, Rebecca Y, James, Olga G, Borges-Neto, Salvador, Bisanar, Tiffany, Li, Yi-Ju, Qi, Wenjing, Berger, Miles, Terrando, Niccolò, Newman, Mark F, Doraiswamy, P Murali, Mathew, Joseph P, Weiner, Michael W, Aisen, Paul, Weiner, Michael, 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, Khachaturian, Zaven, Sorensen, Greg, Carrillo, Maria, Kuller, Lew, Raichle, Marc, Paul, Steven, Davies, Peter, Fillit, Howard, Hefti, Franz, Holtzman, David, Mesulam, M Marcel, Potter, William, Snyder, Peter, Schwartz, Adam, Montine, Tom, Thomas, Ronald G, Donohue, Michael, Walter, Sarah, Gessert, Devon, Sather, Tamie, Jiminez, Gus, Balasubramanian, Archana B, Mason, Jennifer, Sim, Iris, 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, Morris, John C, Cairns, Louis Nigel J, Franklin, Erin, Taylor-Reinwald, Lisa, Lee, Virginia, Korecka, Magdalena, Figurski, Michal, Crawford, Karen, Neu, Scott, Foroud, Tatiana M, Potkin, Steven, Shen, Li, Faber, Kelley, Kim, Sungeun, Nho, Kwangsik, Thal, Lean, Thal, Leon, and Buckholtz, Neil

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Mental Health, Aging, Brain Disorders, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Behavioral and Social Science, Biomedical Imaging, Clinical Research, Neurosciences, Alzheimer's Disease, Dementia, Neurodegenerative, Acquired Cognitive Impairment, 2.1 Biological and endogenous factors, Neurological, Aged, Amyloid beta-Peptides, Aniline Compounds, Brain, Cardiac Surgical Procedures, Cognitive Dysfunction, Ethylene Glycols, Female, Fluorine Radioisotopes, Humans, Male, Mental Status and Dementia Tests, Middle Aged, Positron-Emission Tomography, Postoperative Complications, Prospective Studies, Alzheimer’s Disease Neuroimaging Initiative (ADNI) Study Group, Neurologic Outcomes Research Group, Anesthesiology, Clinical sciences
Abstract

BackgroundAmyloid deposition is a potential contributor to postoperative cognitive dysfunction. The authors hypothesized that 6-week global cortical amyloid burden, determined by F-florbetapir positron emission tomography, would be greater in those patients manifesting cognitive dysfunction at 6 weeks postoperatively.MethodsAmyloid deposition was evaluated in cardiac surgical patients at 6 weeks (n = 40) and 1 yr (n = 12); neurocognitive function was assessed at baseline (n = 40), 6 weeks (n = 37), 1 yr (n = 13), and 3 yr (n = 9). The association of 6-week amyloid deposition with cognitive dysfunction was assessed by multivariable regression, accounting for age, years of education, and baseline cognition. Differences between the surgical cohort with cognitive deficit and the Alzheimer's Disease Neuroimaging Initiative cohorts (normal and early/late mild cognitive impairment) was assessed, adjusting for age, education, and apolipoprotein E4 genotype.ResultsThe authors found that 6-week abnormal global cortical amyloid deposition was not associated with cognitive dysfunction (13 of 37, 35%) at 6 weeks postoperatively (median standard uptake value ratio [interquartile range]: cognitive dysfunction 0.92 [0.89 to 1.07] vs. 0.98 [0.93 to 1.05]; P = 0.455). In post hoc analyses, global cortical amyloid was also not associated with cognitive dysfunction at 1 or 3 yr postoperatively. Amyloid deposition at 6 weeks in the surgical cohort was not different from that in normal Alzheimer's Disease Neuroimaging Initiative subjects, but increased over 1 yr in many areas at a rate greater than in controls.ConclusionsIn this study, postoperative cognitive dysfunction was not associated with 6-week cortical amyloid deposition. The relationship between cognitive dysfunction and regional amyloid burden and the rate of postoperative amyloid deposition merit further investigation.

Published
2018

28. Identification of genetic risk factors in the Chinese population implicates a role of immune system in Alzheimer’s disease pathogenesis

Author

Zhou, Xiaopu, Chen, Yu, Mok, Kin Y, Zhao, Qianhua, Chen, Keliang, Chen, Yuewen, Hardy, John, Li, Yun, Fu, Amy KY, Guo, Qihao, Ip, Nancy Y, Saykin, Andrew J, Toga, Arthur W, Borowski, Bret, Ward, Chad, DeCarli, Charles, Mathis, Chet, Jack, Clifford R, Harvey, Danielle, Holtzman, David, Jones, David, Gessert, Devon, Lilly, Eli, Reiman, Eric M, Franklin, Erin, Hefti, Franz, Sorensen, Greg, Jimenez, Gustavo, Fillit, Howard, Gunter, Jeff, Salazar, Jennifer, Hsiao, John, Morris, John, Trojanowki, John Q, Neu, Karen Crawford Scott, Kantarci, Kejal, Faber, Kelley, Harless, Kelly, Chen, Kewei, Nho, Kwangsik, Beckett, Laurel, Thal, Lean, Thal, Leon, Shaw, Leslie M, Kuller, Lew, Shen, Li, Hergesheimer, Lindsey, Taylor-Reinwald, Lisa, Mesulam, M Marcel, Korecka, Magdalena, Raichle, Marc, Carrillo, Maria, Albert, Marilyn, Senjem, Matt, Bernstein, Matthew, Donohue, Michael, Weiner, Michael, Figurski, Michal, Buckholtz, Neil, Fox, Nick, Cairns, Nigel J, Schuff, Norbert, Foster, Norm, Aisen, Paul, Thompson, Paul, Davies, Peter, Snyder, Peter J, Snyder, Peter, Vemuri, Prashanthi, Frank, Richard, Koeppe, Robert A, Green, Robert C, Petersen, Ronald, Walter, Sarah, Paul, Steven, Potkin, Steven, Kim, Sungeun, Foroud, Tatiana M, Montine, Tom, Lee, Virginia, Jagust, William, Potter, William, Cabrera, Yuliana, Khachaturian, Zaven, Fleisher, Adam, Pierce, Aimee, Mintz, Akiva, Lerner, Alan, Norbash, Alexander, Levey, Allan I, Rosen, Allyson, Smith, Amanda, Ulysse, Anaztasia, Budson, Andrew E, Kertesz, Andrew, Oliver, Angela, Hake, Ann Marie, Burke, Anna, Sarrael, Antero, and Porsteinsson, Anton P

Subjects
Biological Sciences, Genetics, Dementia, Acquired Cognitive Impairment, Prevention, Brain Disorders, Aging, Human Genome, Neurosciences, Alzheimer's Disease, Neurodegenerative, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), 2.1 Biological and endogenous factors, Aetiology, Detection, screening and diagnosis, 4.1 Discovery and preclinical testing of markers and technologies, Good Health and Well Being, Age of Onset, Aged, Aged, 80 and over, Alzheimer Disease, Apolipoproteins E, Asian People, China, Cohort Studies, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, Genotype, Humans, Immune System, Male, Middle Aged, Potassium Channels, Inwardly Rectifying, Risk Factors, Alzheimer’s Disease Neuroimaging Initiative, Alzheimer’s disease, GWAS, immune, risk variant, whole-genome sequencing
Abstract

Alzheimer's disease (AD) is a leading cause of mortality among the elderly. We performed a whole-genome sequencing study of AD in the Chinese population. In addition to the variants identified in or around the APOE locus (sentinel variant rs73052335, P = 1.44 × 10-14), two common variants, GCH1 (rs72713460, P = 4.36 × 10-5) and KCNJ15 (rs928771, P = 3.60 × 10-6), were identified and further verified for their possible risk effects for AD in three small non-Asian AD cohorts. Genotype-phenotype analysis showed that KCNJ15 variant rs928771 affects the onset age of AD, with earlier disease onset in minor allele carriers. In addition, altered expression level of the KCNJ15 transcript can be observed in the blood of AD subjects. Moreover, the risk variants of GCH1 and KCNJ15 are associated with changes in their transcript levels in specific tissues, as well as changes of plasma biomarkers levels in AD subjects. Importantly, network analysis of hippocampus and blood transcriptome datasets suggests that the risk variants in the APOE, GCH1, and KCNJ15 loci might exert their functions through their regulatory effects on immune-related pathways. Taking these data together, we identified common variants of GCH1 and KCNJ15 in the Chinese population that contribute to AD risk. These variants may exert their functional effects through the immune system.

Published
2018

29. Anxiety in late-life depression: Associations with brain volume, amyloid beta, white matter lesions, cognition, and functional ability

Author

Kryza-Lacombe, Maria, primary, Kassel, Michelle T., additional, Insel, Philip S., additional, Rhodes, Emma, additional, Bickford, David, additional, Burns, Emily, additional, Butters, Meryl A., additional, Tosun, Duygu, additional, Aisen, Paul, additional, Raman, Rema, additional, Landau, Susan, additional, Saykin, Andrew J., additional, Toga, Arthur W., additional, Jack, Clifford R., additional, Koeppe, Robert, additional, Weiner, Michael W., additional, Nelson, Craig, additional, and Mackin, R. Scott, additional

Published
2024
Full Text
View/download PDF

30. A trial of gantenerumab or solanezumab in dominantly inherited Alzheimer’s disease

Author

Salloway, Stephen, Farlow, Martin, McDade, Eric, Clifford, David B., Wang, Guoqiao, Llibre-Guerra, Jorge J., Hitchcock, Janice M., Mills, Susan L., Santacruz, Anna M., Aschenbrenner, Andrew J., Hassenstab, Jason, Benzinger, Tammie L. S., Gordon, Brian A., Fagan, Anne M., Coalier, Kelley A., Cruchaga, Carlos, Goate, Alison A., Perrin, Richard J., Xiong, Chengjie, Li, Yan, Morris, John C., Snider, B. Joy, Mummery, Catherine, Surti, G. Mustafa, Hannequin, Didier, Wallon, David, Berman, Sarah B., Lah, James J., Jimenez-Velazquez, Ivonne Z., Roberson, Erik D., van Dyck, Christopher H., Honig, Lawrence S., Sánchez-Valle, Raquel, Brooks, William S., Gauthier, Serge, Galasko, Douglas R., Masters, Colin L., Brosch, Jared R., Hsiung, Ging-Yuek Robin, Jayadev, Suman, Formaglio, Maité, Masellis, Mario, Clarnette, Roger, Pariente, Jérémie, Dubois, Bruno, Pasquier, Florence, Jack, Jr, Clifford R., Koeppe, Robert, Snyder, Peter J., Aisen, Paul S., Thomas, Ronald G., Berry, Scott M., Wendelberger, Barbara A., Andersen, Scott W., Holdridge, Karen C., Mintun, Mark A., Yaari, Roy, Sims, John R., Baudler, Monika, Delmar, Paul, Doody, Rachelle S., Fontoura, Paulo, Giacobino, Caroline, Kerchner, Geoffrey A., and Bateman, Randall J.

Published
2021
Full Text
View/download PDF

31. An updated synthesis of [11C]carfentanil for positron emission tomography (PET) imaging of the μ‐opioid receptor

Author

Blecha, Joseph E, Henderson, Bradford D, Hockley, Brian G, VanBrocklin, Henry F, Zubieta, Jon‐Kar, DaSilva, Alexandre F, Kilbourn, Michael R, Koeppe, Robert A, Scott, Peter JH, and Shao, Xia

Subjects
Biomedical Imaging, Good Health and Well Being, Carbon Radioisotopes, Chemistry Techniques, Synthetic, Fentanyl, Positron-Emission Tomography, Radiochemistry, Receptors, Opioid, mu, C-11, carbon-11, opioid, PET radiochemistry, radiosynthesis, Organic Chemistry, Pharmacology and Pharmaceutical Sciences, Medicinal & Biomolecular Chemistry
Abstract

[11 C]Carfentanil ([11 C]CFN) is a selective radiotracer for in vivo positron emission tomography imaging studies of the μ-opioid system that, in our laboratories, is synthesized by methylation of the corresponding carboxylate precursor with [11 C]MeOTf, and purified using a C2 solid-phase extraction cartridge. Changes in the commercial availability of common C2 cartridges have necessitated future proofing the synthesis of [11 C]CFN to maintain reliable delivery of the radiotracer for clinical imaging studies. An updated synthesis of [11 C]CFN is reported that replaces a now obsolete purification cartridge with a new commercially available version and also substitutes the organic solvents used in traditional production methods with ethanol.

Published
2017

32. Bayesian model reveals latent atrophy factors with dissociable cognitive trajectories in Alzheimer’s disease

Author

Zhang, Xiuming, Mormino, Elizabeth C, Sun, Nanbo, Sperling, Reisa A, Sabuncu, Mert R, Yeo, BT Thomas, Weiner, Michael W, Aisen, Paul, Weiner, Michael, 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, Khachaturian, Zaven, Sorensen, Greg, Carrillo, Maria, Kuller, Lew, Raichle, Marc, Paul, Steven, Davies, Peter, Fillit, Howard, Hefti, Franz, Holtzman, David, Mesulam, M Marcel, Potter, William, Snyder, Peter, Schwartz, Adam, Montine, Tom, Thomas, Ronald G, Donohue, Michael, Walter, Sarah, Gessert, Devon, Sather, Tamie, Jiminez, Gus, Balasubramanian, Archana B, Mason, Jennifer, Sim, Iris, Harvey, Danielle, Bernstein, Matthew, Fox, Nick, Thompson, Paul, Schuff, Norbert, DeCArli, Charles, Borowski, Davis 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, Morris, John C, Cairns, Nigel J, Franklin, Erin, Taylor-Reinwald, Lisa, Lee, Virginia, Korecka, Magdalena, Figurski, Michal, Crawford, Karen, Neu, Scott, Foroud, Tatiana M, Potkin, Steven, Shen, Li, Faber, Kelley, Kim, Sungeun, Nho, Kwangsik, Thal, Lean, Thal, Leon, Buckholtz, Neil, Snyder, Peter J, Albert, Marilyn, and Frank, Richard

Subjects
Biological Psychology, Psychology, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Alzheimer's Disease, Clinical Research, Aging, Brain Disorders, Dementia, Neurosciences, Neurodegenerative, Acquired Cognitive Impairment, Aetiology, 2.1 Biological and endogenous factors, Neurological, Alzheimer Disease, Atrophy, Bayes Theorem, Brain, Cognitive Dysfunction, Female, Humans, Magnetic Resonance Imaging, Male, Risk Factors, mental disorder subtypes, Alzheimer's disease subtypes, Alzheimer's disease heterogeneity, voxel-based morphometry, unsupervised machine learning, Alzheimer’s Disease Neuroimaging Initiative, Alzheimer’s disease heterogeneity, Alzheimer’s disease subtypes
Abstract

We used a data-driven Bayesian model to automatically identify distinct latent factors of overlapping atrophy patterns from voxelwise structural MRIs of late-onset Alzheimer's disease (AD) dementia patients. Our approach estimated the extent to which multiple distinct atrophy patterns were expressed within each participant rather than assuming that each participant expressed a single atrophy factor. The model revealed a temporal atrophy factor (medial temporal cortex, hippocampus, and amygdala), a subcortical atrophy factor (striatum, thalamus, and cerebellum), and a cortical atrophy factor (frontal, parietal, lateral temporal, and lateral occipital cortices). To explore the influence of each factor in early AD, atrophy factor compositions were inferred in beta-amyloid-positive (Aβ+) mild cognitively impaired (MCI) and cognitively normal (CN) participants. All three factors were associated with memory decline across the entire clinical spectrum, whereas the cortical factor was associated with executive function decline in Aβ+ MCI participants and AD dementia patients. Direct comparison between factors revealed that the temporal factor showed the strongest association with memory, whereas the cortical factor showed the strongest association with executive function. The subcortical factor was associated with the slowest decline for both memory and executive function compared with temporal and cortical factors. These results suggest that distinct patterns of atrophy influence decline across different cognitive domains. Quantification of this heterogeneity may enable the computation of individual-level predictions relevant for disease monitoring and customized therapies. Factor compositions of participants and code used in this article are publicly available for future research.

Published
2016

34. Accelerating rates of cognitive decline and imaging markers associated with &bgr;-amyloid pathology

Author

Insel, Philip S, Mattsson, Niklas, Mackin, R Scott, Schöll, Michael, Nosheny, Rachel L, Tosun, Duygu, Donohue, Michael C, Aisen, Paul S, Jagust, William J, Weiner, Michael W, 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, Liu, Enchi, Montine, Tom, Gamst, Anthony, Thomas, Ronald G, Donohue, Michael, Walter, Sarah, Gessert, Devon, Sather, Tamie, Harvey, Danielle, Kornak, John, Dale, Anders, Bernstein, Matthew, Felmlee, Joel, Fox, Nick, Thompson, Paul, Schuff, Norbert, Alexander, Gene, DeCarli, Charles, Bandy, Dan, Koeppe, Robert A, Foster, Norm, Reiman, Eric M, Chen, Kewei, Mathis, Chet, Cairns, Nigel J, Taylor-Reinwald, Lisa, Trojanowki, JQ, Shaw, Les, Lee, Virginia MY, Korecka, Magdalena, Crawford, Karen, Neu, Scott, 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, 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, and Griffith, Randall

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Acquired Cognitive Impairment, Dementia, Neurodegenerative, Biomedical Imaging, Brain Disorders, Aging, Alzheimer's Disease, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Neurosciences, Neurological, Aged, Amyloid beta-Peptides, Aniline Compounds, Atrophy, Biomarkers, Brain, Cognition, Cognitive Dysfunction, Disease Progression, Ethylene Glycols, Female, Fluorodeoxyglucose F18, Humans, Longitudinal Studies, Magnetic Resonance Imaging, Male, Mental Status Schedule, Neuropsychological Tests, Peptide Fragments, Positron-Emission Tomography, Radiopharmaceuticals, Regression Analysis, Alzheimer's Disease Neuroimaging Initiative, Cognitive Sciences, Neurology & Neurosurgery, Clinical sciences
Abstract

ObjectiveTo estimate points along the spectrum of β-amyloid pathology at which rates of change of several measures of neuronal injury and cognitive decline begin to accelerate.MethodsIn 460 patients with mild cognitive impairment (MCI), we estimated the points at which rates of florbetapir PET, fluorodeoxyglucose (FDG) PET, MRI, and cognitive and functional decline begin to accelerate with respect to baseline CSF Aβ42. Points of initial acceleration in rates of decline were estimated using mixed-effects regression.ResultsRates of neuronal injury and cognitive and even functional decline accelerate substantially before the conventional threshold for amyloid positivity, with rates of florbetapir PET and FDG PET accelerating early. Temporal lobe atrophy rates also accelerate prior to the threshold, but not before the acceleration of cognitive and functional decline.ConclusionsA considerable proportion of patients with MCI would not meet inclusion criteria for a trial using the current threshold for amyloid positivity, even though on average, they are experiencing cognitive/functional decline associated with prethreshold levels of CSF Aβ42. Future trials in early Alzheimer disease might consider revising the criteria regarding β-amyloid thresholds to include the range of amyloid associated with the first signs of accelerating rates of decline.

Published
2016

35. Better verbal memory in women than men in MCI despite similar levels of hippocampal atrophy

Author

Sundermann, Erin E, Biegon, Anat, Rubin, Leah H, Lipton, Richard B, Mowrey, Wenzhu, Landau, Susan, Maki, Pauline M, 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, Liu, Enchi, Montine, Tom, Gamst, Anthony, Thomas, Ronald G, Donohue, Michael, Walter, Sarah, Gessert, Devon, Sather, Tamie, Harvey, Danielle, Kornak, John, Dale, Anders, Bernstein, Matthew, Felmlee, Joel, Fox, Nick, Thompson, Paul, Schuff, Norbert, Alexander, Gene, DeCarli, Charles, Bandy, Dan, Koeppe, Robert A, Foster, Norm, Reiman, Eric M, Chen, Kewei, Mathis, Chet, Cairns, Nigel J, Taylor-Reinwald, Lisa, Trojanowki, JQ, Shaw, Les, Lee, Virginia MY, Korecka, Magdalena, Crawford, Karen, Neu, Scott, 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, 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, and Mitsis, Effie

Subjects
Biomedical and Clinical Sciences, Neurosciences, Clinical Sciences, Prevention, Aging, Behavioral and Social Science, Clinical Research, Alzheimer's Disease, Brain Disorders, Acquired Cognitive Impairment, Neurodegenerative, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Clinical Trials and Supportive Activities, Dementia, 2.1 Biological and endogenous factors, Aetiology, Neurological, Aged, Aged, 80 and over, Atrophy, Cognitive Dysfunction, Cross-Sectional Studies, Female, Hippocampus, Humans, Magnetic Resonance Imaging, Male, Memory, Middle Aged, Sex Characteristics, Verbal Learning, Alzheimer's Disease Neuroimaging Initiative, Cognitive Sciences, Neurology & Neurosurgery, Clinical sciences
Abstract

ObjectiveTo examine sex differences in the relationship between clinical symptoms related to Alzheimer disease (AD) (verbal memory deficits) and neurodegeneration (hippocampal volume/intracranial volume ratio [HpVR]) across AD stages.MethodsThe sample included 379 healthy participants, 694 participants with amnestic mild cognitive impairment (aMCI), and 235 participants with AD and dementia from the Alzheimer's Disease Neuroimaging Initiative who completed the Rey Auditory Verbal Learning Test (RAVLT). Cross-sectional analyses were conducted using linear regression to examine the interaction between sex and HpVR on RAVLT across and within diagnostic groups adjusting for age, education, and APOE ε4 status.ResultsAcross groups, there were significant sex × HpVR interactions for immediate and delayed recall (p < 0.01). Women outperformed men among individuals with moderate to larger HpVR, but not among individuals with smaller HpVR. In diagnosis-stratified analyses, the HpVR × sex interaction was significant in the aMCI group, but not in the control or AD dementia groups, for immediate and delayed recall (p < 0.01). Among controls, women outperformed men on both outcomes irrespective of HpVR (p < 0.001). In AD dementia, better RAVLT performance was independently associated with female sex (immediate, p = 0.04) and larger HpVR (delayed, p = 0.001).ConclusionWomen showed an advantage in verbal memory despite evidence of moderate hippocampal atrophy. This advantage may represent a sex-specific form of cognitive reserve delaying verbal memory decline until more advanced disease stages.

Published
2016

36. Periventricular hyperintensities are associated with elevated cerebral amyloid

Author

Marnane, Michael, Al-Jawadi, Osama O, Mortazavi, Shervin, Pogorzelec, Kathleen J, Wang, Bing Wei, Feldman, Howard H, Hsiung, Ging-Yuek R, 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, Liu, Enchi, Montine, Tom, Gamst, Anthony, Thomas, Ronald G, Donohue, Michael, Walter, Sarah, Gessert, Devon, Sather, Tamie, Harvey, Danielle, Kornak, John, Dale, Anders, Bernstein, Matthew, Felmlee, Joel, Fox, Nick, Thompson, Paul, Schuff, Norbert, Alexander, Gene, DeCarli, Charles, Bandy, Dan, Koeppe, Robert A, Foster, Norm, Reiman, Eric M, Chen, Kewei, Mathis, Chet, Cairns, Nigel J, Taylor-Reinwald, Lisa, Trojanowki, JQ, Shaw, Les, Lee, Virginia MY, Korecka, Magdalena, Crawford, Karen, Neu, Scott, 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, 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, and Mitsis, Effie

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Prevention, Aging, Clinical Research, Alzheimer's Disease, Neurosciences, Brain Disorders, Acquired Cognitive Impairment, Neurodegenerative, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Dementia, 2.1 Biological and endogenous factors, Aetiology, Neurological, Adult, Aged, Aged, 80 and over, Amyloid beta-Peptides, Biomarkers, Cerebral Ventricles, Cognitive Dysfunction, Female, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Positron-Emission Tomography, Prospective Studies, Alzheimer's Disease Neuroimaging Initiative, Cognitive Sciences, Neurology & Neurosurgery, Clinical sciences
Abstract

ObjectiveTo investigate the association between periventricular white mater hyperintensities (PVWMH) and biomarkers of elevated cerebral β-amyloid (Aβ) in the Alzheimer's Disease Neuroimaging Initiative, a large prospective multicenter observational study.MethodsThe burden of frontal, parietal, and occipital PVWMH on 3T fluid-attenuated inversion recovery MRI was evaluated in 698 cognitively normal participants and participants with mild cognitive impairment (MCI) using a novel semiquantitative visual rating scale. Results were correlated with CSF-Aβ, florbetapir-PET, and fluorodeoxyglucose (FDG)-PET.ResultsIncreased burden of parietal, occipital, and frontal PVWMH was associated with elevated cerebral amyloid evidenced by high florbetapir-PET signal (p < 0.01) and low CSF-Aβ (p < 0.01). In logistic regression models, including PVWMH, age, sex, APOE status, vascular risk factors, pulse pressure, vascular secondary prevention medications, education, ethnicity, and race, parietal, occipital, and frontal PVWMH burden was independently associated with high florbetapir-PET uptake (p < 0.05). In a similar logistic regression model, parietal and occipital (p < 0.05) but not frontal (p = 0.05) PVWMH were independently associated with CSF-Aβ. Weaker associations were found between parieto-occipital PVWMH and elevated CSF-tau (p < 0.05) and occipital PVWMH and elevated CSF-phospho-tau (p < 0.05). PVWMH were associated with cerebral hypometabolism on FDG-PET independent of CSF-Aβ levels (p < 0.05). Absolute and consistency of agreement intraclass correlation coefficients were, respectively, 0.83 and 0.83 for frontal, 0.78 and 0.8 for parietal, and 0.45 and 0.75 for occipital PVWMH measurements.ConclusionsIncreased PVWMH were associated with elevated cerebral amyloid independent of potential confounders such as age, APOE genotype, and vascular risk factors. The mechanisms underlying the association between PVWMH and cerebral amyloid remain to be clarified.

Published
2016

37. Correction: Quantitative Amyloid Imaging in Autosomal Dominant Alzheimer’s Disease: Results from the DIAN Study Group

Author

Su, Yi, Blazey, Tyler M, Owen, Christopher J, Christensen, Jon J, Friedrichsen, Karl, Joseph-Mathurin, Nelly, Wang, Qing, Hornbeck, Russ C, Ances, Beau M, Snyder, Abraham Z, Cash, Lisa A, Koeppe, Robert A, Klunk, William E, Galasko, Douglas, Brickman, Adam M, McDade, Eric, Ringman, John M, Thompson, Paul M, Saykin, Andrew J, Ghetti, Bernardino, Sperling, Reisa A, Johnson, Keith A, Salloway, Stephen P, Schofield, Peter R, Masters, Colin L, Villemagne, Victor L, Fox, Nick C, Förster, Stefan, Chen, Kewei, Reiman, Eric M, Xiong, Chengjie, Marcus, Daniel S, Weiner, Michael W, Morris, John C, Bateman, Randall J, and Benzinger, Tammie LS

Subjects
Biochemistry and Cell Biology, Health Sciences, Biological Sciences, Dominantly Inherited Alzheimer Network, General Science & Technology
Abstract

[This corrects the article DOI: 10.1371/journal.pone.0152082.].

Published
2016

38. Quantitative Amyloid Imaging in Autosomal Dominant Alzheimer’s Disease: Results from the DIAN Study Group

Author

Su, Yi, Blazey, Tyler M, Owen, Christopher J, Christensen, Jon J, Friedrichsen, Karl, Joseph-Mathurin, Nelly, Wang, Qing, Hornbeck, Russ C, Ances, Beau M, Snyder, Abraham Z, Cash, Lisa A, Koeppe, Robert A, Klunk, William E, Galasko, Douglas, Brickman, Adam M, McDade, Eric, Ringman, John M, Thompson, Paul M, Saykin, Andrew J, Ghetti, Bernardino, Sperling, Reisa A, Johnson, Keith A, Salloway, Stephen P, Schofield, Peter R, Masters, Colin L, Villemagne, Victor L, Fox, Nick C, Förster, Stefan, Chen, Kewei, Reiman, Eric M, Xiong, Chengjie, Marcus, Daniel S, Weiner, Michael W, Morris, John C, Bateman, Randall J, and Benzinger, Tammie LS

Subjects
Alzheimer's Disease, Aging, Biomedical Imaging, Neurosciences, Neurodegenerative, Dementia, Acquired Cognitive Impairment, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Brain Disorders, Neurological, Adult, Alzheimer Disease, Amyloid, Brain, Carbon Isotopes, Cross-Sectional Studies, DNA Mutational Analysis, Family Health, Female, Genes, Dominant, Heterozygote, Humans, Image Processing, Computer-Assisted, Longitudinal Studies, Male, Middle Aged, Mutation, Positron-Emission Tomography, Reference Values, Dominantly Inherited Alzheimer Network, General Science & Technology
Abstract

Amyloid imaging plays an important role in the research and diagnosis of dementing disorders. Substantial variation in quantitative methods to measure brain amyloid burden exists in the field. The aim of this work is to investigate the impact of methodological variations to the quantification of amyloid burden using data from the Dominantly Inherited Alzheimer's Network (DIAN), an autosomal dominant Alzheimer's disease population. Cross-sectional and longitudinal [11C]-Pittsburgh Compound B (PiB) PET imaging data from the DIAN study were analyzed. Four candidate reference regions were investigated for estimation of brain amyloid burden. A regional spread function based technique was also investigated for the correction of partial volume effects. Cerebellar cortex, brain-stem, and white matter regions all had stable tracer retention during the course of disease. Partial volume correction consistently improves sensitivity to group differences and longitudinal changes over time. White matter referencing improved statistical power in the detecting longitudinal changes in relative tracer retention; however, the reason for this improvement is unclear and requires further investigation. Full dynamic acquisition and kinetic modeling improved statistical power although it may add cost and time. Several technical variations to amyloid burden quantification were examined in this study. Partial volume correction emerged as the strategy that most consistently improved statistical power for the detection of both longitudinal changes and across-group differences. For the autosomal dominant Alzheimer's disease population with PiB imaging, utilizing brainstem as a reference region with partial volume correction may be optimal for current interventional trials. Further investigation of technical issues in quantitative amyloid imaging in different study populations using different amyloid imaging tracers is warranted.

Published
2016

39. Cognitive Clusters of Early‐onset non‐Alzheimer’s disease

Author

Kim, Hee Jin, primary, Lane, Kathleen A., additional, Gao, Sujuan, additional, Hammers, Dustin B., additional, Logan, Paige E., additional, Aisen, Paul S. S, additional, Dage, Jeff L., additional, Eloyan, Ani, additional, Foroud, Tatiana M., additional, Grinberg, Lea T., additional, Iaccarino, Leo, additional, Jack, Clifford R., additional, Kramer, Joel H., additional, Koeppe, Robert A., additional, Kukull, Walter A., additional, La Joie, Renaud, additional, Mundada, Nidhi S, additional, Murray, Melissa E., additional, Nudelman, Kelly N. H., additional, Rumbaugh, Malia C., additional, Soleimani‐Meigooni, David N., additional, Toga, Arthur W., additional, Taurone, Alexander, additional, Vemuri, Prashanthi, additional, Atri, Alireza, additional, Day, Gregory S., additional, Duara, Ranjan, additional, Graff‐Radford, Neill R., additional, Honig, Lawrence S., additional, Jones, David T., additional, Masdeu, Joseph C., additional, Mendez, Mario F., additional, Musiek, Erik S., additional, Onyike, Chiadi, additional, Riddle, Meghan C., additional, Rogalski, Emily J, additional, Salloway, Stephen, additional, Sha, Sharon, additional, Turner, R. Scott, additional, Wingo, Thomas S., additional, Wolk, David, additional, Carrillo, Maria C., additional, Dickerson, Brad C., additional, Rabinovici, Gil D., additional, and Apostolova, Liana G., additional

Published
2023
Full Text
View/download PDF

40. Cohort heterogeneity and AD biomarkers in older adults without significant cognitive impairment: A comparison of U.S. POINTER and ADNI

Author

Landau, Susan M., primary, Harrison, Theresa M., additional, Ward, Tyler J., additional, Baker, Suzanne L., additional, Koeppe, Robert A., additional, Vemuri, Prashanthi, additional, Lockhart, Samuel N., additional, Jung, Youngkyoo, additional, Harvey, Danielle J., additional, Lovato, Laura, additional, Toga, Arthur W., additional, Masdeu, Joseph C., additional, Oh, Hwamee, additional, Gitelman, Darren R., additional, Aggarwal, Neelum T., additional, Farias, Sarah Tomaszewski, additional, Papp, Kathryn V., additional, Snyder, Heather M, additional, Baker, Laura D, additional, Decarli, Charles, additional, and Jagust, William J., additional

Published
2023
Full Text
View/download PDF

41. Sex‐associated differences in plasma and cerebrospinal fluid biomarkers in Early‐onset Alzheimer’s disease

Author

Nemes, Sára, primary, Logan, Paige E., additional, Dage, Jeff L., additional, Hammers, Dustin B., additional, Fagan, Anne M., additional, Manchella, Mohit K., additional, Eloyan, Ani, additional, Foroud, Tatiana M., additional, Zetterberg, Henrik, additional, Koeppe, Robert, additional, Aisen, Paul S. S, additional, Carrillo, Maria C., additional, Blennow, Kaj, additional, Schindler, Suzanne E., additional, Gray, Julia D, additional, Dickerson, Brad C., additional, Rabinovici, Gil D., additional, and Apostolova, Liana G., additional

Published
2023
Full Text
View/download PDF

42. Amyloid‐, tau‐, and FDG‐PET in amyloid‐negative patients clinically diagnosed with early‐onset Alzheimer’s disease in the LEADS study

Author

Mundada, Nidhi S., primary, Soleimani‐Meigooni, David N., additional, Zeltzer, Ehud, additional, Windon, Charles, additional, Tanner, Jeremy A., additional, Heath, Courtney Lawh, additional, Iaccarino, Leonardo, additional, Shankar, Ranjani, additional, Amuiri, Alinda, additional, Aisen, Paul S. S, additional, Eloyan, Ani, additional, Koeppe, Robert A., additional, Carrillo, Maria C., additional, Dickerson, Brad C., additional, Apostolova, Liana G., additional, Rabinovici, Gil D., additional, and La Joie, Renaud, additional

Published
2023
Full Text
View/download PDF

43. Harmonization of amyloid and tau PET tracers in a multi‐center cohort from NIA Alzheimer’s disease research centers in the United States

Author

Harrison, Theresa M., primary, Landau, Susan M., additional, Baker, Suzanne L., additional, Lee, JiaQie, additional, Ward, Tyler J., additional, Murphy, Alice, additional, Chadwick, Trevor, additional, Mormino, Elizabeth C., additional, Johnson, Sterling C, additional, Rogalski, Emily J, additional, Koeppe, Robert A., additional, Decarli, Charles, additional, Toga, Arthur W., additional, Kukull, Walter A., additional, Biber, Sarah, additional, Jack, Clifford R., additional, and Jagust, William J., additional

Published
2023
Full Text
View/download PDF

44. Quantitative Amyloid‐PET in Real‐World Practice: Lessons from the Imaging Dementia—Evidence for Amyloid Scanning (IDEAS) study

Author

La Joie, Renaud, primary, Mundada, Nidhi S., additional, Blazhenets, Ganna, additional, Mejía‐Perez, Jhony Alejandro, additional, Schonhaut, Daniel R, additional, Zeltzer, Ehud, additional, Soleimani‐Meigooni, David N., additional, Cho, Hanna, additional, Ranasinghe, Kamalini G, additional, Windon, Charles, additional, Yadollahikhales, Golnaz, additional, Iaccarino, Leonardo, additional, Koeppe, Robert, additional, Carrillo, Maria C., additional, Hanna, Lucy, additional, Gatsonis, Constantine, additional, March, Andrew, additional, Siegel, Barry A, additional, Hillner, Bruce E, additional, Whitmer, Rachel A., additional, and Rabinovici, Gil D., additional

Published
2023
Full Text
View/download PDF

45. Associations of plasma GFAP, NfL, and p‐tau231 with early‐onset Alzheimer’s Disease pathology

Author

Logan, Paige E., primary, Dage, Jeff L., additional, Hammers, Dustin B., additional, Manchella, Mohit K., additional, Eloyan, Ani, additional, Mundada, Nidhi S., additional, La Joie, Renaud, additional, Iaccarino, Leonardo, additional, Fagan, Anne M., additional, Foroud, Tatiana M., additional, Zetterberg, Henrik, additional, Blennow, Kaj, additional, Koeppe, Robert A., additional, Aisen, Paul S. S, additional, Carrillo, Maria C., additional, Rabinovici, Gil D., additional, Dickerson, Brad C., additional, and Apostolova, Liana G., additional

Published
2023
Full Text
View/download PDF

46. Amyloid‐PET, tau‐PET, and their association in sporadic early‐onset Alzheimer’s Disease: Cross‐sectional and longitudinal data from the LEADS study

Author

La Joie, Renaud, primary, Mundada, Nidhi, additional, Iaccarino, Leonardo, additional, soleimani‐Meigooni, David N., additional, Zeltzer, Ehud, additional, Windon, Charles, additional, Tanner, Jeremy A., additional, Heath, Courtney Lawh, additional, Shankar, Ranjani, additional, Amuiri, Alinda, additional, Cho, Hanna, additional, Ackley, Sarah F, additional, Blazhenets, Ganna, additional, Aisen, Paul S. S, additional, Eloyan, Ani, additional, Koeppe, Robert A., additional, Carrillo, Maria C., additional, Dickerson, Brad C., additional, Apostolova, Liana G., additional, and Rabinovici, Gil D., additional

Published
2023
Full Text
View/download PDF

47. Estimated Age of Amyloid Onset in Participants with Early‐ versus Late‐Onset Alzheimer’s Disease: Results from the LEADS & ADNI Studies

Author

Blazhenets, Ganna, primary, Mundada, Nidhi, additional, Lee, JiaQie, additional, Landau, Susan M., additional, Koeppe, Robert A., additional, Carrillo, Maria C., additional, Dickerson, Brad C., additional, Jagust, William J., additional, Apostolova, Liana G., additional, Rabinovici, Gil D., additional, and La Joie, Renaud, additional

Published
2023
Full Text
View/download PDF

48. Regional patterns of pathological tau accumulation in sporadic early‐onset Alzheimer’s disease: Longitudinal tau‐PET in the LEADS Cohort

Author

Schonhaut, Daniel R, primary, Mundada, Nidhi S., additional, Insel, Philip S., additional, soleimani‐Meigooni, David N., additional, Zeltzer, Ehud, additional, Windon, Charles, additional, Tanner, Jeremy A., additional, Heath, Courtney Lawh, additional, Shankar, Ranjani, additional, Amuiri, Alinda, additional, Aisen, Paul S. S, additional, Eloyan, Ani, additional, Koeppe, Robert A., additional, Carrillo, Maria C., additional, Dickerson, Brad C., additional, Apostolova, Liana G., additional, Rabinovici, Gil D., additional, and La Joie, Renaud, additional

Published
2023
Full Text
View/download PDF

50. Baseline neuropsychiatric symptoms and psychotropic medication use midway through data collection of the Longitudinal Early‐ Onset Alzheimer’s Disease Study (LEADS) Cohort

Author

Polsinelli, Angelina J, primary, Wonderlin, Ryan J, additional, Hammers, Dustin B., additional, Garcia, Alex Pena, additional, Eloyan, Ani, additional, Taurone, Alexander, additional, Thangarajah, Maryanne, additional, Beckett, Laurel, additional, Gao, Sujuan, additional, Wang, Sophia, additional, Kirby, Kala, additional, Logan, Paige E., additional, Aisen, Paul S. S, additional, Dage, Jeff L., additional, Foroud, Tatiana M., additional, Griffin, Percy, additional, Iaccarino, Leo, additional, Kramer, Joel H., additional, Koeppe, Robert A., additional, Kukull, Walter A., additional, La Joie, Renaud, additional, Mundada, Nidhi S, additional, Murray, Melissa E., additional, Nudelman, Kelly N. H., additional, Soleimani‐Meigooni, David N., additional, Rumbaugh, Malia C., additional, Toga, Arthur W., additional, Touroutoglou, Alexandra, additional, Vemuri, Prashanthi, additional, Atri, Alireza, additional, Day, Gregory S., additional, Duara, Ranjan, additional, Graff‐Radford, Neill R, additional, Honig, Lawrence S., additional, Jones, David T., additional, Masdeu, Joseph C., additional, Mendez, Mario F., additional, Musiek, Erik S., additional, Onyike, Chiadi, additional, Riddle, Meghan C., additional, Rogalski, Emily J, additional, Salloway, Stephen, additional, Sha, Sharon, additional, Turner, Raymond Scott, additional, Wingo, Thomas S., additional, Wolk, David, additional, Womack, Kyle B., additional, Carrillo, Maria C., additional, Dickerson, Brad C., additional, Rabinovici, Gil D., additional, and Apostolova, Liana G., additional

Published
2023
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results