1,386 results on '"Snitz BE"'
Search Results
2. Multi-analyte proteomic analysis identifies blood-based neuroinflammation, cerebrovascular and synaptic biomarkers in preclinical Alzheimer’s disease
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Zeng, Xuemei, Lafferty, Tara K., Sehrawat, Anuradha, Chen, Yijun, Ferreira, Pamela C. L., Bellaver, Bruna, Povala, Guilherme, Kamboh, M. Ilyas, Klunk, William E., Cohen, Ann D., Lopez, Oscar L., Ikonomovic, Milos D., Pascoal, Tharick A., Ganguli, Mary, Villemagne, Victor L., Snitz, Beth E., and Karikari, Thomas K.
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- 2024
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3. Alzheimer blood biomarkers: practical guidelines for study design, sample collection, processing, biobanking, measurement and result reporting
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Zeng, Xuemei, Chen, Yijun, Sehrawat, Anuradha, Lee, Jihui, Lafferty, Tara K., Kofler, Julia, Berman, Sarah B., Sweet, Robert A., Tudorascu, Dana L., Klunk, William E., Ikonomovic, Milos D., Pfister, Anna, Zetterberg, Henrik, Snitz, Beth E., Cohen, Anne D., Villemagne, Victor L., Pascoal, Tharick A., Kamboh, M. llyas, Lopez, Oscar I., Blennow, Kaj, and Karikari, Thomas K.
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- 2024
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4. Discriminating Parkinson’s disease patients from healthy controls using nasal respiratory airflow
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Michal Andelman-Gur, Kobi Snitz, Danielle Honigstein, Aharon Weissbrod, Timna Soroka, Aharon Ravia, Lior Gorodisky, Liron Pinchover, Adi Ezra, Neomi Hezi, Tanya Gurevich, and Noam Sobel
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Medicine - Abstract
Abstract Background Breathing patterns may inform on health. We note that the sites of earliest brain damage in Parkinson’s disease (PD) house the neural pace-makers of respiration. We therefore hypothesized that ongoing long-term temporal dynamics of respiration may be altered in PD. Methods We applied a wearable device that precisely logs nasal airflow over time in 28 PD patients (mostly H&Y stage-II) and 33 matched healthy controls. Each participant wore the device for 24 h of otherwise routine daily living. Results We observe significantly altered temporal patterns of nasal airflow in PD, where inhalations are longer and less variable than in matched controls (mean PD = −1.22 ± 1.9 (combined respiratory features score), Control = 1.04 ± 2.16, Wilcoxon rank-sum test, z = −4.1, effect size Cliff’s δ = −0.61, 95% confidence interval = −0.79 – (−0.34), P = 4.3 × 10−5). The extent of alteration is such that using only 30 min of recording we detect PD at 87% accuracy (AUC = 0.85, 79% sensitivity (22 of 28), 94% specificity (31 of 33), z = 5.7, p = 3.5 × 10−9), and also predict disease severity (correlation with UPDRS-Total score: r = 0.49; P = 0.008). Conclusions We conclude that breathing patterns are altered by H&Y stage-II in the disease cascade, and our methods may be further refined in the future to provide an indication with diagnostic and prognostic value.
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- 2024
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5. Multi-analyte proteomic analysis identifies blood-based neuroinflammation, cerebrovascular and synaptic biomarkers in preclinical Alzheimer’s disease
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Xuemei Zeng, Tara K. Lafferty, Anuradha Sehrawat, Yijun Chen, Pamela C. L. Ferreira, Bruna Bellaver, Guilherme Povala, M. Ilyas Kamboh, William E. Klunk, Ann D. Cohen, Oscar L. Lopez, Milos D. Ikonomovic, Tharick A. Pascoal, Mary Ganguli, Victor L. Villemagne, Beth E. Snitz, and Thomas K. Karikari
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Preclinical Alzheimer’s disease ,Plasma biomarkers ,Proteomics ,Amyloid pathology ,Tau pathology ,Neurodegeneration ,Neurology. Diseases of the nervous system ,RC346-429 ,Geriatrics ,RC952-954.6 - Abstract
Abstract Background Blood-based biomarkers are gaining grounds for the detection of Alzheimer’s disease (AD) and related disorders (ADRDs). However, two key obstacles remain: the lack of methods for multi-analyte assessments and the need for biomarkers for related pathophysiological processes like neuroinflammation, vascular, and synaptic dysfunction. A novel proteomic method for pre-selected analytes, based on proximity extension technology, was recently introduced. Referred to as the NULISAseq CNS disease panel, the assay simultaneously measures ~ 120 analytes related to neurodegenerative diseases, including those linked to both core (i.e., tau and amyloid-beta (Aβ)) and non-core AD processes. This study aimed to evaluate the technical and clinical performance of this novel targeted proteomic panel. Methods The NULISAseq CNS disease panel was applied to 176 plasma samples from 113 individuals in the MYHAT-NI cohort of predominantly cognitively normal participants from an economically underserved region in southwestern Pennsylvania, USA. Classical AD biomarkers, including p-tau181, p-tau217, p-tau231, GFAP, NEFL, Aβ40, and Aβ42, were independently measured using Single Molecule Array (Simoa) and correlations and diagnostic performances compared. Aβ pathology, tau pathology, and neurodegeneration (AT(N) statuses) were evaluated with [11C] PiB PET, [18F]AV-1451 PET, and an MRI-based AD-signature composite cortical thickness index, respectively. Linear mixed models were used to examine cross-sectional and Wilcoxon rank sum tests for longitudinal associations between NULISA and neuroimaging-determined AT(N) biomarkers. Results NULISA concurrently measured 116 plasma biomarkers with good technical performance (97.2 ± 13.9% targets gave signals above assay limits of detection), and significant correlation with Simoa assays for the classical biomarkers. Cross-sectionally, p-tau217 was the top hit to identify Aβ pathology, with age, sex, and APOE genotype-adjusted AUC of 0.930 (95%CI: 0.878–0.983). Fourteen markers were significantly decreased in Aβ-PET + participants, including TIMP3, BDNF, MDH1, and several cytokines. Longitudinally, FGF2, IL4, and IL9 exhibited Aβ PET-dependent yearly increases in Aβ-PET + participants. Novel plasma biomarkers with tau PET-dependent longitudinal changes included proteins associated with neuroinflammation, synaptic function, and cerebrovascular integrity, such as CHIT1, CHI3L1, NPTX1, PGF, PDGFRB, and VEGFA; all previously linked to AD but only reliable when measured in cerebrospinal fluid. The autophagosome cargo protein SQSTM1 exhibited significant association with neurodegeneration after adjusting age, sex, and APOE ε4 genotype. Conclusions Together, our results demonstrate the feasibility and potential of immunoassay-based multiplexing to provide a comprehensive view of AD-associated proteomic changes, consistent with the recently revised biological and diagnostic framework. Further validation of the identified inflammation, synaptic, and vascular markers will be important for establishing disease state markers in asymptomatic AD.
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- 2024
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6. Alzheimer blood biomarkers: practical guidelines for study design, sample collection, processing, biobanking, measurement and result reporting
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Xuemei Zeng, Yijun Chen, Anuradha Sehrawat, Jihui Lee, Tara K. Lafferty, Julia Kofler, Sarah B. Berman, Robert A. Sweet, Dana L. Tudorascu, William E. Klunk, Milos D. Ikonomovic, Anna Pfister, Henrik Zetterberg, Beth E. Snitz, Anne D. Cohen, Victor L. Villemagne, Tharick A. Pascoal, M. llyas Kamboh, Oscar I. Lopez, Kaj Blennow, and Thomas K. Karikari
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Blood biomarker ,Standardization ,Preanalytical factors ,Alzheimer’s disease ,Biobanking ,Neurodegeneration ,Neurology. Diseases of the nervous system ,RC346-429 ,Geriatrics ,RC952-954.6 - Abstract
Abstract Alzheimer’s disease (AD), the most common form of dementia, remains challenging to understand and treat despite decades of research and clinical investigation. This might be partly due to a lack of widely available and cost-effective modalities for diagnosis and prognosis. Recently, the blood-based AD biomarker field has seen significant progress driven by technological advances, mainly improved analytical sensitivity and precision of the assays and measurement platforms. Several blood-based biomarkers have shown high potential for accurately detecting AD pathophysiology. As a result, there has been considerable interest in applying these biomarkers for diagnosis and prognosis, as surrogate metrics to investigate the impact of various covariates on AD pathophysiology and to accelerate AD therapeutic trials and monitor treatment effects. However, the lack of standardization of how blood samples and collected, processed, stored analyzed and reported can affect the reproducibility of these biomarker measurements, potentially hindering progress toward their widespread use in clinical and research settings. To help address these issues, we provide fundamental guidelines developed according to recent research findings on the impact of sample handling on blood biomarker measurements. These guidelines cover important considerations including study design, blood collection, blood processing, biobanking, biomarker measurement, and result reporting. Furthermore, the proposed guidelines include best practices for appropriate blood handling procedures for genetic and ribonucleic acid analyses. While we focus on the key blood-based AD biomarkers for the AT(N) criteria (e.g., amyloid-beta [Aβ]40, Aβ42, Aβ42/40 ratio, total-tau, phosphorylated-tau, neurofilament light chain, brain-derived tau and glial fibrillary acidic protein), we anticipate that these guidelines will generally be applicable to other types of blood biomarkers. We also anticipate that these guidelines will assist investigators in planning and executing biomarker research, enabling harmonization of sample handling to improve comparability across studies.
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- 2024
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7. Generation of a gene-corrected human isogenic iPSC line from an Alzheimer’s disease iPSC line carrying the PSEN1 H163R mutation
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Damián Hernández, Stephanie Morgan Schlicht, Jordan Elli Clarke, Maciej Daniszewski, Celeste M. Karch, Alison M. Goate, Alice Pébay, Sarah Adams, Ricardo Allegri, Aki Araki, Nicolas Barthelemy, Randall Bateman, Jacob Bechara, Tammie Benzinger, Sarah Berman, Courtney Bodge, Sus Brandon, William (Bill) Brooks, Jared Brosch, Jill Buck, Virginia Buckles, Kathleen Carter, Lisa Cash, Charlie Chen, Jasmeer Chhatwal, Patricio Chrem Mendez, Jasmin Chua, Helena Chui, Laura Courtney, Carlos Cruchaga, Gregory S Day, Chrismary DeLaCruz, Darcy Denner, Anna Diffenbacher, Aylin Dincer, Tamara Donahue, Jane Douglas, Duc Duong, Noelia Egido, Bianca Esposito, Anne Fagan, Marty Farlow, Becca Feldman, Colleen Fitzpatrick, Shaney Flores, Nick Fox, Erin Franklin, Nelly Joseph-Mathurin, Hisako Fujii, Samantha Gardener, Bernardino Ghetti, Alison Goate, Sarah Goldberg, Jill Goldman, Alyssa Gonzalez, Brian Gordon, Susanne Gr¨aber-Sultan, Neill Graff-Radford, Morgan Graham, Julia Gray, Emily Gremminger, Miguel Grilo, Alex Groves, Christian Haass, Lisa H¨asler, Jason Hassenstab, Cortaiga Hellm, Elizabeth Herries, Laura Hoechst-Swisher, Anna Hofmann, David Holtzman, Russ Hornbeck, Yakushev Igor, Ryoko Ihara, Takeshi Ikeuchi, Snezana Ikonomovic, Kenji Ishii, Clifford Jack, Gina Jerome, Erik Johnson, Mathias Jucker, Celeste Karch, Stephan K¨aser, Kensaku Kasuga, Sarah Keefe, William Klunk, Robert Koeppe, Deb Koudelis, Elke Kuder-Buletta, Christoph Laske, Allan Levey, Johannes Levin, Yan Li, Oscar Lopez, Jacob Marsh, Ralph Martins, Neal Scott Mason, Colin Masters, Kwasi Mawuenyega, Austin McCullough, Eric McDade, Arlene Mejia, Estrella Morenas-Rodriguez, John Morris, James Mountz, Cath Mummery, Neelesh Nadkarni, Akemi Nagamatsu, Katie Neimeyer, Yoshiki Niimi, James Noble, Joanne Norton, Brigitte Nuscher, Ulricke Obermüller, Antoinette O’Connor, Riddhi Patira, Richard Perrin, Lingyan Ping, Oliver Preische, Alan Renton, John Ringman, Stephen Salloway, Peter Schofield, Michio Senda, Nicholas T Seyfried, Kristine Shady, Hiroyuki Shimada, Wendy Sigurdson, Jennifer Smith, Lori Smith, Beth Snitz, Hamid Sohrabi, Sochenda Stephens, Kevin Taddei, Sarah Thompson, Jonathan V¨oglein, Peter Wang, Qing Wang, Elise Weamer, Chengjie Xiong, Jinbin Xu, and Xiong Xu
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Biology (General) ,QH301-705.5 - Abstract
We report the generation of a gene-edited human induced pluripotent stem cell (iPSC) line from an Alzheimer’s disease patient-derived iPSC line harbouring the PSEN1 H163R mutation. This line demonstrates pluripotent stem cell morphology, expression of pluripotency markers, and maintains a normal karyotype.
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- 2024
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8. Genome-wide analysis identifies novel loci influencing plasma apolipoprotein E concentration and Alzheimer’s disease risk
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Aslam, M. Muaaz, Fan, Kang-Hsien, Lawrence, Elizabeth, Bedison, Margaret Anne, Snitz, Beth E., DeKosky, Steven T., Lopez, Oscar L., Feingold, Eleanor, and Kamboh, M. Ilyas
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- 2023
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9. Apolipoprotein E and Alzheimer’s disease pathology in African American older adults
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Royse, Sarah K., Snitz, Beth E., Hill, Ashley V., Reese, Alexandria C., Roush, Rebecca E., Kamboh, M. Ilyas, Bertolet, Marnie, Saeed, Anum, Lopresti, Brian J., Villemagne, Victor L., Lopez, Oscar L., Reis, Steven E., Becker, James T., and Cohen, Ann D.
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- 2024
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10. Astrocyte reactivity influences amyloid-β effects on tau pathology in preclinical Alzheimer’s disease
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Bellaver, Bruna, Povala, Guilherme, Ferreira, Pamela C. L., Ferrari-Souza, João Pedro, Leffa, Douglas T., Lussier, Firoza Z., Benedet, Andréa L., Ashton, Nicholas J., Triana-Baltzer, Gallen, Kolb, Hartmuth C., Tissot, Cécile, Therriault, Joseph, Servaes, Stijn, Stevenson, Jenna, Rahmouni, Nesrine, Lopez, Oscar L., Tudorascu, Dana L., Villemagne, Victor L., Ikonomovic, Milos D., Gauthier, Serge, Zimmer, Eduardo R., Zetterberg, Henrik, Blennow, Kaj, Aizenstein, Howard J., Klunk, William E., Snitz, Beth E., Maki, Pauline, Thurston, Rebecca C., Cohen, Ann D., Ganguli, Mary, Karikari, Thomas K., Rosa-Neto, Pedro, and Pascoal, Tharick A.
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- 2023
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11. APOE ε4 and the Influence of Sex, Age, Vascular Risk Factors, and Ethnicity on Cognitive Decline
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Makkar, Steve R, Lipnicki, Darren M, Crawford, John D, Kochan, Nicole A, Castro-Costa, Erico, Lima-Costa, Maria Fernanda, Diniz, Breno Satler, Brayne, Carol, Stephan, Blossom, Matthews, Fiona, Llibre-Rodriguez, Juan J, Llibre-Guerra, Jorge J, Valhuerdi-Cepero, Adolfo J, Lipton, Richard B, Katz, Mindy J, Wang, Cuiling, Ritchie, Karen, Carles, Sophie, Carriere, Isabelle, Scarmeas, Nikolaos, Yannakoulia, Mary, Kosmidis, Mary, Lam, Linda, Chan, Wai Chi, Fung, Ada, Guaita, Antonio, Vaccaro, Roberta, Davin, Annalisa, Kim, Ki Woong, Han, Ji Won, Suh, Seung Wan, Riedel-Heller, Steffi G, Roehr, Susanne, Pabst, Alexander, Ganguli, Mary, Hughes, Tiffany F, Snitz, Beth, Anstey, Kaarin J, Cherbuin, Nicolas, Easteal, Simon, Haan, Mary N, Aiello, Allison E, Dang, Kristina, Ng, Tze Pin, Gao, Qi, Nyunt, Ma Shwe Zin, Brodaty, Henry, Trollor, Julian N, Leung, Yvonne, Lo, Jessica W, and Sachdev, Perminder
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Health Sciences ,Alzheimer's Disease ,Acquired Cognitive Impairment ,Genetics ,Brain Disorders ,Mental Health ,Clinical Research ,Cerebrovascular ,Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Vascular Cognitive Impairment/Dementia ,Dementia ,Aging ,Neurosciences ,Prevention ,Alzheimer's Disease Related Dementias (ADRD) ,Women's Health ,Neurodegenerative ,Behavioral and Social Science ,2.4 Surveillance and distribution ,Age Factors ,Aged ,Aged ,80 and over ,Alleles ,Apolipoprotein E4 ,Cognitive Dysfunction ,Female ,Genotype ,Humans ,Longitudinal Studies ,Male ,Middle Aged ,Risk Factors ,Sex Factors ,Cognitive decline ,APOE genotype ,Epidemiology ,Sex ,Ethnicity ,Clinical Sciences ,Gerontology ,Biomedical and clinical sciences ,Health sciences - Abstract
We aimed to examine the relationship between Apolipoprotein E ε4 (APOE*4) carriage on cognitive decline, and whether these associations were moderated by sex, baseline age, ethnicity, and vascular risk factors. Participants were 19,225 individuals aged 54-103 years from 15 longitudinal cohort studies with a mean follow-up duration ranging between 1.2 and 10.7 years. Two-step individual participant data meta-analysis was used to pool results of study-wise analyses predicting memory and general cognitive decline from carriage of one or two APOE*4 alleles, and moderation of these associations by age, sex, vascular risk factors, and ethnicity. Separate pooled estimates were calculated in both men and women who were younger (ie, 62 years) and older (ie, 80 years) at baseline. Results showed that APOE*4 carriage was related to faster general cognitive decline in women, and faster memory decline in men. A stronger dose-dependent effect was observed in older men, with faster general cognitive and memory decline in those carrying two versus one APOE*4 allele. Vascular risk factors were related to an increased effect of APOE*4 on memory decline in younger women, but a weaker effect of APOE*4 on general cognitive decline in older men. The relationship between APOE*4 carriage and memory decline was larger in older-aged Asians than Whites. In sum, APOE*4 is related to cognitive decline in men and women, although these effects are enhanced by age and carriage of two APOE*4 alleles in men, a higher numbers of vascular risk factors during the early stages of late adulthood in women, and Asian ethnicity.
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- 2020
12. Identifying sex-specific risk architectures for predicting amyloid deposition using neural networks
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Wang, Linghai, Kolobaric, Antonija, Aizenstein, Howard, Lopresti, Brian, Tudorascu, Dana, Snitz, Beth, Klunk, William, and Wu, Minjie
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- 2023
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13. In Pre-Clinical AD Small Vessel Disease is Associated With Altered Hippocampal Connectivity and Atrophy
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Wu, Minjie, Schweitzer, Noah, Iordanova, Bistra E., Halligan-Eddy, Edythe, Tudorascu, Dana L., Mathis, Chester A., Lopresti, Brian J., Kamboh, M. Ilyas, Cohen, Ann D., Snitz, Beth E., Klunk, William E., and Aizenstein, Howard J.
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- 2023
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14. Low thalamic activity during a digit-symbol substitution task is associated with symptoms of subjective cognitive decline
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Akiko Mizuno, Helmet Talib Karim, Maria J. Ly, Brian J. Lopresti, Ann D. Cohen, Areej A. Ali, Chester A. Mathis, William E. Klunk, Howard J. Aizenstein, and Beth E. Snitz
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subjective cognitive decline ,fMRI ,digit-symbol substitution task ,executive function ,amyloid ,Psychiatry ,RC435-571 - Abstract
IntroductionSubjective cognitive decline (SCD) may represent the earliest preclinical stage of Alzheimer's Disease (AD) for some older adults. However, the underlying neurobiology of SCD is not completely understood. Since executive function may be affected earlier than memory function in the progression of AD, we aimed to characterize SCD symptoms in terms of fMRI brain activity during the computerized digit-symbol substitution task (DSST), an executive function task. We also explored associations of DSST task performance with brain activation, SCD severity, and amyloid-ß (Aß) load.MethodsWe analyzed data from 63 cognitively normal older individuals (mean age 73.6 ± 7.2) with varying degree of SCD symptoms. Participants completed a computerized version of DSST in the MR scanner and a Pittsburgh Compound-B (PiB)-PET scan to measure global cerebral Aß load.ResultsA voxel-wise analysis revealed that greater SCD severity was associated with lower dorsomedial thalamus activation. While task performance was not associated with brain activation nor Aß load, slower reaction time was associated with greater SCD severity.DiscussionThe observed lower dorsomedial thalamus activation may reflect declining familiarity-based working memory and the trans-thalamic executive function pathway in SCD. SCD symptoms may reflect altered neural function and subtle decline of executive function, while Aß load may have an indirect impact on neural function and performance. Self-perceived cognitive decline may serve as a psychological/subjective marker reflecting subtle brain changes.
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- 2023
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15. Comparison of amyloid burden in individuals with Down syndrome versus autosomal dominant Alzheimer's disease: a cross-sectional study
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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
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- 2023
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16. Identifying sex-specific risk architectures for predicting amyloid deposition using neural networks
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Linghai Wang, Antonija Kolobaric, Howard Aizenstein, Brian Lopresti, Dana Tudorascu, Beth Snitz, William Klunk, and Minjie Wu
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Alzheimer's disease ,Small vessel disease ,Machine learning ,Beta-amyloid ,Sex differences ,Neurosciences. Biological psychiatry. Neuropsychiatry ,RC321-571 - Abstract
In older adults without dementia, White Matter Hyperintensities (WMH) in MRI have been shown to be highly associated with cerebral amyloid deposition, measured by the Pittsburgh compound B (PiB) PET. However, the relation to age, sex, and education in explaining this association is not well understood. We use the voxel counts of regional WMH, age, one-hot encoded sex, and education to predict the regional PiB using a multilayer perceptron with only rectilinear activations using mean squared error. We then develop a novel, robust metric to understand the relevance of each input variable for prediction. Our observations indicate that sex is the most relevant predictor of PiB and that WMH is not relevant for prediction. These results indicate that there is a sex-specific risk architecture for Aβ deposition.
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- 2023
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17. Predicting brain age from functional connectivity in symptomatic and preclinical Alzheimer disease
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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.
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- 2022
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18. Soluble TREM2 in CSF and its association with other biomarkers and cognition in autosomal-dominant Alzheimer's disease: a longitudinal observational study
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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
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- 2022
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19. Sex Differences in Magnetoencephalography-Identified Functional Connectivity in the Human Connectome Project Connectomics of Brain Aging and Dementia Cohort.
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Ricardo Bruña, Fernando Maestú, David López-Sanz, Anto Bagic, Ann D. Cohen, Yue-Fang Chang, Yu Cheng, Jack Doman, Ted Huppert, Tae Kim, Rebecca E. Roush, Beth E. Snitz, and James T. Becker
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- 2022
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20. An olfactory self-test effectively screens for COVID-19
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Kobi Snitz, Danielle Honigstein, Reut Weissgross, Aharon Ravia, Eva Mishor, Ofer Perl, Shiri Karagach, Abebe Medhanie, Nir Harel, Sagit Shushan, Yehudah Roth, Behzad Iravani, Artin Arshamian, Gernot Ernst, Masako Okamoto, Cindy Poo, Niccolò Bonacchi, Zachary Mainen, Erminio Monteleone, Caterina Dinnella, Sara Spinelli, Franklin Mariño-Sánchez, Camille Ferdenzi, Monique Smeets, Kazushige Touhara, Moustafa Bensafi, Thomas Hummel, Johan N. Lundström, and Noam Sobel
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Medicine - Abstract
Snitz et al. develop a web-based olfactory screening tool for COVID-19, which relies on users smelling household odorants. Based on data from participants in 134 countries, the authors report that olfactory ratings are indicative of COVID-19 status.
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- 2022
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21. Predictors of Driving Cessation in Older Adults: A 12-year Population-based Study
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Wood, Isabella, Bhojak, Tejal, Jia, Yichen, Jacobsen, Erin, Snitz, Beth E., Chang, Chung-Chou H., and Ganguli, Mary
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- 2023
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22. An olfactory self-test effectively screens for COVID-19
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Snitz, Kobi, Honigstein, Danielle, Weissgross, Reut, Ravia, Aharon, Mishor, Eva, Perl, Ofer, Karagach, Shiri, Medhanie, Abebe, Harel, Nir, Shushan, Sagit, Roth, Yehudah, Iravani, Behzad, Arshamian, Artin, Ernst, Gernot, Okamoto, Masako, Poo, Cindy, Bonacchi, Niccolò, Mainen, Zachary, Monteleone, Erminio, Dinnella, Caterina, Spinelli, Sara, Mariño-Sánchez, Franklin, Ferdenzi, Camille, Smeets, Monique, Touhara, Kazushige, Bensafi, Moustafa, Hummel, Thomas, Lundström, Johan N., and Sobel, Noam
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- 2022
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23. Reading the Mind in the Eyes: A Population-Based Study of Social Cognition in Older Adults
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Lee, Soyoung, Jacobsen, Erin P., Jia, Yichen, Snitz, Beth E., Chang, Chung-Chou H., and Ganguli, Mary
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- 2021
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24. Peripheral inflammatory biomarkers predict the deposition and progression of amyloid-β in cognitively unimpaired older adults
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Oberlin, Lauren E., Erickson, Kirk I., Mackey, Rachel, Klunk, William E., Aizenstein, Howard, Lopresti, Brian J., Kuller, Lewis H., Lopez, Oscar L., and Snitz, Beth E.
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- 2021
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25. Cardiac-induced cerebral pulsatility, brain structure, and cognition in middle and older-aged adults
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Kim, Tae, Kim, Sang-Young, Agarwal, Vikas, Cohen, Annie, Roush, Rebecca, Chang, Yue-Fang, Cheng, Yu, Snitz, Beth, Huppert, Theodore J, Bagic, Anto, Kamboh, M. Ilyas, Doman, Jack, and Becker, James T.
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- 2021
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26. Predicting brain age from functional connectivity in symptomatic and preclinical Alzheimer disease
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Peter R. Millar, Patrick H. Luckett, Brian A. Gordon, Tammie L.S. Benzinger, Suzanne E. Schindler, Anne M. Fagan, Carlos Cruchaga, Randall J. Bateman, Ricardo Allegri, Mathias Jucker, Jae-Hong Lee, Hiroshi Mori, Stephen P Salloway, Igor Yakushev, John C. Morris, Beau M. Ances, Sarah Adams, MS, Ricardo Allegri, PhD, Aki Araki, Nicolas Barthelemy, PhD, Randall Bateman, MD, Jacob Bechara, BS, Tammie Benzinger, MD, PhD, Sarah Berman, MD, PhD, Courtney Bodge, PhD, Susan Brandon, BS, William (Bill) Brooks, MBBS,MPH, Jared Brosch, MD, PhD, Jill Buck, BSN, Virginia Buckles, PhD, Kathleen Carter, PhD, Lisa Cash, BFA, Charlie Chen, BA, Jasmeer Chhatwal, MD,PhD, Patricio Chrem Mendez, MD, Jasmin Chua, BS, Helena Chui, MD, Laura Courtney, BS, Carlos Cruchaga, PhD, Gregory S Day, MD, Chrismary DeLaCruz, BA, Darcy Denner, PhD, Anna Diffenbacher, MS, Aylin Dincer, BS, Tamara Donahue, MS, Jane Douglas, MPh, Duc Duong, BS, Noelia Egido, BS, Bianca Esposito, BS, Anne Fagan, PhD, Marty Farlow, MD, Becca Feldman, BS,BA, Colleen Fitzpatrick, MS, Shaney Flores, BS, Nick Fox, MD, Erin Franklin, MS, Nelly Joseph-Mathurin, PhD, Hisako Fujii, PhD, Samantha Gardener, PhD, Bernardino Ghetti, MD, Alison Goate, PhD, Sarah Goldberg, MS,LPC,NCC, Jill Goldman, MS,MPhil,CGC, Alyssa Gonzalez, BS, Brian Gordon, PhD, Susanne Gräber-Sultan, PhD, Neill Graff-Radford, MD, Morgan Graham, BA, Julia Gray, MS, Emily Gremminger, BA, Miguel Grilo, MD, Alex Groves, Christian Haass, PhD, Lisa Häsler, MSc, Jason Hassenstab, PhD, Cortaiga Hellm, BA, Elizabeth Herries, BA, Laura Hoechst-Swisher, MS, Anna Hofmann, MD, Anna Hofmann, David Holtzman, MD, Russ Hornbeck, MSCS, MPM, Yakushev Igor, MD, Ryoko Ihara, MD, Takeshi Ikeuchi, MD, Snezana Ikonomovic, MD, Kenji Ishii, MD, Clifford Jack, MD, Gina Jerome, MS, Erik Johnson, MD, PHD, Mathias Jucker, PhD, Celeste Karch, PhD, Stephan Käser, PHD, Kensaku Kasuga, MD, Sarah Keefe, BS, William Klunk, MD, PHD, Robert Koeppe, PHD, Deb Koudelis, MHS,RN, Elke Kuder-Buletta, RN, Christoph Laske, PhD, Allan Levey, MD, PHD, Johannes Levin, MD, Yan Li, PHD, Oscar Lopez, MD, MD, Jacob Marsh, BA, Ralph Martins, PhD, Neal Scott Mason, PhD, Colin Masters, MD, Kwasi Mawuenyega, PhD, Austin McCullough, PhD Candidate, Eric McDade, DO, Arlene Mejia, MD, Estrella Morenas-Rodriguez, MD, PhD, John Morris, MD, James Mountz, MD, Cath Mummery, PhD, N eelesh Nadkarni, MD, PhD, Akemi Nagamatsu, RN, Katie Neimeyer, MS, Yoshiki Niimi, MD, James Noble, MD, Joanne Norton, MSN, RN, PMHCNS-BC, Brigitte Nuscher, Ulricke Obermüller, Antoinette O'Connor, MRCPI, Riddhi Patira, MD, Richard Perrin, MD, PhD, Lingyan Ping, PhD, Oliver Preische, MD, Alan Renton, PhD, John Ringman, MD, Stephen Salloway, MD, Peter Schofield, PhD, Michio Senda, MD, PhD, Nicholas T Seyfried, D.Phil, Kristine Shady, BA, BS, Hiroyuki Shimada, MD, PhD, Wendy Sigurdson, RN, Jennifer Smith, PhD, Lori Smith, PA-C, Beth Snitz, PhD, Hamid Sohrabi, PhD, Sochenda Stephens, BS, CCRP, Kevin Taddei, BS, Sarah Thompson, PA-C, Jonathan Vöglein, MD, Peter Wang, PhD, Qing Wang, PhD, Elise Weamer, MPH, Chengjie Xiong, PhD, Jinbin Xu, PhD, and Xiong Xu, BS, MS
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Brain aging ,Alzheimer disease ,Resting-state functional connectivity ,fMRI ,Machine learning ,Neurosciences. Biological psychiatry. Neuropsychiatry ,RC321-571 - Abstract
“Brain-predicted age” quantifies apparent brain age compared to normative neuroimaging trajectories. Advanced brain-predicted age has been well established in symptomatic Alzheimer disease (AD), but is underexplored in preclinical AD. Prior brain-predicted age studies have typically used structural MRI, but resting-state functional connectivity (FC) remains underexplored. Our model predicted age from FC in 391 cognitively normal, amyloid-negative controls (ages 18–89). We applied the trained model to 145 amyloid-negative, 151 preclinical AD, and 156 symptomatic AD participants to test group differences. The model accurately predicted age in the training set. FC-predicted brain age gaps (FC-BAG) were significantly older in symptomatic AD and significantly younger in preclinical AD compared to controls. There was minimal correspondence between networks predictive of age and AD. Elevated FC-BAG may reflect network disruption during symptomatic AD. Reduced FC-BAG in preclinical AD was opposite to the expected direction, and may reflect a biphasic response to preclinical AD pathology or may be driven by inconsistency between age-related vs. AD-related networks. Overall, FC-predicted brain age may be a sensitive AD biomarker.
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- 2022
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27. Alzheimer’s disease pathology in a community-based sample of older adults without dementia: The MYHAT neuroimaging study
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Sullivan, Kevin J., Liu, Anran, Chang, Chung-Chou H., Cohen, Ann D., Lopresti, Brian J., Minhas, Davneet S., Laymon, Charles M., Klunk, William E., Aizenstein, Howard, Nadkarni, Neelesh K., Loewenstein, David, Kamboh, M. Ilyas, Ganguli, Mary, and Snitz, Beth E.
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- 2021
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28. Psychosocial implications of early COVID-19 restrictions on older adults in a small-town region in Southwestern, Pennsylvania (USA).
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Hughes, Tiffany F., Ran, Xinhui, Fang, Fang, Jacobsen, Erin, Snitz, Beth E., Chang, Chung-Chou H., and Ganguli, Mary
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Objectives: The restrictions put in place in 2020 to mitigate the spread of the coronavirus disease 2019 limited or eliminated social connections that are vital for psychosocial well-being. The objectives of this research were to examine the impact of early pandemic-related restrictions on feelings of loneliness, depression, and anxiety as well as social activity disruption and their concomitant associations in a sample of community-dwelling older adults residing in a small-town region in the USA. Design and Setting: Cross-sectional data collected from an ongoing population-based cohort study in Southwestern, Pennsylvania. Participants: Analyses included 360 adults aged 65 years and older whose annual study assessment occurred during the first 120 days of pandemic-related restrictions. Measurements: Self-reported feelings of loneliness, depression, and anxiety due to the pandemic-related restrictions were each measured using a single question. Depressive symptoms and anxiety were also assessed with the modified Center for Epidemiologic Studies-Depression and Generalized Anxiety Disorder-7 item tools. Disruption in a variety of common social activities was also assessed. Results: Feeling lonely affected 36% of participants who were more likely to be female, not currently married, and living alone. Giving up in-person visits with family was associated with significantly higher odds of feeling lonely, and feeling lonely was associated with significantly higher odds of feelings of anxiety and depression. Conclusions: Loneliness is a serious outcome of pandemic-related restrictions among older adults, potentially linked to loss of connection with family, and may be associated with increased feelings of depression and anxiety. [ABSTRACT FROM AUTHOR]
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- 2024
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29. Implementation and Assessment of Tau Thresholds in Non-Demented Individuals as Predictors of Cognitive Decline in Tau Imaging Studies.
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Gogola, Alexandra, Cohen, Ann D., Snitz, Beth, Minhas, Davneet, Tudorascu, Dana, Ikonomovic, Milos D., Shaaban, C. Elizabeth, Doré, Vincent, Matan, Cristy, Bourgeat, Pierrick, Mason, N. Scott, Leuzy, Antoine, Aizenstein, Howard, Mathis, Chester A., Lopez, Oscar L., Lopresti, Brian J., and Villemagne, Victor L.
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ALZHEIMER'S disease ,TEMPORAL lobe ,COGNITION disorders ,DISEASE progression ,TAU proteins - Abstract
Background: Tau accumulation in Alzheimer's disease is associated with short term clinical progression and faster rates of cognitive decline in individuals with high amyloid-β deposition. Defining an optimal threshold of tau accumulation predictive of cognitive decline remains a challenge. Objective: We tested the ability of regional tau PET sensitivity and specificity thresholds to predict longitudinal cognitive decline. We also tested the predictive performance of thresholds in the proposed new NIA-AA biological staging for Alzheimer's disease where multiple levels of tau positivity are used to stage participants. Methods:
18 F-flortaucipir scans from 301 non-demented participants were processed and sampled. Four cognitive measures were assessed longitudinally. Regional standardized uptake value ratios were split into infra- and suprathreshold groups at baseline using previously derived thresholds. Survival analysis, log rank testing, and Generalized Estimation Equations assessed the relationship between the application of regional sensitivity/specificity thresholds and change in cognitive measures as well as tau threshold performance in predicting cognitive decline within the new NIA-AA biological staging. Results: The meta temporal region was best for predicting risk of short-term cognitive decline in suprathreshold, as compared to infrathreshold participants. When applying multiple levels of tau positivity, each subsequent level of tau identified cognitive decline at earlier timepoints. Conclusions: When using18 F-flortaucipir, meta temporal suprathreshold classification was associated with increased risk of cognitive decline, suggesting that abnormal tau deposition in the cortex predicts decline. Likewise, the application of multiple levels of tau clearly predicts the distinctive cognitive trajectories in the new NIA-AA biological staging framework. [ABSTRACT FROM AUTHOR]- Published
- 2024
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30. Influence of apolipoprotein-E genotype on brain amyloid load and longitudinal trajectories
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Lopresti, Brian J., Campbell, Elizabeth M., Yu, Zheming, Anderson, Stewart J., Cohen, Ann D., Minhas, Davneet S., Snitz, Beth E., Royse, Sarah K., Becker, Carl R., Aizenstein, Howard J., Mathis, Chester A., Lopez, Oscar L., Klunk, William E., and Tudorascu, Dana L.
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- 2020
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31. Voxel-wise hemispheric Amyloid Asymmetry and its association with cerebral metabolism and grey matter density in cognitively normal older adults
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Jayaprakash, Hunsica J., primary, Mizuno, Akiko, additional, Snitz, Beth E., additional, Cohen, Ann D., additional, Klunk, Willian E., additional, Aizenstein, Howard J., additional, and Karim, Helmet T., additional
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- 2024
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32. Estimating prevalence of subjective cognitive decline in and across international cohort studies of aging: a COSMIC study
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Susanne Röhr, Alexander Pabst, Steffi G. Riedel-Heller, Frank Jessen, Yuda Turana, Yvonne S. Handajani, Carol Brayne, Fiona E. Matthews, Blossom C. M. Stephan, Richard B. Lipton, Mindy J. Katz, Cuiling Wang, Maëlenn Guerchet, Pierre-Marie Preux, Pascal Mbelesso, Karen Ritchie, Marie-Laure Ancelin, Isabelle Carrière, Antonio Guaita, Annalisa Davin, Roberta Vaccaro, Ki Woong Kim, Ji Won Han, Seung Wan Suh, Suzana Shahar, Normah C. Din, Divya Vanoh, Martin van Boxtel, Sebastian Köhler, Mary Ganguli, Erin P. Jacobsen, Beth E. Snitz, Kaarin J. Anstey, Nicolas Cherbuin, Shuzo Kumagai, Sanmei Chen, Kenji Narazaki, Tze Pin Ng, Qi Gao, Xinyi Gwee, Henry Brodaty, Nicole A. Kochan, Julian Trollor, Antonio Lobo, Raúl López-Antón, Javier Santabárbara, John D. Crawford, Darren M. Lipnicki, Perminder S. Sachdev, and for Cohort Studies of Memory in an International Consortium (COSMIC)
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Subjective cognitive decline ,Prevalence ,Epidemiology ,Individual participant data ,Data harmonization ,Cohort study ,Neurosciences. Biological psychiatry. Neuropsychiatry ,RC321-571 ,Neurology. Diseases of the nervous system ,RC346-429 - Abstract
Abstract Background Subjective cognitive decline (SCD) is recognized as a risk stage for Alzheimer’s disease (AD) and other dementias, but its prevalence is not well known. We aimed to use uniform criteria to better estimate SCD prevalence across international cohorts. Methods We combined individual participant data for 16 cohorts from 15 countries (members of the COSMIC consortium) and used qualitative and quantitative (Item Response Theory/IRT) harmonization techniques to estimate SCD prevalence. Results The sample comprised 39,387 cognitively unimpaired individuals above age 60. The prevalence of SCD across studies was around one quarter with both qualitative harmonization/QH (23.8%, 95%CI = 23.3–24.4%) and IRT (25.6%, 95%CI = 25.1–26.1%); however, prevalence estimates varied largely between studies (QH 6.1%, 95%CI = 5.1–7.0%, to 52.7%, 95%CI = 47.4–58.0%; IRT: 7.8%, 95%CI = 6.8–8.9%, to 52.7%, 95%CI = 47.4–58.0%). Across studies, SCD prevalence was higher in men than women, in lower levels of education, in Asian and Black African people compared to White people, in lower- and middle-income countries compared to high-income countries, and in studies conducted in later decades. Conclusions SCD is frequent in old age. Having a quarter of older individuals with SCD warrants further investigation of its significance, as a risk stage for AD and other dementias, and of ways to help individuals with SCD who seek medical advice. Moreover, a standardized instrument to measure SCD is needed to overcome the measurement variability currently dominant in the field.
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- 2020
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33. Hippocampal sclerosis, TDP‐43, and the duration of the symptoms of dementia of AD patients
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Oscar L. Lopez, Julia Kofler, YueFang Chang, Sarah B. Berman, James T. Becker, Robert A. Sweet, Neelesh Nadkarni, Riddhi Patira, M. Ilyas Kamboh, Ann D. Cohen, Beth E. Snitz, Lewis H. Kuller, and William E. Klunk
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Neurosciences. Biological psychiatry. Neuropsychiatry ,RC321-571 ,Neurology. Diseases of the nervous system ,RC346-429 - Abstract
Abstract Objectives To examine the relationship between duration of the cognitive symptoms, from the earliest reported symptom to death, and hippocampal sclerosis (HS) and TAR‐DNA binding protein of 43kDA (TDP‐43) in Alzheimer’s disease (AD) patients. Methods The study was conducted in 359 cognitively impaired patients who met the pathological criteria for AD (NIA‐Reagan intermediate or high). The mean age at onset was 69.5 ± 8.8 years (range 37‐95) and the mean duration of the symptoms was 10.5 ± 4.2 years. The association between symptoms duration and HS and TDP‐43 was examined with logistic regression analyses controlling for age at death, atherosclerosis in the Circle of Willis (CW), cerebral infarcts, gender, baseline Mini Mental State Examination scores, APOE‐4 allele, and presence of Lewy bodies (LB). Results HS was present in 18% (n = 64) and TDP‐43 in 51.5% (n = 185) of the patients. HS and TDP‐43 were more frequent in patients whose symptoms lasted more than 10 years. LBs were present in 72% of the patients with HS and in 64% of the patients with TDP‐43. Age at onset was not associated with TDP‐43 or HS. HS was associated with duration of symptoms and LB, TDP‐43, and atherosclerosis in the CW. TDP‐43 was associated with duration of symptoms, LB, and HS. Interpretation HS and TDP‐43 are present in early and late onset AD. However, their presence is mainly driven by the duration of symptoms and the presence of LB. This suggests that HS and TDP‐43 are part of the later neuropathological changes in AD.
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- 2020
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34. Tract Specific White Matter Lesion Load Affects White Matter Microstructure and Their Relationships With Functional Connectivity and Cognitive Decline
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Tae Kim, Howard J. Aizenstein, Beth E. Snitz, Yu Cheng, Yue-Fang Chang, Rebecca E. Roush, Theodore J. Huppert, Annie Cohen, Jack Doman, and James T. Becker
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white matter fiber tracts ,Alzheimer’s disease ,cognitive impairment ,aging ,white matter hyperintensity (WMH) ,white matter lesion (WML) ,Neurosciences. Biological psychiatry. Neuropsychiatry ,RC321-571 - Abstract
White matter hyperintensities (WMHs) are associated with cognitive decline. Assessing the effect of WMH on WM microstructural changes and its relationships with structural and functional connectivity to multiple cognitive domains are helpful to better understand the pathophysiological processes of cognitive impairment. 65 participants (49 normal and 16 MCI subjects, age: 67.4 ± 8.3 years, 44 females) were studied at 3T. The WMHs and fifty fiber tracts were automatically segmented from the T1/T2-weighted images and diffusion-weighted images, respectively. Tract-profiles of WMH were compared with those of apparent fiber density (AFD). The relationship between AFD and tract connectivity (TC) was assessed. Functional connectivity (FC) between tract ends obtained from resting-state functional MRI was examined in relation to TC. Tract-specific relationships of WMH, TC and FC with a multi-domain neuropsychological test battery and Montreal Cognitive Assessment (MoCA) were also separately assessed by lasso linear regression. Indirect pathways of TC and FC between WMH and multiple cognitive measures were tested using the mediation analysis. Higher WMH loads in WM tracts were locally matched with the reduced AFD, which was related to decrease in TC. However, no direct relationship was found between TC and FC. Tract-specific changes on WMH, TC and FC for each cognitive performance may explain that macro- and microstructural and functional changes are associated differently with each cognitive domain in a fiber specific manner. In these identified tracts, the differences between normal and MCI for WMH and TC were increased, and the relationships of WMH, TC and FC with cognitive outcomes were more significant, compared to the results from all tracts. Indirect pathways of two-step (TC-FC) between WMH and all cognitive domains were significant (p < 0.0083 with Bonferroni correction), while the separated indirect pathways through TC and through FC were different depending on cognitive domain. Deterioration in specific cognitive domains may be affected by alterations in a set of different tracts that are differently associated with macrostructural, microstructural, and function changes. Thus, assessments of WMH and its associated changes on specific tracts help for better understanding of the interrelationships of multiple changes in cognitive impairment.
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- 2022
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35. A measure of smell enables the creation of olfactory metamers
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Ravia, Aharon, Snitz, Kobi, Honigstein, Danielle, Finkel, Maya, Zirler, Rotem, Perl, Ofer, Secundo, Lavi, Laudamiel, Christophe, Harel, David, and Sobel, Noam
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- 2020
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36. Relationships Between Executive Control Circuit Activity, Amyloid Burden, and Education in Cognitively Healthy Older Adults
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Karim, Helmet T., Tudorascu, Dana L., Cohen, Ann, Price, Julie C., Lopresti, Brian, Mathis, Chester, Klunk, William, Snitz, Beth E., and Aizenstein, Howard J.
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- 2019
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37. Blood amyloid levels and risk of dementia in the Ginkgo Evaluation of Memory Study (GEMS): A longitudinal analysis
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Lopez, Oscar L., Chang, Yuefang, Ives, Diane G., Snitz, Beth E., Fitzpatrick, Annette L., Carlson, Michelle C., Rapp, Stephen R., Williamson, Jeffrey D., Tracy, Russell P., DeKosky, Steven T., and Kuller, Lewis H.
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- 2019
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38. Fluid and PET biomarkers for amyloid pathology in Alzheimer's disease
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Cohen, Ann D., Landau, Susan M., Snitz, Beth E., Klunk, William E., Blennow, Kaj, and Zetterberg, Henrik
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- 2019
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39. Amyloid deposition is associated with different patterns of hippocampal connectivity in men versus women
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Wu, Minjie, Thurston, Rebecca C., Tudorascu, Dana L., Karim, Helmet T., Mathis, Chester A., Lopresti, Brian J., Kamboh, M. Ilyas, Cohen, Ann D., Snitz, Beth E., Klunk, William E., and Aizenstein, Howard J.
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- 2019
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40. Connectomics in Brain Aging and Dementia – The Background and Design of a Study of a Connectome Related to Human Disease
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Ann D. Cohen, Ricardo Bruña, Yue-Fang Chang, Yu Cheng, Jack Doman, Ted Huppert, Tae Kim, Fernando Maestu, Rebecca E. Roush, Beth E. Snitz, and James T. Becker
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aging ,MRI ,amyloid PET imaging ,magnetoencepalography ,Connectome Related to Human Disease ,neuropsychology ,Neurosciences. Biological psychiatry. Neuropsychiatry ,RC321-571 - Abstract
The natural history of Alzheimer’s Disease (AD) includes significant alterations in the human connectome, and this disconnection results in the dementia of AD. The organizing principle of our research project is the idea that the expression of cognitive dysfunction in the elderly is the result of two independent processes — the neuropathology associated with AD, and second the neuropathological changes of cerebrovascular disease. Synaptic loss, senile plaques, and neurofibrillary tangles are the functional and diagnostic hallmarks of AD, but it is the structural changes as a consequence of vascular disease that reduce brain reserve and compensation, resulting in an earlier expression of the clinical dementia syndrome. This work is being completed under the auspices of the Human Connectome Project (HCP). We have achieved an equal representation of Black individuals (vs. White individuals) and enrolled 60% Women. Each of the participants contributes demographic, behavioral and laboratory data. We acquire data relative to vascular risk, and the participants also undergo in vivo amyloid imaging, and magnetoencephalography (MEG). All of the data are publicly available under the HCP guidelines using the Connectome Coordinating Facility and the NIMH Data Archive. Locally, we use these data to address specific questions related to structure, function, AD, aging and vascular disease in multi-modality studies leveraging the differential advantages of magnetic resonance imaging (MRI), functional magnetic resonance imaging (fMRI), MEG, and in vivo beta amyloid imaging.
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- 2021
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41. The effect of amyloid deposition on longitudinal resting-state functional connectivity in cognitively normal older adults
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Chemin Lin, Maria Ly, Helmet T. Karim, Wenjing Wei, Beth E. Snitz, William E. Klunk, and Howard J. Aizenstein
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Preclinical Alzheimer’s disease ,Resting-state fMRI ,Longitudinal ,Compensation ,Homeostatic regulation ,Amyloid ,Neurosciences. Biological psychiatry. Neuropsychiatry ,RC321-571 ,Neurology. Diseases of the nervous system ,RC346-429 - Abstract
Abstract Background Pathological processes contributing to Alzheimer’s disease begin decades prior to the onset of clinical symptoms. There is significant variation in cognitive changes in the presence of pathology, functional connectivity may be a marker of compensation to amyloid; however, this is not well understood. Methods We recruited 64 cognitively normal older adults who underwent neuropsychological testing and biannual magnetic resonance imaging (MRI), amyloid imaging with Pittsburgh compound B (PiB)-PET, and glucose metabolism (FDG)-PET imaging for up to 6 years. Resting-state MRI was used to estimate connectivity of seven canonical neural networks using template-based rotation. Using voxel-wise paired t-tests, we identified neural networks that displayed significant changes in connectivity across time. We investigated associations among amyloid and longitudinal changes in connectivity and cognitive function by domains. Results Left middle frontal gyrus connectivity within the memory encoding network increased over time, but the rate of change was lower with greater amyloid. This was no longer significant in an analysis where we limited the sample to only those with two time points. We found limited decline in cognitive domains overall. Greater functional connectivity was associated with better attention/processing speed and executive function (independent of time) in those with lower amyloid but was associated with worse function with greater amyloid. Conclusions Increased functional connectivity serves to preserve cognitive function in normal aging and may fail in the presence of pathology consistent with compensatory models.
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- 2020
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42. Association Between β-Amyloid Accumulation and Incident Dementia in Individuals 80 Years or Older Without Dementia
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Lopez, Oscar L., primary, Villemagne, Victor L., additional, Chang, Yue-Fang, additional, Cohen, Ann D., additional, Klunk, William E., additional, Mathis, Chester A., additional, Pascoal, Tharick, additional, Ikonomovic, Milos D., additional, Rowe, Christopher, additional, Dore, Vincent, additional, Snitz, Beth E., additional, Lopresti, Brian J., additional, Kamboh, M. Ilyas, additional, Aizenstein, Howard J., additional, and Kuller, Lewis H., additional
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- 2024
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43. Longitudinal Cognitive Decline in Alzheimer Disease Prevention Trials
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Castilhos, Raphael M., primary and Snitz, Beth E., additional
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- 2024
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44. An electronic nose can identify humans by the smell of their ear
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Brener, Stephanie, primary, Snitz, Kobi, additional, and Sobel, Noam, additional
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- 2024
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45. Association of plasma biomarkers of Alzheimer's disease and related disorders with cognition and cognitive decline: The MYHAT population‐based study.
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Zhang, Yingjin, Ferreira, Pamela C. L., Jacobsen, Erin, Bellaver, Bruna, Pascoal, Tharick A., Snitz, Beth E., Chang, Chung‐Chou H., Villemagne, Victor L., Ganguli, Mary, and Karikari, Thomas K.
- Abstract
INTRODUCTION: Plasma biomarkers of Alzheimer's disease and related dementias predict global cognitive performance and decline over time; it remains unclear how they associate with changes in different dementia syndromes affecting distinct cognitive domains. METHODS: In a prospective study with repeated assessments of a randomly selected population‐based cohort (n = 787, median age 73), we evaluated performance and decline in different cognitive domains over up to 8 years in relation to plasma concentrations of amyloid beta 42/40 (Aβ42/40) ratio, phosphorylated tau181 (p‐tau181), neurofilament light chain (NfL), and glial fibrillary acidic protein (GFAP). RESULTS: Cross‐sectionally, memory showed the strongest associations with p‐tau181, and attention, executive, and visuospatial functions with NfL. Longitudinally, memory decline was distinguishable with all biomarker profiles dichotomized according to data‐driven cutoffs, most efficiently with Aβ42/40. GFAP and Aβ42/40 were the best discriminators of decline patterns in language and visuospatial functions, respectively. DISCUSSION: These relatively non‐invasive tests may be beneficial for clinical screening after replication in other populations and validation through neuroimaging or cerebrospinal fluid analysis. Highlights: We performed a prospective study with up to 8 years of repeated domain‐specific cognitive assessments and baseline plasma Alzheimer's disease and related dementias biomarker measurements in a randomly selected population‐based cohort.We considered distinct growth curves of trajectories of different cognitive domains and survival bias induced by missing data by adding quadratic time and applying joint modeling technique.Cross‐sectionally, memory showed the strongest associations with plasma phosphorylated tau181, while attention, executive, and visuospatial functions were most strongly associated with neurofilament light chain.Longitudinally, memory and visuospatial declines were most efficiently distinguished by dichotomized amyloid beta 42/40 profile among all plasma biomarkers, while language was by dichotomized glial fibrillary acidic protein.These relatively non‐invasive tests may be beneficial for clinical screening; however, they will need replication in other populations and validation through neuroimaging and/or cerebrospinal fluid assessments. [ABSTRACT FROM AUTHOR]
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- 2024
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46. Comparison of longitudinal Aβ in nondemented elderly and Down syndrome
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Tudorascu, Dana L., Anderson, Stewart J., Minhas, Davneet S., Yu, Zheming, Comer, Diane, Lao, Patrick, Hartley, Sigan, Laymon, Charles M., Snitz, Beth E., Lopresti, Brian J., Johnson, Sterling, Price, Julie C., Mathis, Chester A., Aizenstein, Howard J., Klunk, William E., Handen, Benjamin L., Christian, Brad T., and Cohen, Ann D.
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- 2019
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47. Risk architecture for altered hippocampal connectivity in normal aging differ between men and women
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Schweitzer, Noah, primary, Li, Jinghang, additional, Lopresti, Brian J, additional, Klunk, William E, additional, Snitz, Beth E., additional, Tudorascu, Dana, additional, Cohen, Ann D., additional, Kamboh, M. Ilyas, additional, Halligan, Edye, additional, Thurston, Rebecca C, additional, Villemagne, Victor L, additional, Iordanova, Bistra, additional, Aizenstein, Howard J, additional, and Wu, Minjie, additional
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- 2023
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48. Amyloid β‐dependent tau phosphorylation is triggered by reactive astrocytes in preclinical Alzheimer’s disease
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Bellaver, Bruna, primary, Povala, Guilherme, additional, Ferreira, Pamela C.L., additional, Ferrari‐Souza, João Pedro, additional, Leffa, Douglas Teixeira, additional, Lussier, Firoza Z, additional, Benedet, Andrea Lessa, additional, Ashton, Nicholas J., additional, Tissot, Cécile, additional, Therriault, Joseph, additional, Servaes, Stijn, additional, Stevenson, Jenna, additional, Rahmouni, Nesrine, additional, Lopez, Oscar L., additional, Tudorascu, Dana, additional, Villemagne, Victor L, additional, Ikonomovic, Milos D, additional, Gauthier, Serge, additional, Zimmer, Eduardo R, additional, Zetterberg, Henrik, additional, Blennow, Kaj, additional, Aizenstein, Howard J, additional, Klunk, William E, additional, Snitz, Beth E., additional, Maki, Pauline M, additional, Thurston, Rebecca C, additional, Cohen, Ann D., additional, Ganguli, Mary, additional, Karikari, Thomas K, additional, Rosa‐Neto, Pedro, additional, and Pascoal, Tharick Ali, additional
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- 2023
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49. NEIGHBORHOOD DISADVANTAGE, IMAGING BIOMARKERS OF ALZHEIMER’S DISEASE, AND COGNITION IN DIVERSE OLDER ADULTS
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Fan, Erica, primary, Royse, Sarah, additional, Snitz, Beth, additional, Pascoal, Tharick, additional, Shaaban, C, additional, Lopresti, Brian, additional, Villemagne, Victor, additional, and Cohen, Ann, additional
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- 2023
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50. Covid‐19 may have a detrimental impact on sensorimotor function
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Goss, Monica, primary, Bernal, Rebecca, additional, Patel, Vibhuti N, additional, Li, Karl, additional, Garbarino, Valentina R., additional, Nair, Rejani R, additional, Snyder, Heather M, additional, de Erausquin, Gabriel A., additional, Ganguli, Mary, additional, Snitz, Beth E., additional, Girard, Timothy D., additional, Jacobs, Heidi I.L., additional, Hosseini, Akram A., additional, Ibrahim, Tamer, additional, Vahidy, Farhaan S, additional, Satizabal, Claudia L., additional, Himali, Jayandra Jung, additional, and Seshadri, Sudha, additional
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- 2023
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