Michael W. Weiner1,2,3,4,5,6 | Shaveta Kanoria1,6 | Melanie J. Miller1,6 | Paul S. Aisen7 | Laurel A. Beckett8 | Catherine Conti1,6 | Adam Diaz1,6 | Derek Flenniken6 | Robert C. Green9 | Danielle J. Harvey8 | Clifford R. Jack Jr.10 | William Jagust11 | Edward B. Lee12 | John C. Morris13,14,15 | Kwangsik Nho16,17 | Rachel Nosheny1,4 | Ozioma C. Okonkwo18 | Richard J. Perrin13,14,15 | Ronald C. Petersen19 | Monica Rivera-Mindt20,21 | Andrew J. Saykin16,22 | Leslie M. Shaw23 | Arthur W. Toga24 | Duygu Tosun1,2 | Dallas P. Veitch1,6 for the Alzheimer’s Disease Neuroimaging Initiative
1 Department of Veterans Affairs Medical Center, Center for Imaging of Neurodegenerative Diseases, San Francisco, California, USA
2 Department of Radiology and Biomedical Imaging, University of California San Francisco, San Francisco, California, USA
3 Department of Medicine, University of California San Francisco, San Francisco, California, USA
4 Department of Psychiatry and Behavioral Sciences, University of California San Francisco, San Francisco, California, USA
5 Department of Neurology, University of California San Francisco, San Francisco, California, USA
6 Northern California Institute for Research and Education (NCIRE), San Francisco, California, USA
7 Alzheimer’s Therapeutic Research Institute, University of Southern California, San Diego, California, USA
8 Division of Biostatistics, Department of Public Health Sciences, University of California, Medical Sciences 1C, Davis, California, USA
9 Division of Genetics, Department of Medicine, Brigham and Women’s Hospital, Broad Institute Ariadne Labs and Harvard Medical School, Boston, Massachusetts, USA
10 Department of Radiology, Mayo Clinic, Rochester, Minnesota, USA
11 Helen Wills Neuroscience Institute, University of California Berkeley, Berkeley, California, USA
12 Translational Neuropathology Research Laboratory, Department of Pathology and Laboratory Medicine, Perelman School of Medicine at the University of
Pennsylvania, Philadelphia, Pennsylvania, USA
13 Knight Alzheimer’s Disease Research Center, Washington University School of Medicine, Saint Louis, Missouri, USA
14 Department of Neurology, Washington University School of Medicine, Saint Louis, Missouri, USA
15 Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri, USA
16 Department of Radiology and Imaging Sciences and the Indiana Alzheimer’s Disease Research Center, Indiana University School of Medicine, Indianapolis, Indiana, USA
17 Center for Computational Biology and Bioinformatics, Indiana University School of Medicine, Indianapolis, Indiana, USA
18 Wisconsin Alzheimer’s Disease Research Center and Department of Medicine, University of Wisconsin School of Medicine and Public Health, Clinical Science Center, Madison, Wisconsin, USA
19 Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA
20 Department of Psychology, Latin American and Latino Studies Institute, African and African American Studies, Fordham University, Bronx, New York, USA
21 Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, New York, USA
22 Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, Indiana, USA
23 Department of Pathology and Laboratory Medicine and the PENN Alzheimer’s Disease Research Center, Center for Neurodegenerative Research, Perelman School of Medicine, University of Pennsylvania, Philadelphia, USA
24 Laboratory of Neuro Imaging, Institute of Neuroimaging and Informatics, Keck School of Medicine of the University of Southern California, San Diego, California, USA
Correspondence
Michael W. Weiner, Department of Veterans Affairs Medical Center, Center for Imaging of Neurodegenerative Diseases, 4150 Clement St, San Francisco, CA 94121, USA. Email: 该Email地址已收到反垃圾邮件插件保护。要显示它您需要在浏览器中启用JavaScript。 Data used in preparation of this article were obtained from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database (adni.loni.usc.edu). As such, the investigators within the ADNI contributed to the design and implementation of ADNI and/or provided data. Some ADNI investigators participated in analysis or writing of this report. A complete listing of ADNI investigators can be found at: http://adni.loni.usc.edu/wp content/uploads/how_to_apply/ ADNI_Acknowledgement_List.pd
Funding information
NIH, Grant/Award Number: U19 -AG 024904; National Institute on Aging, Grant/Award Number: U19AG024904
This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
© 2024 The Author(s). Alzheimer’s & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer’s Association.
Abstract
The overall goal of the Alzheimer’s Disease Neuroimaging Initiative (ADNI) is to opti mize and validate biomarkers for clinical trials while sharing all data and biofluid samples with the global scientific community. ADNI has been instrumental in stan dardizing and validating amyloid beta (Aβ) and tau positron emission tomography (PET) imaging. ADNI data were used for the US Food and Drug Administration (FDA) approval of the Fujirebio and Roche Elecsys cerebrospinal fluid diagnostic tests. Additionally, ADNI provided data for the trials of the FDA-approved treatments aducanumab, lecanemab, and donanemab. More than 6000 scientific papers have been published using ADNI data, reflecting ADNI’s promotion of open science and data sharing. Despite its enormous success, ADNI has some limitations, particularly in generalizing its data and findings to the entire US/Canadian population. This introduction provides a historical overview of ADNI and highlights its significant accomplishments and future vision to pioneer “the clinical trial of the future” focusing on demographic inclusivity.
KEYWORDS
Alzheimer’s disease, Alzheimer’s disease biomarkers, Alzheimer’s disease clinical trials, Alzheimer’s Disease Neuroimaging Initiative, Alzheimer’s disease progression, amyloid, Lab oratory of Neuro Imaging, magnetic resonance imaging, neurodegeneration, positron emission tomography, post-traumatic stress disorder, tau, underrepresented populations
Highlights
∙ The Alzheimer’s Disease Neuroimaging Initiative (ADNI) introduced a novel model for public-private partnerships and data sharing.
∙ It successfully validated amyloid and Tau PET imaging, as well as CSF and plasma biomarkers, for diagnosing Alzheimer’s disease.
∙ ADNI generated and disseminated vital data for designing AD clinical trials.
Jason Mares1,2 Gautam Kumar1,3,4 Anurag Sharma1,3 Sheina Emrani5 Laura Beth McIntire6 Jia Guo7,8 Vilas Menon1,2 Tal Nuriel1,3 for the Alzheimer’s Disease Neuroimaging Initiative
1 Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, Columbia University, New York, New York, USA
2 Department of Neurology, Columbia University, New York, New York, USA
3 Department of Pathology and Cell Biology, Columbia University, New York, New York, USA
4 Department of Neurobiology, University of Maryland, Baltimore, Maryland, USA
5 Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA
6 Lipidomics and Biomarker Discovery Lab, Brain Health Imaging Institute, Department of Radiology, Weill Cornell Medicine, New York, New York, USA
7 Department of Psychiatry, Columbia University, New York, New York, USA
8 Zuckerman Institute, Columbia University, New York, New York, USA
Tal Nuriel, Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, Columbia University, 630 W. 168th St., P&S 12-420E, New York, NY 10032, USA. Email: 该Email地址已收到反垃圾邮件插件保护。要显示它您需要在浏览器中启用JavaScript。 The Alzheimer’s Disease Neuroimaging Initiative: Data used in preparation of this article were obtained from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database (adni.loni.usc.edu). As such, the investigators within the ADNI contributed to the design and implementation of ADNI and/or provided data, but did not participate in analysis or writing of this report.
NIA, Grant/Award Numbers: K01 AG061264, R01 AG070202, R01 AG078800, R01 AG066831, U19 AG024904 This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
© 2025 The Author(s). Alzheimer’s & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer’s Association
INTRODUCTION: While the role of apolipoprotein E (APOE) ε4 in Alzheimer’s dis ease (AD) susceptibility has been studied extensively, much less is known about the differences in disease presentation in APOE ε4 carriers versus non-carriers.
METHODS: To help elucidate these differences, we performed a broad analysis com paring the regional levels of six different neuroimaging biomarkers in the brains of APOE ε4 carriers versus non-carriers who participated in the Alzheimer’s Disease Neuroimaging Initiative (ADNI).
RESULTS:We observed significant APOE ε4–associated heterogeneity in regional amy loid beta deposition, tau accumulation, glucose uptake, brain volume, cerebral blood flow, and white matter hyperintensities within each AD diagnostic group. We also observed important APOE ε4–associated differences in cognitively unimpaired indi viduals who converted to mild cognitive impairment/AD versus those who did not
DISCUSSION: This observed heterogeneity in neuroimaging biomarkers between APOE ε4 carriers versus non-carriers may have important implications regarding the prevention, diagnosis, and treatment of AD in different subpopulations.
Alzheimer’s disease, Alzheimer’s Disease Neuroimaging Initiative, apolipoprotein E, biomarkers, heterogeneity, neuroimaging
∙ An extensive study was performed on the apolipoprotein E (APOE) ε4–associated heterogeneity in neuroimaging biomarkers from the Alzheimer’s Disease Neu roimaging Initiative.
∙ Robust APOE ε4–associated increases in amyloid beta (Aβ) deposition throughout the brain, in every diagnostic group, were observed.
∙ APOE ε4–associated increases in tau pathology, decreases in glucose uptake, and increases in brain atrophy, which expand in regional scope and magnitude with disease progression, were observed.
∙ Significant sex- and age-related differences in APOE ε4–associated neuroimaging biomarker heterogeneity, with overall increases in pathological presentation in female APOE ε4 carriers, were observed.
∙ Regional differences in Aβ deposition, tau accumulation, glucose uptake, ventricle size, and white matter hyperintensities were observed in cognitively normal partic ipants who converted to mild cognitive impairment/Alzheimer’s disease, which may hold potential predictive value.
Janice C. Colwell
Authors
Amit Gefen
Robert Dymarek
Tomasz Halski
Robert G. Smith
Ana Patrícia Araujo Torquato Lopes
Maria das Neves Decesaro
Jason P. Robertson
Jevon Puckett
伤口世界平台生态圈，以“关爱人间所有伤口患者”为愿景，连接、整合和拓展线上和线下的管理慢性伤口的资源，倡导远程、就近和居家管理慢性伤口，解决伤口专家的碎片化时间的价值创造、诊疗经验的裂变复制、和患者的就近、居家和低成本管理慢性伤口的问题。
2019广东省医疗行业协会伤口管理分会年会
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