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1. Analyzing heterogeneity in Alzheimer Disease using multimodal normative modeling on imaging-based ATN biomarkers

Author: Kumar, Sayantan, Earnest, Tom, Yang, Braden, Kothapalli, Deydeep, Aschenbrenner, Andrew J., Hassenstab, Jason, Xiong, Chengie, Ances, Beau, Morris, John, Benzinger, Tammie L. S., Gordon, Brian A., Payne, Philip, and Sotiras, Aristeidis
Subjects: Quantitative Biology - Neurons and Cognition, Computer Science - Machine Learning
Abstract: INTRODUCTION: Previous studies have applied normative modeling on a single neuroimaging modality to investigate Alzheimer Disease (AD) heterogeneity. We employed a deep learning-based multimodal normative framework to analyze individual-level variation across ATN (amyloid-tau-neurodegeneration) imaging biomarkers. METHODS: We selected cross-sectional discovery (n = 665) and replication cohorts (n = 430) with available T1-weighted MRI, amyloid and tau PET. Normative modeling estimated individual-level abnormal deviations in amyloid-positive individuals compared to amyloid-negative controls. Regional abnormality patterns were mapped at different clinical group levels to assess intra-group heterogeneity. An individual-level disease severity index (DSI) was calculated using both the spatial extent and magnitude of abnormal deviations across ATN. RESULTS: Greater intra-group heterogeneity in ATN abnormality patterns was observed in more severe clinical stages of AD. Higher DSI was associated with worse cognitive function and increased risk of disease progression. DISCUSSION: Subject-specific abnormality maps across ATN reveal the heterogeneous impact of AD on the brain., Comment: Under review in Alzheimer's & Dementia
Published: 2024

2. Evolution of white matter hyperintensity segmentation methods and implementation over the past two decades; an incomplete shift towards deep learning

Author: Rahmani, Maryam, Dierker, Donna, Yaeger, Lauren, Saykin, Andrew, Luckett, Patrick H., Vlassenko, Andrei G., Owens, Christopher, Jafri, Hussain, Womack, Kyle, Fripp, Jurgen, Xia, Ying, Tosun, Duygu, Benzinger, Tammie L. S., Masters, Colin L., Lee, Jin-Moo, Morris, John C., Goyal, Manu S., Strain, Jeremy F., Kukull, Walter, Weiner, Michael, Burnham, Samantha, CoxDoecke, Tim James, Fedyashov, Victor, Fripp, Jurgen, Shishegar, Rosita, Xiong, Chengjie, Marcus, Daniel, Raniga, Parnesh, Li, Shenpeng, Aschenbrenner, Andrew, Hassenstab, Jason, Lim, Yen Ying, Maruff, Paul, Sohrabi, Hamid, Robertson, Jo, Markovic, Shaun, Bourgeat, Pierrick, Doré, Vincent, Mayo, Clifford Jack, Mussoumzadeh, Parinaz, Rowe, Chris, Villemagne, Victor, Bateman, Randy, Fowler, Chris, Li, Qiao-Xin, Martins, Ralph, Schindler, Suzanne, Shaw, Les, Cruchaga, Carlos, Harari, Oscar, Laws, Simon, Porter, Tenielle, O’Brien, Eleanor, Perrin, Richard, Kukull, Walter, Bateman, Randy, McDade, Eric, Jack, Clifford, Morris, John, Yassi, Nawaf, Bourgeat, Pierrick, Perrin, Richard, Roberts, Blaine, Villemagne, Victor, Fedyashov, Victor, and Goudey, Benjamin
Published: 2024
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3. Molecular neuroimaging in dominantly inherited versus sporadic early-onset Alzheimer’s disease

Author: Iaccarino, Leonardo, Llibre-Guerra, Jorge J, McDade, Eric, Edwards, Lauren, Gordon, Brian, Benzinger, Tammie, Hassenstab, Jason, Kramer, Joel H, Li, Yan, Miller, Bruce L, Miller, Zachary, Morris, John C, Mundada, Nidhi, Perrin, Richard J, Rosen, Howard J, Soleimani-Meigooni, David, Strom, Amelia, Tsoy, Elena, Wang, Guoqiao, Xiong, Chengjie, Allegri, Ricardo, Chrem, Patricio, Vazquez, Silvia, Berman, Sarah B, Chhatwal, Jasmeer, Masters, Colin L, Farlow, Martin R, Jucker, Mathias, Levin, Johannes, Salloway, Stephen, Fox, Nick C, Day, Gregory S, Gorno-Tempini, Maria Luisa, Boxer, Adam L, La Joie, Renaud, Bateman, Randall, and Rabinovici, Gil D
Subjects: Biomedical and Clinical Sciences, Biological Psychology, Clinical Sciences, Neurosciences, Psychology, Dementia, Alzheimer's Disease, Biomedical Imaging, Brain Disorders, Clinical Research, Acquired Cognitive Impairment, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Aging, Neurodegenerative, 2.1 Biological and endogenous factors, 4.2 Evaluation of markers and technologies, Neurological, Good Health and Well Being, Alzheimer's disease, amyloid-PET, brain glucose metabolism, FDG-PET, Alzheimer’s disease, Clinical sciences, Biological psychology
Abstract: Approximately 5% of Alzheimer's disease patients develop symptoms before age 65 (early-onset Alzheimer's disease), with either sporadic (sporadic early-onset Alzheimer's disease) or dominantly inherited (dominantly inherited Alzheimer's disease) presentations. Both sporadic early-onset Alzheimer's disease and dominantly inherited Alzheimer's disease are characterized by brain amyloid-β accumulation, tau tangles, hypometabolism and neurodegeneration, but differences in topography and magnitude of these pathological changes are not fully elucidated. In this study, we directly compared patterns of amyloid-β plaque deposition and glucose hypometabolism in sporadic early-onset Alzheimer's disease and dominantly inherited Alzheimer's disease individuals. Our analysis included 134 symptomatic sporadic early-onset Alzheimer's disease amyloid-Positron Emission Tomography (PET)-positive cases from the University of California, San Francisco, Alzheimer's Disease Research Center (mean ± SD age 59.7 ± 5.6 years), 89 symptomatic dominantly inherited Alzheimer's disease cases (age 45.8 ± 9.3 years) and 102 cognitively unimpaired non-mutation carriers from the Dominantly Inherited Alzheimer Network study (age 44.9 ± 9.2). Each group underwent clinical and cognitive examinations, 11C-labelled Pittsburgh Compound B-PET and structural MRI. 18F-Fluorodeoxyglucose-PET was also available for most participants. Positron Emission Tomography scans from both studies were uniformly processed to obtain a standardized uptake value ratio (PIB50-70 cerebellar grey reference and FDG30-60 pons reference) images. Statistical analyses included pairwise global and voxelwise group comparisons and group-independent component analyses. Analyses were performed also adjusting for covariates including age, sex, Mini-Mental State Examination, apolipoprotein ε4 status and average composite cortical of standardized uptake value ratio. Compared with dominantly inherited Alzheimer's disease, sporadic early-onset Alzheimer's disease participants were older at age of onset (mean ± SD, 54.8 ± 8.2 versus 41.9 ± 8.2, Cohen's d = 1.91), with more years of education (16.4 ± 2.8 versus 13.5 ± 3.2, d = 1) and more likely to be apolipoprotein ε4 carriers (54.6% ε4 versus 28.1%, Cramer's V = 0.26), but similar Mini-Mental State Examination (20.6 ± 6.1 versus 21.2 ± 7.4, d = 0.08). Sporadic early-onset Alzheimer's disease had higher global cortical Pittsburgh Compound B-PET binding (mean ± SD standardized uptake value ratio, 1.92 ± 0.29 versus 1.58 ± 0.44, d = 0.96) and greater global cortical 18F-fluorodeoxyglucose-PET hypometabolism (mean ± SD standardized uptake value ratio, 1.32 ± 0.1 versus 1.39 ± 0.19, d = 0.48) compared with dominantly inherited Alzheimer's disease. Fully adjusted comparisons demonstrated relatively higher Pittsburgh Compound B-PET standardized uptake value ratio in the medial occipital, thalami, basal ganglia and medial/dorsal frontal regions in dominantly inherited Alzheimer's disease versus sporadic early-onset Alzheimer's disease. Sporadic early-onset Alzheimer's disease showed relatively greater 18F-fluorodeoxyglucose-PET hypometabolism in Alzheimer's disease signature temporoparietal regions and caudate nuclei, whereas dominantly inherited Alzheimer's disease showed relatively greater hypometabolism in frontal white matter and pericentral regions. Independent component analyses largely replicated these findings by highlighting common and unique Pittsburgh Compound B-PET and 18F-fluorodeoxyglucose-PET binding patterns. In summary, our findings suggest both common and distinct patterns of amyloid and glucose hypometabolism in sporadic and dominantly inherited early-onset Alzheimer's disease.
Published: 2024

4. Genetic and multi-omic resources for Alzheimer disease and related dementia from the Knight Alzheimer Disease Research Center

Author: Fernandez, Maria Victoria, Liu, Menghan, Beric, Aleksandra, Johnson, Matt, Cetin, Arda, Patel, Maulik, Budde, John, Kohlfeld, Pat, Bergmann, Kristy, Lowery, Joseph, Flynn, Allison, Brock, William, Sanchez Montejo, Brenda, Gentsch, Jen, Sykora, Nicholas, Norton, Joanne, Gentsch, Jen, Valdez, Olga, Gorijala, Priyanka, Sanford, Jessie, Sun, Yichen, Wang, Ciyang, Western, Dan, Timsina, Jigyasha, Mangetti Goncalves, Tassia, Do, Anh N., Sung, Yun Ju, Zhao, Guoyan, Morris, John C., Moulder, Krista, Holtzman, David M., Bateman, Randall J., Karch, Celeste, Hassenstab, Jason, Xiong, Chengjie, Schindler, Suzanne E., Balls-Berry, Joyce (Joy), Benzinger, Tammie L. S., Perrin, Richard J., Denny, Andrea, Snider, B. Joy, Stark, Susan L., Ibanez, Laura, and Cruchaga, Carlos
Published: 2024
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5. Personality predictors of dementia diagnosis and neuropathological burden: An individual participant data meta‐analysis

Author: Beck, Emorie D, Yoneda, Tomiko, James, Bryan D, Bennett, David A, Hassenstab, Jason, Katz, Mindy J, Lipton, Richard B, Morris, John, Mroczek, Daniel K, and Graham, Eileen K
Subjects: Social and Personality Psychology, Psychology, Aging, Dementia, Behavioral and Social Science, Prevention, Neurodegenerative, Acquired Cognitive Impairment, Clinical Research, Neurosciences, Brain Disorders, Neurological, agreeableness, arteriosclerosis, Braak stage, CERAD, cerebral amyloid angiopathy, cerebral atherosclerosis, extraversion, gross cerebral infarcts, gross cerebral microinfarcts, hippocampal sclerosis, individual participant data meta-analysis, Lewy body disease, openness, positive affect, satisfaction with life, TDP-43, Clinical Sciences, Geriatrics, Clinical sciences, Biological psychology
Abstract: IntroductionThe extent to which the Big Five personality traits and subjective well-being (SWB) are discriminatory predictors of clinical manifestation of dementia versus dementia-related neuropathology is unclear.MethodsUsing data from eight independent studies (Ntotal = 44,531; Ndementia = 1703; baseline Mage = 49 to 81 years, 26 to 61% female; Mfollow-up range = 3.53 to 21.00 years), Bayesian multilevel models tested whether personality traits and SWB differentially predicted neuropsychological and neuropathological characteristics of dementia.ResultsSynthesized and individual study results indicate that high neuroticism and negative affect and low conscientiousness, extraversion, and positive affect were associated with increased risk of long-term dementia diagnosis. There were no consistent associations with neuropathology.DiscussionThis multistudy project provides robust, conceptually replicated and extended evidence that psychosocial factors are strong predictors of dementia diagnosis but not consistently associated with neuropathology at autopsy.HighlightsN(+), C(-), E(-), PA(-), and NA(+) were associated with incident diagnosis. Results were consistent despite self-report versus clinical diagnosis of dementia. Psychological factors were not associated with neuropathology at autopsy. Individuals with higher conscientiousness and no diagnosis had less neuropathology. High C individuals may withstand neuropathology for longer before death.
Published: 2023

6. Longitudinal clinical, cognitive and biomarker profiles in dominantly inherited versus sporadic early-onset Alzheimer’s disease

Author: Llibre-Guerra, Jorge J, Iaccarino, Leonardo, Coble, Dean, Edwards, Lauren, Li, Yan, McDade, Eric, Strom, Amelia, Gordon, Brian, Mundada, Nidhi, Schindler, Suzanne E, Tsoy, Elena, Ma, Yinjiao, Lu, Ruijin, Fagan, Anne M, Benzinger, Tammie LS, Soleimani-Meigooni, David, Aschenbrenner, Andrew J, Miller, Zachary, Wang, Guoqiao, Kramer, Joel H, Hassenstab, Jason, Rosen, Howard J, Morris, John C, Miller, Bruce L, Xiong, Chengjie, Perrin, Richard J, Allegri, Ricardo, Chrem, Patricio, Surace, Ezequiel, Berman, Sarah B, Chhatwal, Jasmeer, Masters, Colin L, Farlow, Martin R, Jucker, Mathias, Levin, Johannes, Fox, Nick C, Day, Gregory, Gorno-Tempini, Maria Luisa, Boxer, Adam L, La Joie, Renaud, Rabinovici, Gil D, and Bateman, Randall
Subjects: Biomedical and Clinical Sciences, Biological Psychology, Clinical Sciences, Neurosciences, Psychology, Neurodegenerative, Acquired Cognitive Impairment, Genetics, Brain Disorders, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Clinical Research, Alzheimer's Disease, Aging, Dementia, 2.1 Biological and endogenous factors, Neurological, early-onset Alzheimer's disease, sporadic, dominantly inherited, early-onset Alzheimer’s disease, Clinical sciences, Biological psychology
Abstract: Approximately 5% of Alzheimer's disease cases have an early age at onset (
Published: 2023

7. Association of Stages of Objective Memory Impairment With Incident Symptomatic Cognitive Impairment in Cognitively Normal Individuals

Author: Grober, Ellen, Petersen, Kellen K, Lipton, Richard B, Hassenstab, Jason, Morris, John C, Gordon, Brian A, and Ezzati, Ali
Subjects: Biomedical and Clinical Sciences, Neurosciences, Clinical Sciences, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Dementia, Brain Disorders, Aging, Neurodegenerative, Behavioral and Social Science, Mental Health, Alzheimer's Disease, Acquired Cognitive Impairment, Prevention, 2.1 Biological and endogenous factors, 4.2 Evaluation of markers and technologies, 4.1 Discovery and preclinical testing of markers and technologies, Neurological, Humans, Female, Aged, Male, tau Proteins, Alzheimer Disease, Cognitive Dysfunction, Amyloid beta-Peptides, Memory Disorders, Biomarkers, Disease Progression, Cognitive Sciences, Neurology & Neurosurgery, Clinical sciences
Abstract: Background and objectivesIncreasing evidence indicates that a subset of cognitively normal individuals has subtle cognitive impairment at baseline. We sought to identify them using the Stages of Objective Memory Impairment (SOMI) system. Symptomatic cognitive impairment was operationalized by a Clinical Dementia Rating (CDR) ≥0.5. We hypothesized that incident impairment would be higher for participants with subtle retrieval impairment (SOMI-1), higher still for those with moderate retrieval impairment (SOMI-2), and highest for those with storage impairment (SOMI-3/4) after adjusting for demographics and APOE ε4 status. A secondary objective was to determine whether including biomarkers of β-amyloid, tau pathology, and neurodegeneration in the models affect prediction. We hypothesized that even after adjusting for in vivo biomarkers, SOMI would remain a significant predictor of time to incident symptomatic cognitive impairment.MethodsAmong 969 cognitively normal participants, defined by a CDR = 0, from the Knight Alzheimer Disease Research Center, SOMI stage was determined from their baseline Free and Cued Selective Reminding Test scores, 555 had CSF and structural MRI measures and comprised the biomarker subgroup, and 144 of them were amyloid positive. Cox proportional hazards models tested associations of SOMI stages at baseline and biomarkers with time to incident cognitive impairment defined as the transition to CDR ≥0.5.ResultsAmong all participants, the mean age was 69.35 years, 59.6% were female, and mean follow-up was 6.36 years. Participants in SOMI-1-4 had elevated hazard ratios for the transition from normal to impaired cognition in comparison with those who were SOMI-0 (no memory impairment). Individuals in SOMI-1 (mildly impaired retrieval) and SOMI-2 (moderately impaired retrieval) were at nearly double the risk of clinical progression compared with persons with no memory problems. When memory storage impairment emerges (SOMI-3/4), the hazard ratio for clinical progression increased approximately 3 times. SOMI stage remained an independent predictor of incident cognitive impairment after adjusting for all biomarkers.DiscussionSOMI predicts the transition from normal cognition to incident symptomatic cognitive impairment (CDR ≥0.5). The results support the use of SOMI to identify those cognitively normal participants most likely to develop incident cognitive impairment who can then be referred for biomarker screening.
Published: 2023

8. 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

9. Comparison of amyloid burden in individuals with Down syndrome versus autosomal dominant Alzheimer's disease: a cross-sectional study

Author: Boerwinkle, Anna H, Gordon, Brian A, Wisch, Julie, Flores, Shaney, Henson, Rachel L, Butt, Omar H, McKay, Nicole, Chen, Charles D, Benzinger, Tammie LS, 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, Ances, Beau M, Syndrome, Alzheimer's Biomarker Consortium-Down, Aizenstein, Howard J, Andrews, Howard F, Bell, Karen, Birn, Rasmus M, Bulova, Peter, Cheema, Amrita, Chen, Kewei, Clare, Isabel, Clark, Lorraine, Cohen, Ann D, Constantino, John N, Doran, Eric W, Feingold, Eleanor, Foroud, Tatiana M, Hartley, Sigan L, Hom, Christy, Honig, Lawrence, Ikonomovic, Milos D, Johnson, Sterling C, Jordan, Courtney, Kamboh, M Ilyas, Keator, David, Klunk, William E, Kofler, Julia K, Kreisl, William C, McHale, Sharon J Krinsky-, 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, Network, Dominantly Inherited Alzheimer, 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, and DeLaCruz, Chrismary
Subjects: Biomedical and Clinical Sciences, Neurosciences, Clinical Sciences, Biomedical Imaging, Aging, Alzheimer's Disease, Clinical Research, Neurodegenerative, Brain Disorders, Dementia, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Intellectual and Developmental Disabilities (IDD), Genetics, Acquired Cognitive Impairment, 2.1 Biological and endogenous factors, Aetiology, Neurological, Adult, Aged, Humans, Middle Aged, Alzheimer Disease, Amyloid beta-Peptides, Apolipoproteins E, Biomarkers, Cross-Sectional Studies, Down Syndrome, Positron-Emission Tomography, Cerebral Cortex, Alzheimer's Biomarker Consortium-Down Syndrome, Dominantly Inherited Alzheimer Network, Neurology & Neurosurgery, Clinical sciences
Abstract: BackgroundImportant insights into the early pathogenesis of Alzheimer's disease can be provided by studies of autosomal dominant Alzheimer's disease and Down syndrome. However, it is unclear whether the timing and spatial distribution of amyloid accumulation differs between people with autosomal dominant Alzheimer's disease and those with Down syndrome. We aimed to directly compare amyloid changes between these two groups of people.MethodsIn this cross-sectional study, we included participants (aged ≥25 years) with Down syndrome and sibling controls who had MRI and amyloid PET scans in the first data release (January, 2020) of the Alzheimer's Biomarker Consortium-Down Syndrome (ABC-DS) study. We also included carriers of autosomal dominant Alzheimer's disease genetic mutations and non-carrier familial controls who were within a similar age range to ABC-DS participants (25-73 years) and had MRI and amyloid PET scans at the time of a data freeze (December, 2020) of the Dominantly Inherited Alzheimer Network (DIAN) study. Controls from the two studies were combined into a single group. All DIAN study participants had genetic testing to determine PSEN1, PSEN2, or APP mutation status. APOE genotype was determined from blood samples. CSF samples were collected in a subset of ABC-DS and DIAN participants and the ratio of amyloid β42 (Aβ42) to Aβ40 (Aβ42/40) was measured to evaluate its Spearman's correlation with amyloid PET. Global PET amyloid burden was compared with regards to cognitive status, APOE ɛ4 status, sex, age, and estimated years to symptom onset. We further analysed amyloid PET deposition by autosomal dominant mutation type. We also assessed regional patterns of amyloid accumulation by estimated number of years to symptom onset. Within a subset of participants the relationship between amyloid PET and CSF Aβ42/40 was evaluated.Findings192 individuals with Down syndrome and 33 sibling controls from the ABC-DS study and 265 carriers of autosomal dominant Alzheimer's disease mutations and 169 non-carrier familial controls from the DIAN study were included in our analyses. PET amyloid centiloid and CSF Aβ42/40 were negatively correlated in carriers of autosomal dominant Alzheimer's disease mutations (n=216; r=-0·565; p
Published: 2023

10. Sex-Specific Patterns of Body Mass Index Relationship with White Matter Connectivity

Author: Rahmani, Farzaneh, primary, Wang, Qing, additional, McKay, Nicole S., additional, Keefe, Sarah, additional, Hantler, Nancy, additional, Hornbeck, Russ, additional, Wang, Yong, additional, Hassenstab, Jason, additional, Schindler, Suzanne, additional, Xiong, Chengjie, additional, Morris, John C., additional, Benzinger, Tammie L.S., additional, and Raji, Cyrus A., additional
Published: 2024
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11. Autosomal dominant and sporadic late onset Alzheimer's disease share a common in vivo pathophysiology

Author: Morris, John C, Weiner, Michael, Xiong, Chengjie, Beckett, Laurel, Coble, Dean, Saito, Naomi, Aisen, Paul S, Allegri, Ricardo, Benzinger, Tammie LS, Berman, Sarah B, Cairns, Nigel J, Carrillo, Maria C, Chui, Helena C, Chhatwal, Jasmeer P, Cruchaga, Carlos, Fagan, Anne M, Farlow, Martin, Fox, Nick C, Ghetti, Bernardino, Goate, Alison M, Gordon, Brian A, Graff-Radford, Neill, Day, Gregory S, Hassenstab, Jason, Ikeuchi, Takeshi, Jack, Clifford R, Jagust, William J, Jucker, Mathias, Levin, Johannes, Massoumzadeh, Parinaz, Masters, Colin L, Martins, Ralph, McDade, Eric, Mori, Hiroshi, Noble, James M, Petersen, Ronald C, Ringman, John M, Salloway, Stephen, Saykin, Andrew J, Schofield, Peter R, Shaw, Leslie M, Toga, Arthur W, Trojanowski, John Q, Vöglein, Jonathan, Weninger, Stacie, Bateman, Randall J, and Buckles, Virginia D
Subjects: Biomedical and Clinical Sciences, Health Sciences, Psychology, Brain Disorders, Clinical Trials and Supportive Activities, Alzheimer's Disease, Clinical Research, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Biomedical Imaging, Genetics, Aging, Acquired Cognitive Impairment, Neurosciences, Neurodegenerative, Dementia, 2.1 Biological and endogenous factors, Aetiology, Neurological, Humans, Alzheimer Disease, Amyloid beta-Peptides, Magnetic Resonance Imaging, Amyloidosis, Biomarkers, Alzheimer pathophysiology, biomarkers, rates of change, Medical and Health Sciences, Psychology and Cognitive Sciences, Neurology & Neurosurgery, Biomedical and clinical sciences, Health sciences
Abstract: The extent to which the pathophysiology of autosomal dominant Alzheimer's disease corresponds to the pathophysiology of 'sporadic' late onset Alzheimer's disease is unknown, thus limiting the extrapolation of study findings and clinical trial results in autosomal dominant Alzheimer's disease to late onset Alzheimer's disease. We compared brain MRI and amyloid PET data, as well as CSF concentrations of amyloid-β42, amyloid-β40, tau and tau phosphorylated at position 181, in 292 carriers of pathogenic variants for Alzheimer's disease from the Dominantly Inherited Alzheimer Network, with corresponding data from 559 participants from the Alzheimer's Disease Neuroimaging Initiative. Imaging data and CSF samples were reprocessed as appropriate to guarantee uniform pipelines and assays. Data analyses yielded rates of change before and after symptomatic onset of Alzheimer's disease, allowing the alignment of the ∼30-year age difference between the cohorts on a clinically meaningful anchor point, namely the participant age at symptomatic onset. Biomarker profiles were similar for both autosomal dominant Alzheimer's disease and late onset Alzheimer's disease. Both groups demonstrated accelerated rates of decline in cognitive performance and in regional brain volume loss after symptomatic onset. Although amyloid burden accumulation as determined by PET was greater after symptomatic onset in autosomal dominant Alzheimer's disease than in late onset Alzheimer's disease participants, CSF assays of amyloid-β42, amyloid-β40, tau and p-tau181 were largely overlapping in both groups. Rates of change in cognitive performance and hippocampal volume loss after symptomatic onset were more aggressive for autosomal dominant Alzheimer's disease participants. These findings suggest a similar pathophysiology of autosomal dominant Alzheimer's disease and late onset Alzheimer's disease, supporting a shared pathobiological construct.
Published: 2022

12. CSF proteomics identifies early changes in autosomal dominant Alzheimer’s disease

Author: Noble, James M., Day, Gregory S., Graff-Radford, Neill R., Voglein, Jonathan, Allegri, Ricardo, Mendez, Patricio Chrem, Surace, Ezequiel, Berman, Sarah B., Ikonomovic, Snezana, Nadkarni, Neelesh, Lopera, Francisco, Ramirez, Laura, Aguillon, David, Leon, Yudy, Ramos, Claudia, Alzate, Diana, Baena, Ana, Londono, Natalia, Mathias Jucker, Sonia Moreno, Laske, Christoph, Kuder-Buletta, Elke, Graber-Sultan, Susanne, Preische, Oliver, Hofmann, Anna, Ikeuchi, Takeshi, Kasuga, Kensaku, Niimi, Yoshiki, Ishii, Kenji, Senda, Michio, Sanchez-Valle, Raquel, Rosa-Neto, Pedro, Fox, Nick, Cash, Dave, Lee, Jae-Hong, Roh, Jee Hoon, Riddle, Meghan, Menard, William, Bodge, Courtney, Surti, Mustafa, Takada, Leonel Tadao, Farlow, Martin, Chhatwal, Jasmeer P., Sanchez-Gonzalez, V.J., Orozco-Barajas, Maribel, Goate, Alison, Renton, Alan, Esposito, Bianca, Karch, Celeste M., Marsh, Jacob, Cruchaga, Carlos, Fernandez, Victoria, Gordon, Brian A., Fagan, Anne M., Jerome, Gina, Herries, Elizabeth, Llibre-Guerra, Jorge, Levey, Allan I., Johnson, Erik C.B., Seyfried, Nicholas T., Schofield, Peter R., Brooks, William, Bechara, Jacob, Bateman, Randall J., McDade, Eric, Hassenstab, Jason, Perrin, Richard J., Franklin, Erin, Benzinger, Tammie L.S., Chen, Allison, Chen, Charles, Flores, Shaney, Friedrichsen, Nelly, Hantler, Nancy, Hornbeck, Russ, Jarman, Steve, Keefe, Sarah, Koudelis, Deborah, Massoumzadeh, Parinaz, McCullough, Austin, McKay, Nicole, Nicklaus, Joyce, Pulizos, Christine, Wang, Qing, Mishall, Sheetal, Sabaredzovic, Edita, Deng, Emily, Candela, Madison, Smith, Hunter, Hobbs, Diana, Scott, Jalen, Levin, Johannes, Xiong, Chengjie, Wang, Peter, Xu, Xiong, Li, Yan, Gremminger, Emily, Ma, Yinjiao, Bui, Ryan, Lu, Ruijin, Martins, Ralph, Sosa Ortiz, Ana Luisa, Daniels, Alisha, Courtney, Laura, Mori, Hiroshi, Supnet-Bell, Charlene, Xu, Jinbin, Ringman, John, Shen, Yuanyuan, Timsina, Jigyasha, Heo, Gyujin, Beric, Aleksandra, Ali, Muhammad, Wang, Ciyang, Yang, Chengran, Wang, Yueyao, Western, Daniel, Liu, Menghan, Gorijala, Priyanka, Budde, John, Do, Anh, Liu, Haiyan, Gordon, Brian, Llibre-Guerra, Jorge J., Joseph-Mathurin, Nelly, Maschi, Dario, Wyss-Coray, Tony, Pastor, Pau, Renton, Alan E., Surace, Ezequiel I., Alvarez, Ignacio, Ringman, John M., Allegri, Ricardo Francisco, Seyfried, Nicholas, Day, Gregg S., Wu, Qisi, Fernández, M. Victoria, Tarawneh, Rawan, Morris, John C., Ibanez, Laura, and Sung, Yun Ju
Published: 2024
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13. γ-Secretase activity, clinical features, and biomarkers of autosomal dominant Alzheimer's disease: cross-sectional and longitudinal analysis of the Dominantly Inherited Alzheimer Network observational study (DIAN-OBS)

Author: Aguillon, David, Allegri, Ricardo F., Aschenbrenner, Andrew J., Baker, Bryce, Barthelemy, Nicolas, Bechara, Jacob A., Berman, Sarah B., Brooks, William S., Cash, David M., Chen, Allison, Chrem Mendez, Patricio, Courtney, Laura, Cruchaga, Carlos, Daniels, Alisha J., Fagan, Anne M., Flores, Shaney, Fox, Nick C., Franklin, Erin, Goate, Alison M., Graber-Sultan, Susanne, Graff-Radford, Neill R., Gremminger, Emily, Herries, Elizabeth, Hofmann, Anna, Holtzman, David M., Hornbeck, Russ, Huey, Edward D., Ibanez, Laura, Ikeuchi, Takeshi, Ikonomovic, Snezana, Jackson, Kelley, Jarman, Steve, Jerome, Gina, Johnson, Erik C.B, Kasuga, Kensaku, Keefe, Sarah, Koudelis, Deborah, Kuder-Buletta, Elke, Laske, Christoph, Leon, Yudy Milena, Levey, Allan I., Li, Yan, Llibre-Guerra, Jorge J., Lopera, Francisco, Lu, Ruijin, Marsh, Jacob, Martins, Ralph, Massoumzadeh, Parinaz, Masters, Colin, McCullough, Austin, McKay, Nicole, Minton, Matthew, Mori, Hiroshi, Morris, John C., Nadkarni, Neelesh K., Nicklaus, Joyce, Niimi, Yoshiki, Noble, James M., Obermueller, Ulrike, Picarello, Danielle M., Pulizos, Christine, Ramirez, Laura, Renton, Alan E., Ringman, John, Rizzo, Jacqueline, Roedenbeck, Yvonne, Roh, Jee Hoon, Rosa-Neto, Pedro, Ryan, Natalie S., Sabaredzovic, Edita, Salloway, Stephen, Sanchez-Valle, Raquel, Scott, Jalen, Seyfried, Nicholas T., Simmons, Ashlee, Smith, Jennifer, Smith, Hunter, Stauber, Jennifer, Stout, Sarah, Supnet-Bell, Charlene, Surace, Ezequiel, Vazquez, Silvia, Vöglein, Jonathan, Wang, Guoqiao, Wang, Qing, Xu, Xiong, Xu, Jinbin, Schultz, Stephanie A, Liu, Lei, Schultz, Aaron P, Fitzpatrick, Colleen D, Levin, Raina, Bellier, Jean-Pierre, Shirzadi, Zahra, Joseph-Mathurin, Nelly, Chen, Charles D, Benzinger, Tammie L S, Day, Gregory S, Farlow, Martin R, Gordon, Brian A, Hassenstab, Jason J, Jack, Clifford R, Jr, Jucker, Mathias, Karch, Celeste M, Lee, Jae-Hong, Levin, Johannes, Perrin, Richard J, Schofield, Peter R, Xiong, Chengjie, Johnson, Keith A, McDade, Eric, Bateman, Randall J, Sperling, Reisa A, Selkoe, Dennis J, and Chhatwal, Jasmeer P
Published: 2024
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14. To BYOD or not: Are device latencies important for bring-your-own-device (BYOD) smartphone cognitive testing?

Author: Nicosia, Jessica, Wang, Benjamin, Aschenbrenner, Andrew J., Sliwinski, Martin J., Yabiku, Scott T., Roque, Nelson A., Germine, Laura T., Bateman, Randall J., Morris, John C., and Hassenstab, Jason
Published: 2023
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15. 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
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16. Deconstructing pathological tau by biological process in early stages of Alzheimer disease: a method for quantifying tau spatial spread in neuroimaging

Author: Noble, James M., Day, Gregory S., Graff-Radford, Neill R., Voglein, Jonathan, Levin, Johannes, Allegri, Ricardo F., Mendez, Patricio Chrem, Surace, Ezequiel, Berman, Sarah B., Ikonomovic, Snezana, Nadkarni, Neelesh K., Lopera, Francisco, Ramirez, Laura, Aguillon, David, Leon, Yudy, Ramos, Claudia, Alzate, Diana, Baena, Ana, Londono, Natalia, Moreno, Sonia, Jucker, Mathias, Laske, Christoph, Kuder-Buletta, Elke, Graber-Sultan, Susanne, Preische, Oliver, Hofmann, Anna, Ikeuchi, Takeshi, Kasuga, Kensaku, Niimi, Yoshiki, Ishii, Kenji, Senda, Michio, Sanchez-Valle, Raquel, Rosa-Neto, Pedro, Fox, Nick C., Cash, Dave, Lee, Jae-Hong, Roh, Jee Hoon, Salloway, Stephen, Riddle, Meghan C., Menard, William, Bodge, Courtney, Surti, Mustafa, Takada, Leonel Tadao, Farlow, Martin, Chhatwal, Jasmeer P., Sanchez-Gonzalez, V.J., Orozco-Barajas, Maribel, Goate, Alison M., Renton, Alan E., Esposito, Bianca T., Karch, Celeste M., Marsh, Jacob, Cruchaga, Carlos, Fernanadez, Victoria, Gordon, Brian A., Fagan, Anne M., Jerome, Gina, Herries, Elizabeth, Llibre-Guerra, Jorge, Levey, Allan I., Johnson, Erik C.B., Seyfried, Nicholas T., Schofield, Peter R., Brooks, William S., Bechara, Jacob A., Bateman, Randall, McDade, Eric, Hassenstab, Jason, Perrin, Richard J., Franklin, Erin E., Benzinger, Tammie, Chen, Allison, Chen, Charles, Flores, Shaney, Friedrichsen, Nelly, Gordon, Brian, Hantler, Nancy, Hornbeck, Russ, Jarman, Steve, Keefe, Sarah, Koudelis, Deborah, Massoumzadeh, Parinaz, McCullough, Austin, McKay, Nicole, Nicklaus, Joyce, Pulizos, Christine, Wang, Qing, Mishall, Sheetal, Sabaredzovic, Edita, Deng, Emily, Candela, Madison, Smith, Hunter, Hobbs, Diana, Scott, Jalen, Xiong, Chengjie, Wang, Peter, Xu, Xiong, Li, Yan, Gremminger, Emily, Ma, Yinjiao, Bui, Ryan, Lu, Ruijin, Martins, Ralph, Sosa Ortiz, Ana Luisa, Daniels, Alisha, Courtney, Laura, Mori, Hiroshi, Supnet-Bell, Charlene, Xu, Jinbin, Ringman, John, Barthelemy, Nicolas, Morris, John, Smith, Jennifer, Doering, Stephanie, Chen, Charles D., Jarman, Stephen, Jackson, Kelley, Hornbeck, Russ C., Ances, Beau M., Aschenbrenner, Andrew J., Bateman, Randall J., Morris, John C., and Benzinger, Tammie L.S.
Published: 2024
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17. Comparison of tau spread in people with Down syndrome versus autosomal-dominant Alzheimer's disease: a cross-sectional study

Author: Aizenstein, Howard J., Andrews, Howard F., Bell, Karen, Birn, Rasmus M., Bulova, Peter, Cheema, Amrita, Chen, Kewei, Clare, Isabel, Clark, Lorraine, Cohen, Ann D., Constantino, John N., Doran, Eric W., Feingold, Eleanor, Foroud, Tatiana M., Hartley, Sigan L., Hom, Christy, Honig, Lawrence, Ikonomovic, Milos D., Johnson, Sterling C., Jordan, Courtney, Kamboh, M. Ilyas, Keator, David, Klunk, William E., Kofler, Julia K., Kreisl, William C., Krinsky-McHale, Sharon J., Lao, Patrick, Laymon, Charles, Lott, Ira T., Lupson, Victoria, Mathis, Chester A., Minhas, Davneet S., Nadkarni, Neelesh, Pang, Deborah, Petersen, Melissa, Price, Julie C., Pulsifer, Margaret, Reiman, Eric, Rizvi, Batool, Sabbagh, Marwan N., Schupf, Nicole, Tudorascu, Dana L., Tumuluru, Rameshwari, Tycko, Benjamin, Varadarajan, Badri, White, Desiree A., Yassa, Michael A., Zaman, Shahid, Zhang, Fan, Bateman, Randall, Daniels, Alisha J., Courtney, Laura, McDade, Eric, Llibre-Guerra, Jorge J., Supnet-Bell, Charlene, Xiong, Chengie, Xu, Xiong, Lu, Ruijin, Wang, Guoqiao, Li, Yan, Gremminger, Emily, Perrin, Richard J., Franklin, Erin, Ibanez, Laura, Jerome, Gina, Herries, Elizabeth, Stauber, Jennifer, Baker, Bryce, Minton, Matthew, Cruchaga, Carlos, Goate, Alison M., Renton, Alan E., Picarello, Danielle M., Benzinger, Tammie, Gordon, Brian A., Hornbeck, Russall, Hassenstab, Jason, Smith, Jennifer, Stout, Sarah, Aschenbrenner, Andrew J., Karch, Celeste M., Marsh, Jacob, Morris, John C., Holtzman, David M., Barthelemy, Nicolas, Xu, Jinbin, Noble, James M., Berman, Sarah B., Ikonomovic, Snezana, Nadkarni, Neelesh K., Day, Gregory, Graff-Radford, Neill R., Farlow, Martin, Chhatwal, Jasmeer P., Ikeuchi, Takeshi, Kasuga, Kensaku, Niimi, Yoshiki, Huey, Edward D., Salloway, Stephen, Schofield, Peter R., Brooks, William S., Bechara, Jacob A., Martins, Ralph, Fox, Nick C., Cash, David M., Ryan, Natalie S., Jucker, Mathias, Laske, Christoph, Hofmann, Anna, Kuder-Buletta, Elke, Graber-Sultan, Susanne, Obermueller, Ulrike, Levin, Johannes, Roedenbeck, Yvonne, Vöglein, Jonathan, Lee, Jae-Hong, Roh, Jee Hoon, Sanchez-Valle, Raquel, Rosa-Neto, Pedro, Allegri, Ricardo F., Chrem Mendez, Patricio, Surace, Ezequiel, Vazquez, Silvia, Lopera, Francisco, Leon, Yudy Milena, Ramirez, Laura, Aguillon, David, Levey, Allan I., Johnson, Erik C.B, Seyfried, Nicholas T., Ringman, John, Mori, Hiroshi, Wisch, Julie K, McKay, Nicole S, Boerwinkle, Anna H, Kennedy, James, Flores, Shaney, Handen, Benjamin L, Christian, Bradley T, Head, Elizabeth, Mapstone, Mark, Rafii, Michael S, O’Bryant, Sid E, Price, Julie C, Laymon, Charles M, Krinsky-McHale, Sharon J, Lai, Florence, Rosas, H Diana, Hartley, Sigan L, Lott, Ira T, Tudorascu, Dana, Zammit, Matthew, Brickman, Adam M, Lee, Joseph H, Bird, Thomas D, Cohen, Annie, Chrem, Patricio, Daniels, Alisha, Chhatwal, Jasmeer P, Karch, Celeste M, Day, Gregory S, Llibre-Guerra, Jorge, Ringman, John M, van Dyck, Christopher H, Xiong, Chengjie, Morris, John C, Bateman, Randall J, Benzinger, Tammie L S, Gordon, Brian A, and Ances, Beau M
Published: 2024
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18. Assessing depression recurrence, cognitive burden, and neurobiological homeostasis in late life: Design and rationale of the REMBRANDT study

Author: Taylor, Warren D., Ajilore, Olusola, Karim, Helmet T., Butters, Meryl A., Krafty, Robert, Boyd, Brian D., Banihashemi, Layla, Szymkowicz, Sarah M., Ryan, Claire, Hassenstab, Jason, Landman, Bennett A., and Andreescu, Carmen
Published: 2024
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19. Predicting cognitive decline: Which is more useful, baseline amyloid levels or longitudinal change?

Author: Chen, Gengsheng, McKay, Nicole S., Gordon, Brian A., Liu, Jingxia, Joseph-Mathurin, Nelly, Schindler, Suzanne E., Hassenstab, Jason, Aschenbrenner, Andrew J., Wang, Qing, Schultz, Stephanie A., Su, Yi, LaMontagne, Pamela J, Keefe, Sarah J., Massoumzadeh, Parinaz, Cruchaga, Carlos, Xiong, Chengjie, Morris, John C., and Benzinger, Tammie L.S.
Published: 2024
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20. Advanced structural brain aging in preclinical autosomal dominant Alzheimer disease

Author: Millar, Peter R, Gordon, Brian A, Wisch, Julie K, Schultz, Stephanie A, Benzinger, Tammie LS, Cruchaga, Carlos, Hassenstab, Jason J, Ibanez, Laura, Karch, Celeste, Llibre-Guerra, Jorge J, Morris, John C, Perrin, Richard J, Supnet-Bell, Charlene, Xiong, Chengjie, Allegri, Ricardo F, Berman, Sarah B, Chhatwal, Jasmeer P, Chrem Mendez, Patricio A, Day, Gregory S, Hofmann, Anna, Ikeuchi, Takeshi, Jucker, Mathias, Lee, Jae-Hong, Levin, Johannes, Lopera, Francisco, Niimi, Yoshiki, Sánchez-González, Victor J, Schofield, Peter R, Sosa-Ortiz, Ana Luisa, Vöglein, Jonathan, Bateman, Randall J, Ances, Beau M, and McDade, Eric M
Published: 2023
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21. Alzheimer’s disease genetic risk and cognitive reserve in relationship to long-term cognitive trajectories among cognitively normal individuals

Author: Pettigrew, Corinne, Nazarovs, Jurijs, Soldan, Anja, Singh, Vikas, Wang, Jiangxia, Hohman, Timothy, Dumitrescu, Logan, Libby, Julia, Kunkle, Brian, Gross, Alden L., Johnson, Sterling, Lu, Qiongshi, Engelman, Corinne, Masters, Colin L., Maruff, Paul, Laws, Simon M., Morris, John C., Hassenstab, Jason, Cruchaga, Carlos, Resnick, Susan M., Kitner-Triolo, Melissa H., An, Yang, and Albert, Marilyn
Published: 2023
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22. Item response theory analysis of the Clinical Dementia Rating.

Author: Li, Yan, Xiong, Chengjie, Aschenbrenner, Andrew J, Chang, Chih-Hung, Weiner, Michael W, Nosheny, Rachel L, Mungas, Dan, Bateman, Randall J, Hassenstab, Jason, Moulder, Krista L, and Morris, John C
Subjects: Humans, Alzheimer Disease, Psychiatric Status Rating Scales, Algorithms, Aged, Female, Male, Cognitive Dysfunction, Mental Status and Dementia Tests, Alzheimer's disease, Clinical Dementia Rating, bi-factor model, cognitive assessment, dementia severity, item response theory, Alzheimer's Disease, Brain Disorders, Neurosciences, Dementia, Acquired Cognitive Impairment, Neurodegenerative, Aging, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Neurological, Alzheimer&apos, s disease, bi&#8208, factor model, Clinical Sciences, Geriatrics
Abstract: IntroductionThe Clinical Dementia Rating (CDR) is widely used in Alzheimer's disease research studies and has well established reliability and validity. To facilitate the development of an online, electronic CDR (eCDR) for more efficient clinical applications, this study aims to produce a shortened version of the CDR, and to develop the statistical model for automatic scoring.MethodsItem response theory (IRT) was used for item evaluation and model development. An automatic scoring algorithm was validated using existing CDR global and domain box scores as the reference standard.ResultsMost CDR items discriminate well at mild and very mild levels of cognitive impairment. The bi-factor IRT model fits best and the shortened CDR still demonstrates very high classification accuracy (81%∼92%).DiscussionThe shortened version of the CDR and the automatic scoring algorithm has established a good foundation for developing an eCDR and will ultimately improve the efficiency of cognitive assessment.
Published: 2021

23. Markers of early changes in cognition across cohorts of adults with Down syndrome at risk of Alzheimer's disease

Author: Aschenbrenner, Andrew J, Baksh, R Asaad, Benejam, Bessy, Beresford‐Webb, Jessica A, Coppus, Antonia, Fortea, Juan, Handen, Benjamin L, Hartley, Sigan, Head, Elizabeth, Jaeger, Judith, Levin, Johannes, Loosli, Sandra V, Rebillat, Anne‐Sophie, Sacco, Silvia, Schmitt, Frederick A, Thurlow, Kate E, Zaman, Shahid, Hassenstab, Jason, and Strydom, Andre
Subjects: Biological Psychology, Psychology, Alzheimer's Disease, Acquired Cognitive Impairment, Neurosciences, Down Syndrome, Behavioral and Social Science, Aging, Neurodegenerative, Intellectual and Developmental Disabilities (IDD), Dementia, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Prevention, Brain Disorders, Neurological, Congenital, Alzheimer's disease, clinical trial outcome, composite measure, Down syndrome, early cognitive decline, Genetics, Biological psychology
Abstract: IntroductionDown syndrome (DS), a genetic variant of early onset Alzheimer's disease (AD), lacks a suitable outcome measure for prevention trials targeting pre-dementia stages.MethodsWe used cognitive test data collected in several longitudinal aging studies internationally from 312 participants with DS without dementia to identify composites that were sensitive to change over time. We then conducted additional analyses to provide support for the utility of the composites. The composites were presented to an expert panel to determine the most optimal cognitive battery based on predetermined criteria.ResultsThere were common cognitive domains across site composites, which were sensitive to early decline. The final composite consisted of memory, language/executive functioning, selective attention, orientation, and praxis tests.DiscussionWe have identified a composite that is sensitive to early decline and thus may have utility as an outcome measure in trials to prevent or delay symptoms of AD in DS.
Published: 2021

24. Enabling Technologies for Personalized and Precision Medicine

Author: Ho, Dean, Quake, Stephen R, McCabe, Edward RB, Chng, Wee Joo, Chow, Edward K, Ding, Xianting, Gelb, Bruce D, Ginsburg, Geoffrey S, Hassenstab, Jason, Ho, Chih-Ming, Mobley, William C, Nolan, Garry P, Rosen, Steven T, Tan, Patrick, Yen, Yun, and Zarrinpar, Ali
Subjects: Bioengineering, Brain Disorders, Clinical Research, Generic health relevance, Good Health and Well Being, Artificial Intelligence, Biomarkers, Diagnosis, Humans, Precision Medicine, Therapeutics, artificial intelligence, clinical trials, diagnostics, personalized medicine, precision medicine, therapeutics, Biological Sciences, Engineering, Technology, Biotechnology
Abstract: Individualizing patient treatment is a core objective of the medical field. Reaching this objective has been elusive owing to the complex set of factors contributing to both disease and health; many factors, from genes to proteins, remain unknown in their role in human physiology. Accurately diagnosing, monitoring, and treating disorders requires advances in biomarker discovery, the subsequent development of accurate signatures that correspond with dynamic disease states, as well as therapeutic interventions that can be continuously optimized and modulated for dose and drug selection. This work highlights key breakthroughs in the development of enabling technologies that further the goal of personalized and precision medicine, and remaining challenges that, when addressed, may forge unprecedented capabilities in realizing truly individualized patient care.
Published: 2020

25. Neuroinflammation and amyloid deposition in the progression of mixed Alzheimer and vascular dementia

Author: Ying, Chunwei, Kang, Peter, Binkley, Michael M., Ford, Andria L., Chen, Yasheng, Hassenstab, Jason, Wang, Qing, Strain, Jeremy, Morris, John C., Lee, Jin-Moo, Benzinger, Tammie L.S., and An, Hongyu
Published: 2023
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26. 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
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27. 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
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28. CSF Tau phosphorylation at Thr205 is associated with loss of white matter integrity in autosomal dominant Alzheimer disease

Author: Strain, Jeremy F., Barthelemy, Nicolas, Horie, Kanta, Gordon, Brian A., Kilgore, Collin, Aschenbrenner, Andrew, Cruchaga, Carlos, Xiong, Chengjie, Joseph-Mathurin, Nelly, Hassenstab, Jason, Fagan, Anne M., Li, Yan, Karch, Celeste M., Perrin, Richard J., Berman, Sarah B., Chhatwal, Jasmeer P., Graff-Radford, Neill R., Mori, Hiroshi, Levin, Johannes, Noble, James M., Allegri, Ricardo, Schofield, Peter R., Marcus, Daniel S., Holtzman, David M., Morris, John C., Benzinger, Tammie L.S., McDade, Eric M., Bateman, Randall J., and Ances, Beau M.
Published: 2022
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29. 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
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30. Beta-amyloid moderates the relationship between cortical thickness and attentional control in middle- and older-aged adults

Author: McKay, Nicole S., Dincer, Aylin, Mehrotra, Vidushri, Aschenbrenner, Andrew J., Balota, David, Hornbeck, Russ C., Hassenstab, Jason, Morris, John C., Benzinger, Tammie L.S., and Gordon, Brian A.
Published: 2022
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31. Unlocking Cognitive Analysis Potential in Alzheimer's Disease Clinical Trials: Investigating Hierarchical Linear Models for Analyzing Novel Measurement Burst Design Data.

Author: Wang, Guoqiao, Hassenstab, Jason, Li, Yan, Aschenbrenner, Andrew J., McDade, Eric M., Llibre‐Guerra, Jorge, Bateman, Randall J., and Xiong, Chengjie
Abstract: Measurement burst designs typically administer brief cognitive tests four times per day for 1 week, resulting in a maximum of 28 data points per week per test for every 6 months. In Alzheimer's disease clinical trials, utilizing measurement burst designs holds great promise for boosting statistical power by collecting huge amount of data. However, appropriate methods for analyzing these complex datasets are not well investigated. Furthermore, the large amount of burst design data also poses tremendous challenges for traditional computational procedures such as SAS mixed or Nlmixed. We propose to analyze burst design data using novel hierarchical linear mixed effects models or hierarchical mixed models for repeated measures. Through simulations and real‐world data applications using the novel SAS procedure Hpmixed, we demonstrate these hierarchical models' efficiency over traditional models. Our sample simulation and analysis code can serve as a catalyst to facilitate the methodology development for burst design data. [ABSTRACT FROM AUTHOR]
Published: 2024
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32. Longitudinal associations between exercise and biomarkers in autosomal dominant Alzheimer's disease.

Author: Sewell, Kelsey R., Doecke, James D., Xiong, Chengjie, Benzinger, Tammie, Masters, Colin L., Laske, Christoph, Jucker, Mathias, Lopera, Francisco, Gordon, Brian A., Llibre‐Guerra, Jorge, Levin, Johannes, Huey, Edward D., Hassenstab, Jason, Schofield, Peter R., Day, Gregory S., Fox, Nick C., Chhatwal, Jasmeer, Ibanez, Laura, Roh, Jee Hoon, and Perrin, Richard
Abstract: INTRODUCTION: We investigated longitudinal associations between self‐reported exercise and Alzheimer's disease (AD)‐related biomarkers in individuals with autosomal dominant AD (ADAD) mutations. METHODS: Participants were 308 ADAD mutation carriers aged 39.7 ± 10.8 years from the Dominantly Inherited Alzheimer's Network. Weekly exercise volume was measured via questionnaire and associations with brain volume (magnetic resonance imaging), cerebrospinal fluid biomarkers, and brain amyloid beta (Aβ) measured by positron emission tomography were investigated. RESULTS: Greater volume of weekly exercise at baseline was associated with slower accumulation of brain Aβ at preclinical disease stages β = –0.16 [–0.23 to –0.08], and a slower decline in multiple brain regions including hippocampal volume β = 0.06 [0.03 to 0.08]. DISCUSSION: Exercise is associated with more favorable profiles of AD‐related biomarkers in individuals with ADAD mutations. Exercise may have therapeutic potential for delaying the onset of AD; however, randomized controlled trials are vital to determine a causal relationship before a clinical recommendation of exercise is implemented. Highlights: Greater self‐reported weekly exercise predicts slower declines in brain volume in autosomal dominant Alzheimer's disease (ADAD).Greater self‐reported weekly exercise predicts slower accumulation of brain amyloid beta in ADAD.Associations varied depending on closeness to estimated symptom onset. [ABSTRACT FROM AUTHOR]
Published: 2024
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33. Sex-specific genetic predictors of Alzheimer’s disease biomarkers

Author: Deming, Yuetiva, Dumitrescu, Logan, Barnes, Lisa L, Thambisetty, Madhav, Kunkle, Brian, Gifford, Katherine A, Bush, William S, Chibnik, Lori B, Mukherjee, Shubhabrata, De Jager, Philip L, Kukull, Walter, Huentelman, Matt, Crane, Paul K, Resnick, Susan M, Keene, C Dirk, Montine, Thomas J, Schellenberg, Gerard D, Haines, Jonathan L, Zetterberg, Henrik, Blennow, Kaj, Larson, Eric B, Johnson, Sterling C, Albert, Marilyn, Moghekar, Abhay, del Aguila, Jorge L, Fernandez, Maria Victoria, Budde, John, Hassenstab, Jason, Fagan, Anne M, Riemenschneider, Matthias, Petersen, Ronald C, Minthon, Lennart, Chao, Michael J, Van Deerlin, Vivianna M, Lee, Virginia M-Y, Shaw, Leslie M, Trojanowski, John Q, Peskind, Elaine R, Li, Gail, Davis, Lea K, Sealock, Julia M, Cox, Nancy J, Alzheimer’s Disease Neuroimaging Initiative (ADNI), The Alzheimer Disease Genetics Consortium (ADGC), Goate, Alison M, Bennett, David A, Schneider, Julie A, Jefferson, Angela L, Cruchaga, Carlos, and Hohman, Timothy J
Subjects: Biomedical and Clinical Sciences, Neurosciences, Women's Health, Neurodegenerative, Brain Disorders, Alzheimer's Disease, Dementia, Human Genome, Acquired Cognitive Impairment, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Aging, Genetics, 2.1 Biological and endogenous factors, Neurological, Aged, 80 and over, Alzheimer Disease, Amyloid beta-Peptides, Amyloidosis, Apolipoproteins E, Biomarkers, Brain, Claudins, Female, Genome-Wide Association Study, Genotype, Humans, Male, Muscle Proteins, Mutation, Peptide Fragments, Serpins, Sex Factors, Transcription Factors, tau Proteins, Alzheimer disease, Cerebrospinal fluid biomarkers, Neuropathology, Sex difference, APOE, Amyloid, Tau, Alzheimer’s Disease Neuroimaging Initiative, Alzheimer Disease Genetics Consortium, Clinical Sciences, Neurology & Neurosurgery
Abstract: Cerebrospinal fluid (CSF) levels of amyloid-β 42 (Aβ42) and tau have been evaluated as endophenotypes in Alzheimer's disease (AD) genetic studies. Although there are sex differences in AD risk, sex differences have not been evaluated in genetic studies of AD endophenotypes. We performed sex-stratified and sex interaction genetic analyses of CSF biomarkers to identify sex-specific associations. Data came from a previous genome-wide association study (GWAS) of CSF Aβ42 and tau (1527 males, 1509 females). We evaluated sex interactions at previous loci, performed sex-stratified GWAS to identify sex-specific associations, and evaluated sex interactions at sex-specific GWAS loci. We then evaluated sex-specific associations between prefrontal cortex (PFC) gene expression at relevant loci and autopsy measures of plaques and tangles using data from the Religious Orders Study and Rush Memory and Aging Project. In Aβ42, we observed sex interactions at one previous and one novel locus: rs316341 within SERPINB1 (p = 0.04) and rs13115400 near LINC00290 (p = 0.002). These loci showed stronger associations among females (β = - 0.03, p = 4.25 × 10-8; β = 0.03, p = 3.97 × 10-8) than males (β = - 0.02, p = 0.009; β = 0.01, p = 0.20). Higher levels of expression of SERPINB1, SERPINB6, and SERPINB9 in PFC was associated with higher levels of amyloidosis among females (corrected p values 0.38). In total tau, we observed a sex interaction at a previous locus, rs1393060 proximal to GMNC (p = 0.004), driven by a stronger association among females (β = 0.05, p = 4.57 × 10-10) compared to males (β = 0.02, p = 0.03). There was also a sex-specific association between rs1393060 and tangle density at autopsy (pfemale = 0.047; pmale = 0.96), and higher levels of expression of two genes within this locus were associated with lower tangle density among females (OSTN p = 0.006; CLDN16 p = 0.002) but not males (p ≥ 0.32). Results suggest a female-specific role for SERPINB1 in amyloidosis and for OSTN and CLDN16 in tau pathology. Sex-specific genetic analyses may improve understanding of AD's genetic architecture.
Published: 2018

34. White matter diffusion alterations precede symptom onset in autosomal dominant Alzheimer’s disease

Author: Caballero, Miguel Ángel Araque, Suárez-Calvet, Marc, Duering, Marco, Franzmeier, Nicolai, Benzinger, Tammie, Fagan, Anne M, Bateman, Randall J, Jack, Clifford R, Levin, Johannes, Dichgans, Martin, Jucker, Mathias, Karch, Celeste, Masters, Colin L, Morris, John C, Weiner, Michael, Rossor, Martin, Fox, Nick C, Lee, Jae-Hong, Salloway, Stephen, Danek, Adrian, Goate, Alison, Yakushev, Igor, Hassenstab, Jason, Schofield, Peter R, Haass, Christian, and Ewers, Michael
Subjects: Health Services and Systems, Health Sciences, Neurosciences, Dementia, Biomedical Imaging, Clinical Research, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Acquired Cognitive Impairment, Brain Disorders, Alzheimer's Disease, Neurodegenerative, Aging, 2.1 Biological and endogenous factors, Aetiology, Neurological, Adult, Alzheimer Disease, Brain, Diffusion Tensor Imaging, Female, Humans, Male, Middle Aged, White Matter, Alzheimer's disease, autosomal dominant, white matter, diffusion tensor imaging, TREM2, Medical and Health Sciences, Psychology and Cognitive Sciences, Neurology & Neurosurgery, Biomedical and clinical sciences, Health sciences, Psychology
Abstract: White matter alterations are present in the majority of patients with Alzheimer's disease type dementia. However, the spatiotemporal pattern of white matter changes preceding dementia symptoms in Alzheimer's disease remains unclear, largely due to the inherent diagnostic uncertainty in the preclinical phase and increased risk of confounding age-related vascular disease and stroke in late-onset Alzheimer's disease. In early-onset autosomal-dominantly inherited Alzheimer's disease, participants are destined to develop dementia, which provides the opportunity to assess brain changes years before the onset of symptoms, and in the absence of ageing-related vascular disease. Here, we assessed mean diffusivity alterations in the white matter in 64 mutation carriers compared to 45 non-carrier family non-carriers. Using tract-based spatial statistics, we mapped the interaction of mutation status by estimated years from symptom onset on mean diffusivity. For major atlas-derived fibre tracts, we determined the earliest time point at which abnormal mean diffusivity changes in the mutation carriers were detectable. Lastly, we assessed the association between mean diffusivity and cerebrospinal fluid biomarkers of amyloid, tau, phosphorylated-tau, and soluble TREM2, i.e. a marker of microglia activity. Results showed a significant interaction of mutations status by estimated years from symptom onset, i.e. a stronger increase of mean diffusivity, within the posterior parietal and medial frontal white matter in mutation carriers compared with non-carriers. The earliest increase of mean diffusivity was observed in the forceps major, forceps minor and long projecting fibres-many connecting default mode network regions-between 5 to 10 years before estimated symptom onset. Higher mean diffusivity in fibre tracts was associated with lower grey matter volume in the tracts' projection zones. Global mean diffusivity was correlated with lower cerebrospinal fluid levels of amyloid-β1-42 but higher levels of tau, phosphorylated-tau and soluble TREM2. Together, these results suggest that regionally selective white matter degeneration occurs years before the estimated symptom onset. Such white matter alterations are associated with primary Alzheimer's disease pathology and microglia activity in the brain.
Published: 2018

35. Spatial patterns of neuroimaging biomarker change in individuals from families with autosomal dominant Alzheimer's disease: a longitudinal study

Author: Gordon, Brian A, Blazey, Tyler M, Su, Yi, Hari-Raj, Amrita, Dincer, Aylin, Flores, Shaney, Christensen, Jon, McDade, Eric, Wang, Guoqiao, Xiong, Chengjie, Cairns, Nigel J, Hassenstab, Jason, Marcus, Daniel S, Fagan, Anne M, Jack, Clifford R, Hornbeck, Russ C, Paumier, Katrina L, Ances, Beau M, Berman, Sarah B, Brickman, Adam M, Cash, David M, Chhatwal, Jasmeer P, Correia, Stephen, Förster, Stefan, Fox, Nick C, Graff-Radford, Neill R, la Fougère, Christian, Levin, Johannes, Masters, Colin L, Rossor, Martin N, Salloway, Stephen, Saykin, Andrew J, Schofield, Peter R, Thompson, Paul M, Weiner, Michael M, Holtzman, David M, Raichle, Marcus E, Morris, John C, Bateman, Randall J, and Benzinger, Tammie LS
Subjects: Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Neurosciences, Acquired Cognitive Impairment, Neurodegenerative, Clinical Research, Dementia, Alzheimer's Disease, Brain Disorders, Biomedical Imaging, Aging, Rare Diseases, Aetiology, Detection, screening and diagnosis, 2.1 Biological and endogenous factors, 4.1 Discovery and preclinical testing of markers and technologies, Neurological, Adult, Alzheimer Disease, Amyloid beta-Protein Precursor, Aniline Compounds, Brain, Brain Mapping, Family Health, Female, Fluorodeoxyglucose F18, Humans, Longitudinal Studies, Magnetic Resonance Imaging, Male, Middle Aged, Positron-Emission Tomography, Presenilin-1, Presenilin-2, Statistics, Nonparametric, Thiazoles, Clinical Sciences, Neurology & Neurosurgery
Abstract: BackgroundModels of Alzheimer's disease propose a sequence of amyloid β (Aβ) accumulation, hypometabolism, and structural decline that precedes the onset of clinical dementia. These pathological features evolve both temporally and spatially in the brain. In this study, we aimed to characterise where in the brain and when in the course of the disease neuroimaging biomarkers become abnormal.MethodsBetween Jan 1, 2009, and Dec 31, 2015, we analysed data from mutation non-carriers, asymptomatic carriers, and symptomatic carriers from families carrying gene mutations in presenilin 1 (PSEN1), presenilin 2 (PSEN2), or amyloid precursor protein (APP) enrolled in the Dominantly Inherited Alzheimer's Network. We analysed 11C-Pittsburgh Compound B (11C-PiB) PET, 18F-Fluorodeoxyglucose (18F-FDG) PET, and structural MRI data using regions of interest to assess change throughout the brain. We estimated rates of biomarker change as a function of estimated years to symptom onset at baseline using linear mixed-effects models and determined the earliest point at which biomarker trajectories differed between mutation carriers and non-carriers. This study is registered at ClinicalTrials.gov (number NCT00869817) FINDINGS: 11C-PiB PET was available for 346 individuals (162 with longitudinal imaging), 18F-FDG PET was available for 352 individuals (175 with longitudinal imaging), and MRI data were available for 377 individuals (201 with longitudinal imaging). We found a sequence to pathological changes, with rates of Aβ deposition in mutation carriers being significantly different from those in non-carriers first (across regions that showed a significant difference, at a mean of 18·9 years [SD 3·3] before expected onset), followed by hypometabolism (14·1 years [5·1] before expected onset), and lastly structural decline (4·7 years [4·2] before expected onset). This biomarker ordering was preserved in most, but not all, regions. The temporal emergence within a biomarker varied across the brain, with the precuneus being the first cortical region for each method to show divergence between groups (22·2 years before expected onset for Aβ accumulation, 18·8 years before expected onset for hypometabolism, and 13·0 years before expected onset for cortical thinning).InterpretationMutation carriers had elevations in Aβ deposition, reduced glucose metabolism, and cortical thinning compared with non-carriers which preceded the expected onset of dementia. Accrual of these pathologies varied throughout the brain, suggesting differential regional and temporal vulnerabilities to Aβ, metabolic decline, and structural atrophy, which should be taken into account when using biomarkers in a clinical setting as well as designing and evaluating clinical trials.FundingUS National Institutes of Health, the German Center for Neurodegenerative Diseases, and the Medical Research Council Dementias Platform UK.
Published: 2018

36. Assessing dynamic cognitive function in the daily lives of youth with and without Type 1 Diabetes (T1D): a pilot and feasibility study (Preprint)

Author: Ray, Mary Katherine, primary, Fleming, Jorie, additional, Aschenbrenner, Andrew, additional, Hassenstab, Jason, additional, Redwine, Brooke, additional, Burns, Carissa, additional, Arbelaez, Ana Maria, additional, Vajravelu, Mary Ellen, additional, and Hershey, Tamara, additional
Published: 2024
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37. Deconstructing pathological tau by biological process in early stages of Alzheimer disease: a method for quantifying tau spatial spread in neuroimaging

Author: Doering, Stephanie, primary, McCullough, Austin, additional, Gordon, Brian A., additional, Chen, Charles D., additional, McKay, Nicole, additional, Hobbs, Diana, additional, Keefe, Sarah, additional, Flores, Shaney, additional, Scott, Jalen, additional, Smith, Hunter, additional, Jarman, Stephen, additional, Jackson, Kelley, additional, Hornbeck, Russ C., additional, Ances, Beau M., additional, Xiong, Chengjie, additional, Aschenbrenner, Andrew J., additional, Hassenstab, Jason, additional, Cruchaga, Carlos, additional, Daniels, Alisha, additional, Bateman, Randall J., additional, Noble, James M., additional, Day, Gregory S., additional, Graff-Radford, Neill R., additional, Voglein, Jonathan, additional, Levin, Johannes, additional, Allegri, Ricardo F., additional, Mendez, Patricio Chrem, additional, Surace, Ezequiel, additional, Berman, Sarah B., additional, Ikonomovic, Snezana, additional, Nadkarni, Neelesh K., additional, Lopera, Francisco, additional, Ramirez, Laura, additional, Aguillon, David, additional, Leon, Yudy, additional, Ramos, Claudia, additional, Alzate, Diana, additional, Baena, Ana, additional, Londono, Natalia, additional, Moreno, Sonia, additional, Jucker, Mathias, additional, Laske, Christoph, additional, Kuder-Buletta, Elke, additional, Graber-Sultan, Susanne, additional, Preische, Oliver, additional, Hofmann, Anna, additional, Ikeuchi, Takeshi, additional, Kasuga, Kensaku, additional, Niimi, Yoshiki, additional, Ishii, Kenji, additional, Senda, Michio, additional, Sanchez-Valle, Raquel, additional, Rosa-Neto, Pedro, additional, Fox, Nick C., additional, Cash, Dave, additional, Lee, Jae-Hong, additional, Roh, Jee Hoon, additional, Salloway, Stephen, additional, Riddle, Meghan C., additional, Menard, William, additional, Bodge, Courtney, additional, Surti, Mustafa, additional, Takada, Leonel Tadao, additional, Farlow, Martin, additional, Chhatwal, Jasmeer P., additional, Sanchez-Gonzalez, V.J., additional, Orozco-Barajas, Maribel, additional, Goate, Alison M., additional, Renton, Alan E., additional, Esposito, Bianca T., additional, Karch, Celeste M., additional, Marsh, Jacob, additional, Fernanadez, Victoria, additional, Fagan, Anne M., additional, Jerome, Gina, additional, Herries, Elizabeth, additional, Llibre-Guerra, Jorge, additional, Levey, Allan I., additional, Johnson, Erik C.B., additional, Seyfried, Nicholas T., additional, Schofield, Peter R., additional, Brooks, William S., additional, Bechara, Jacob A., additional, Bateman, Randall, additional, McDade, Eric, additional, Perrin, Richard J., additional, Franklin, Erin E., additional, Benzinger, Tammie, additional, Chen, Allison, additional, Chen, Charles, additional, Friedrichsen, Nelly, additional, Gordon, Brian, additional, Hantler, Nancy, additional, Hornbeck, Russ, additional, Jarman, Steve, additional, Koudelis, Deborah, additional, Massoumzadeh, Parinaz, additional, Nicklaus, Joyce, additional, Pulizos, Christine, additional, Wang, Qing, additional, Mishall, Sheetal, additional, Sabaredzovic, Edita, additional, Deng, Emily, additional, Candela, Madison, additional, Wang, Peter, additional, Xu, Xiong, additional, Li, Yan, additional, Gremminger, Emily, additional, Ma, Yinjiao, additional, Bui, Ryan, additional, Lu, Ruijin, additional, Martins, Ralph, additional, Sosa Ortiz, Ana Luisa, additional, Courtney, Laura, additional, Mori, Hiroshi, additional, Supnet-Bell, Charlene, additional, Xu, Jinbin, additional, Ringman, John, additional, Barthelemy, Nicolas, additional, Morris, John, additional, Smith, Jennifer, additional, Morris, John C., additional, and Benzinger, Tammie L.S., additional
Published: 2024
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38. Long-term prognosis and educational determinants of brain network decline in older adult individuals

Author: Chan, Micaela Y., Han, Liang, Carreno, Claudia A., Zhang, Ziwei, Rodriguez, Rebekah M., LaRose, Megan, Hassenstab, Jason, and Wig, Gagan S.
Published: 2021
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39. Amyloid and Tau Pathology Associations With Personality Traits, Neuropsychiatric Symptoms, and Cognitive Lifestyle in the Preclinical Phases of Sporadic and Autosomal Dominant Alzheimer’s Disease

Author: Allegri, Ricardo, Amtashar, Fatima, Bateman, Randy, Benzinger, Tammie, Berman, Sarah, Bodge, Courtney, Brandon, Susan, Brooks, William (Bill), Buck, Jill, Buckles, Virginia, Chea, Sochenda, Chhatwal, Jasmeer, Chrem, Patricio, Chui, Helena, Cinco, Jake, Clifford, Jack, Cruchaga, Carlos, D‘Mello, Mirelle, Donahue, Tamara, Douglas, Jane, Edigo, Noelia, Erekin-Taner, Nilufer, Fagan, Anne, Farlow, Marty, Farrar, Angela, Feldman, Howard, Flynn, Gigi, Fox, Nick, Franklin, Erin, Fujii, Hisako, Gant, Cortaiga, Gardener, Samantha, Ghetti, Bernardino, Goate, Alison, Goldman, Jill, Gordon, Brian, Graff-Radford, Neill, Gray, Julia, Gurney, Jenny, Hassenstab, Jason, Hirohara, Mie, Holtzman, David, Hornbeck, Russ, DiBari, Siri Houeland, Ikeuchi, Takeshi, Ikonomovic, Snezana, Jerome, Gina, Jucker, Mathias, Karch, Celeste, Kasuga, Kensaku, Kawarabayashi, Takeshi, Klunk, William (Bill), Koeppe, Robert, Kuder-Buletta, Elke, Laske, Christoph, Lee, Jae-Hong, Levin, Johannes, Marcus, Daniel, Martins, Ralph, Mason, Neal Scott, Masters, Colin, Maue-Dreyfus, Denise, McDade, Eric, Montoya, Lucy, Mori, Hiroshi, Morris, John, Nagamatsu, Akem, Neimeyer, Katie, Noble, James, Norton, Joanne, Perrin, Richard, Raichle, Marc, Ringman, John, Roh, Jee Hoon, Salloway, Stephen, Schofield, Peter, Shimada, Hiroyuki, Shiroto, Tomoyo, Shoji, Mikio, Sigurdson, Wendy, Sohrabi, Hamid, Sparks, Paige, Suzuki, Kazushi, Swisher, Laura, Taddei, Kevin, Wang, Jen, Wang, Peter, Weiner, Mike, Wolfsberger, Mary, Xiong, Chengjie, Xu, Xiong, Tam, Angela, Labonté, Anne, Pichet Binette, Alexa, Faubert, Anne-Marie, Mathieu, Axel, Madjar, Cécile, Carrier, Charles Edouard, Dansereau, Christian, Kazazian, Christina, Lepage, Claude, Picard, Cynthia, Maillet, David, Michaud, Diane, Couture, Doris, Dea, Doris, Cuello, Claudio, Barkun, Alan, Evans, Alan, Courcot, Blandine, Tardif, Christine, Debacker, Clément, Jack, Clifford R., Fontaine, David, Knopman, David S., Maultaup, Gerhard, Near, Jamie, Leoutsakos, Jeannie-Marie, Maltais, Jean-Robert, Brandt, Jason, Pruessner, Jens, Morris, John C., Breitner, John C.S., Poirier, Judes, Cheewakriengkrai, Laksanun, Münter, Lisa-Marie, Collins, Louis, Chakravarty, Mallar, Sager, Mark A., Dauar-Tedeschi, Marina, Eisenberg, Mark, Rajah, Natasha, Aisen, Paul, Toussaint, Joanne, Rosa-Neto, Pedro, Bellec, Pierre, Kostopoulos, Penelope, Etienne, Pierre, Tariot, Pierre N., Orban, Pierre, Sperling, Reisa A., Hoge, Rick, Thomas, Ronald G., Gauthier, Serge, Craft, Suzanne, Villeneuve, Sylvia, Montine, Thomas J., Nair, Vasavan, Bohbot, Véronique, Venugopalan, Vinod, Fonov, Vladimir, Ituria-Medina, Yasser, Khachaturian, Zaven S., Teigner, Eduard, Anthal, Elena, Yu, Elsa, Ferdinand, Fabiola, Pogossova, Galina, Mayrand, Ginette, Duclair, Guerda, Gagné, Guylaine, Newbold-Fox, Holly, Leppert, Illana, Vallée, Isabelle, Vogel, Jacob W., Tremblay-Mercier, Jennifer, Frenette, Joanne, Frappier, Josée, Kat, Justin, Miron, Justin, Wan, Karen, Mahar, Laura, Carmo, Leopoldina, Théroux, Louise, Dadar, Mahsa, Dufour, Marianne, Lafaille-Magnan, Marie-Elyse, Appleby, Melissa, Savard, Mélissa, Tuwaig, Miranda, Petkova, Mirela, Rioux, Pierre, Meyer, Pierre-François, El-Khoury, Rana, Gordon, Renee, Giles, Renuka, Das, Samir, Wang, Seqian, Tabrizi, Shirin, Mathotaarachchi, Sulantha, Dubuc, Sylvie, Lee, Tanya, Beaudry, Thomas, Gervais, Valérie, Pagé, Véronique, Gonneaud, Julie, Ayranci, Gülebru, Pascoal, Tharick A., Desautels, René, Benbouhoud, Fatiha, Saint-Fort, Eunice Farah, Verfaillie, Sander C.J., Farzin, Sarah, Salaciak, Alyssa, Tullo, Stephanie, Vachon-Presseau, Etienne, Daoust, Leslie-Ann, Köbe, Theresa, Spreng, Nathan, McSweeney, Melissa, Nilsson, Nathalie, Pishnamazi, Morteza, Bedetti, Christophe, Vachon-Presseau, Étienne, Bateman, Randall, and Collins, D. Louis
Published: 2021
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40. 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
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41. Axonal damage and inflammation response are biological correlates of decline in small-world values: a cohort study in autosomal dominant Alzheimer's disease.

Author: Vermunt, Lisa, Sutphen, Courtney L, Dicks, Ellen, Leeuw, Diederick M de, Allegri, Ricardo F, Berman, Sarah B, Cash, David M, Chhatwal, Jasmeer P, Cruchaga, Carlos, Day, Gregory S, Ewers, Michael, Farlow, Martin R, Fox, Nick C, Ghetti, Bernardino, Graff-Radford, Neill R, Hassenstab, Jason, Jucker, Mathias, Karch, Celeste M, Kuhle, Jens, and Laske, Christoph
Published: 2024
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42. Serum neurofilament light chain levels are associated with white matter integrity in autosomal dominant Alzheimer's disease

Author: Schultz, Stephanie A., Strain, Jeremy F., Adedokun, Adedamola, Wang, Qing, Preische, Oliver, Kuhle, Jens, Flores, Shaney, Keefe, Sarah, Dincer, Aylin, Ances, Beau M., Berman, Sarah B., Brickman, Adam M., Cash, David M., Chhatwal, Jasmeer, Cruchaga, Carlos, Ewers, Michael, Fox, Nick N., Ghetti, Bernardino, Goate, Alison, Graff-Radford, Neill R., Hassenstab, Jason J., Hornbeck, Russ, Jack, Clifford, Jr, Johnson, Keith, Joseph-Mathurin, Nelly, Karch, Celeste M., Koeppe, Robert A., Lee, Athene K.W., Levin, Johannes, Masters, Colin, McDade, Eric, Perrin, Richard J., Rowe, Christopher C., Salloway, Stephen, Saykin, Andrew J., Sperling, Reisa, Su, Yi, Villemagne, Victor L., Vöglein, Jonathan, Weiner, Michael, Xiong, Chengjie, Fagan, Anne M., Morris, John C., Bateman, Randall J., Benzinger, Tammie L.S., Jucker, Mathias, and Gordon, Brian A.
Published: 2020
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43. Adapting prescribing criteria for amyloid‐targeted antibodies for adults with Down syndrome

Author: Hillerstrom, Hampus, primary, Fisher, Richard, additional, Janicki, Matthew P., additional, Chicoine, Brian, additional, Christian, Bradley T., additional, Esbensen, Anna, additional, Esralew, Lucille, additional, Fortea, Juan, additional, Hartley, Sigan, additional, Hassenstab, Jason, additional, Keller, Seth M., additional, Krinsky‐McHale, Sharon, additional, Lai, Florence, additional, Levin, Johannes, additional, McCarron, Mary, additional, McDade, Eric, additional, Rebillat, Anne Sophie, additional, Rosas, Herminia Diana, additional, Silverman, Wayne, additional, Strydom, Andre, additional, Zaman, Shahid H., additional, and Zetterberg, Henrik, additional
Published: 2024
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44. Continuous Associations Between Remote Self-Administered Cognitive Measures and Imaging Biomarkers of Alzheimer’s Disease

Author: Boots, Elizabeth A., primary, Frank, Ryan D., additional, Fan, Winnie Z., additional, Christianson, Teresa J., additional, Kremers, Walter K., additional, Stricker, John L., additional, Machulda, Mary M., additional, Fields, Julie A., additional, Hassenstab, Jason, additional, Graff-Radford, Jonathan, additional, Vemuri, Prashanthi, additional, Jack, Clifford R., additional, Knopman, David S., additional, Petersen, Ronald C., additional, and Stricker, Nikki H., additional
Published: 2024
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45. Investigating White Matter Neuroinflammation in Alzheimer Disease Using Diffusion-Based Neuroinflammation Imaging

Author: Wang, Qing, primary, Schindler, Suzanne E., additional, Chen, Gengsheng, additional, Mckay, Nicole S., additional, McCullough, Austin, additional, Flores, Shaney, additional, Liu, Jingxia, additional, Sun, Zhexian, additional, Wang, Sicheng, additional, Wang, Wenshang, additional, Hassenstab, Jason, additional, Cruchaga, Carlos, additional, Perrin, Richard J., additional, Fagan, Anne M., additional, Morris, John C., additional, Wang, Yong, additional, and Benzinger, Tammie L.S., additional
Published: 2024
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46. Predictors and outcomes of fluctuations in the clinical dementia rating scale

Author: Wilks, Hannah, primary, Benzinger, Tammie L. S., additional, Schindler, Suzanne E., additional, Cruchaga, Carlos, additional, Morris, John C., additional, and Hassenstab, Jason, additional
Published: 2024
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47. Comparison of cerebrospinal fluid, plasma and neuroimaging biomarker utility in Alzheimer’s disease

Author: Meeker, Karin L, primary, Luckett, Patrick H, additional, Barthélemy, Nicolas R, additional, Hobbs, Diana A, additional, Chen, Charles, additional, Bollinger, James, additional, Ovod, Vitaliy, additional, Flores, Shaney, additional, Keefe, Sarah, additional, Henson, Rachel L, additional, Herries, Elizabeth M, additional, McDade, Eric, additional, Hassenstab, Jason J, additional, Xiong, Chengjie, additional, Cruchaga, Carlos, additional, Benzinger, Tammie L S, additional, Holtzman, David M, additional, Schindler, Suzanne E, additional, Bateman, Randall J, additional, Morris, John C, additional, Gordon, Brian A, additional, and Ances, Beau M, additional
Published: 2024
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48. When Does Alzheimer's Disease Start? Robust Estimates Based on Longitudinal Aβ-Amyloid-PET in Three Large International Cohorts

Author: Burnham, Samantha Claire, primary, Cox, Timothy, additional, Benzinger, Tammie, additional, Bourgeat, Pierrick, additional, Cruchaga, Carlos, additional, Doecke, James D., additional, Doré, Vincent, additional, Fowler, Christopher, additional, Goyal, Manu S., additional, Jin, Liang, additional, Laws, Simon M., additional, Hassenstab, Jason, additional, Maruff, Paul, additional, Williams, Rob, additional, Porter, Tenielle, additional, Saykin, Andrew J., additional, Shishegar, Rosita, additional, Sohrabi, Hamid R., additional, Petersen, Ronald C., additional, Tosun, Duygu, additional, Fripp, Jurgen, additional, Rowe, Christopher C., additional, Morris, John C., additional, Weiner, Michael, additional, Masters, colin, additional, and Villemagne, Victor L., additional
Published: 2024
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49. The BDNFVal66Met SNP modulates the association between beta-amyloid and hippocampal disconnection in Alzheimer’s disease

Author: Franzmeier, Nicolai, Ren, Jinyi, Damm, Alexander, Monté-Rubio, Gemma, Boada, Mercè, Ruiz, Agustín, Ramirez, Alfredo, Jessen, Frank, Düzel, Emrah, Rodríguez Gómez, Octavio, Benzinger, Tammie, Goate, Alison, Karch, Celeste M., Fagan, Anne M., McDade, Eric, Buerger, Katharina, Levin, Johannes, Duering, Marco, Dichgans, Martin, Suárez-Calvet, Marc, Haass, Christian, Gordon, Brian A., Lim, Yen Ying, Masters, Colin L., Janowitz, Daniel, Catak, Cihan, Wolfsgruber, Steffen, Wagner, Michael, Milz, Esther, Moreno-Grau, Sonia, Teipel, Stefan, Grothe, Michel J, Kilimann, Ingo, Rossor, Martin, Fox, Nick, Laske, Christoph, Chhatwal, Jasmeer, Falkai, Peter, Perneczky, Robert, Lee, Jae-Hong, Spottke, Annika, Boecker, Henning, Brosseron, Frederic, Fliessbach, Klaus, Heneka, Michael T., Nestor, Peter, Peters, Oliver, Fuentes, Manuel, Menne, Felix, Priller, Josef, Spruth, Eike J., Franke, Christiana, Schneider, Anja, Westerteicher, Christine, Speck, Oliver, Wiltfang, Jens, Bartels, Claudia, Araque Caballero, Miguel Ángel, Metzger, Coraline, Bittner, Daniel, Salloway, Stephen, Danek, Adrian, Hassenstab, Jason, Yakushev, Igor, Schofield, Peter R., Morris, John C., Bateman, Randall J., and Ewers, Michael
Published: 2021
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50. Baseline Microglial Activation Correlates With Brain Amyloidosis and Longitudinal Cognitive Decline in Alzheimer Disease

Author: Wang, Qing, Chen, Gengsheng, Schindler, Suzanne E., Christensen, Jon, McKay, Nicole S., Liu, Jingxia, Wang, Sicheng, Sun, Zhexian, Hassenstab, Jason, Su, Yi, Flores, Shaney, Hornbeck, Russ, Cash, Lisa, Cruchaga, Carlos, Fagan, Anne M., Tu, Zhude, Morris, John C., Mintun, Mark A., Wang, Yong, and Benzinger, Tammie L.S.
Published: 2022
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