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

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收录情况： ◇ SCIE

作者：
Chen Charles D[1] * ; Joseph-Mathurin Nelly[1] ; Sinha Namita[2,3] ; Zhou Aihong[4] ; Li Yan[5] ; Friedrichsen Karl[6] ; McCullough Austin[1] ; Franklin Erin E[2] ; Hornbeck Russ[1] ; Gordon Brian[1] ; Sharma Vijay[1] ; Cruchaga Carlos[7] ; Goate Alison[8] ; Karch Celeste[7] ; McDade Eric[5] ; Xiong Chengjie[5] ; Bateman Randall J[5] ; Ghetti Bernardino[9] ; Ringman John M[10] ; Chhatwal Jasmeer[11] ; Masters Colin L[12] ; McLean Catriona[13] ; Lashley Tammaryn[14,15] ; Su Yi[16,17] ; Koeppe Robert[18] ; Jack Clifford[19] ; Klunk William E[20] ; Morris John C[5] ; Perrin Richard J[2,5] ; Cairns Nigel J[2,5,21] ; Benzinger Tammie L S[1] ;
机构： [1]Mallinckrodt Institute of Radiology, Washington University in St. Louis, St. Louis, MO, USA [2]Department of Pathology and Immunology, Washington University in St. Louis, St. Louis, MO, USA [3]Department of Pathology, University of Manitoba, Shared Health, Winnipeg, MB, Canada [4]Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, China [5]Department of Neurology, Washington University in St. Louis, St. Louis, MO, USA [6]Department of Ophthalmology and Visual Sciences, Washington University in St. Louis, St. Louis, MO, USA [7]Department of Psychiatry, Washington University in St. Louis, St. Louis, MO, USA [8]Department of Genetics and Genomic Sciences, Ichan School of Medicine at Mount Sinai, New York, NY, USA [9]Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN, USA [10]Department of Neurology, Keck School of Medicine of USC, Los Angeles, CA, USA [11]Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA [12]The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Melbourne, VIC, Australia [13]Department of Anatomic Pathology, Alfred Hospital, Melbourne, VIC, Australia [14]UCL Queen Square Institute of Neurology, University College London, London, UK [15]Queen Square Brain Bank for Neurological Disorders, University College London, London, UK [16]Banner Alzheimer’s Institute, Banner Health, Phoenix, AZ, USA [17]Arizona Alzheimer’s Consortium, Banner Health, Phoenix, AZ, USA [18]Department of Radiology, University of Michigan, Ann Arbor, MI, USA [19]Department of Radiology, Mayo Clinic, Rochester, MN, USA [20]Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA, USA [21]College of Medicine and Health, University of Exeter, Exeter, UK
出处：
DOI： 10.1007/s00401-021-02342-y
ISSN：

关键词： Alzheimer disease Amyloid-β plaques PiB PET Stereology

摘要：
Pittsburgh compound B (PiB) radiotracer for positron emission tomography (PET) imaging can bind to different types of amyloid-β plaques and blood vessels (cerebral amyloid angiopathy). However, the relative contributions of different plaque subtypes (diffuse versus cored/compact) to in vivo PiB PET signal on a region-by-region basis are incompletely understood. Of particular interest is whether the same staging schemes for summarizing amyloid-β burden are appropriate for both late-onset and autosomal dominant forms of Alzheimer disease (LOAD and ADAD). Here, we compared antemortem PiB PET with follow-up postmortem estimation of amyloid-β burden using stereologic methods to estimate the relative area fraction of diffuse and cored/compact amyloid-β plaques across 16 brain regions in 15 individuals with ADAD and 14 individuals with LOAD. In ADAD, we found that PiB PET correlated with diffuse plaques in the frontal, parietal, temporal, and striatal regions commonly used to summarize amyloid-β burden in PiB PET, and correlated with both diffuse and cored/compact plaques in the occipital lobe and parahippocampal gyrus. In LOAD, we found that PiB PET correlated with both diffuse and cored/compact plaques in the anterior cingulate, frontal lobe (middle frontal gyrus), and parietal lobe, and showed additional correlations with diffuse plaque in the amygdala and occipital lobe, and with cored/compact plaque in the temporal lobe. Thus, commonly used PiB PET summary regions predominantly reflect diffuse plaque burden in ADAD and a mixture of diffuse and cored/compact plaque burden in LOAD. In direct comparisons of ADAD and LOAD, postmortem stereology identified much greater mean amyloid-β plaque burdens in ADAD versus LOAD across almost all brain regions studied. However, standard PiB PET did not recapitulate these stereologic findings, likely due to non-trivial amyloid-β plaque burdens in ADAD within the cerebellum and brainstem-commonly used reference regions in PiB PET. Our findings suggest that PiB PET summary regions correlate with amyloid-β plaque burden in both ADAD and LOAD; however, they might not be reliable in direct comparisons of regional amyloid-β plaque burden between the two forms of AD.© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.

基金：
Data collection and sharing for this project was supported by the Knight Alzheimer Disease Research Center (Knight ADRC, P30AG066444, P01AG026276, and P01AG03991) and the Dominantly Inherited Alzheimer Network (DIAN, U19AG032438). This manuscript has been reviewed by DIAN Study investigators for scientific content and consistency of data interpretation with previous DIAN Study publications. We acknowledge the altruism of the participants and their families and contributions of the Knight ADRC and DIAN research and support staff at each of the participating sites for their contributions to this study. For the provision of brain tissue and staining, we acknowledge the Knight ADRC Neuropathology Core and the DIAN Neuropathology Core (P01AG003991). We thank the staff of the Betty Martz Laboratory for Neurodegenerative Disease for their excellent technical support. The authors also acknowledge support from the Neuroimaging Informatics and Analysis Center (P30NS098577). C.D.C. acknowledges support from the NSF GRFP (DGE-1745038). N.J-M. acknowledges support from the Alzheimer’s Association International Research Grant Program (AARFD-20-681815). B.A.G. acknowledges support from the NIH (K01AG053474). J.C.M. acknowledges support from the NIH (UF1AG032438)
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外文
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PubmedID：
中科院(CAS)分区：
出版当年[2020]版：
大类 | 1 区 医学
小类 | 1 区 临床神经病学 1 区 神经科学 1 区 病理学
最新[2023]版：
大类 | 1 区 医学
小类 | 1 区 临床神经病学 1 区 神经科学 1 区 病理学
JCR分区：
出版当年[2019]版：
Q1 NEUROSCIENCES Q1 CLINICAL NEUROLOGY Q1 PATHOLOGY
最新[2023]版：
Q1 NEUROSCIENCES Q1 CLINICAL NEUROLOGY Q1 PATHOLOGY

影响因子： 最新[2023版] 最新五年平均 出版当年[2019版] 出版当年五年平均 出版前一年[2018版] 出版后一年[2020版]

第一作者：
第一作者机构： [1]Mallinckrodt Institute of Radiology, Washington University in St. Louis, St. Louis, MO, USA
通讯作者：
推荐引用方式(GB/T 7714)：
Chen Charles D,Joseph-Mathurin Nelly,Sinha Namita,et al.Comparing amyloid-β plaque burden with antemortem PiB PET in autosomal dominant and late-onset Alzheimer disease.[J].ACTA NEUROPATHOLOGICA.2021,142(4):689-706.doi:10.1007/s00401-021-02342-y.
APA：
Chen Charles D,Joseph-Mathurin Nelly,Sinha Namita,Zhou Aihong,Li Yan...&Benzinger Tammie L S.(2021).Comparing amyloid-β plaque burden with antemortem PiB PET in autosomal dominant and late-onset Alzheimer disease..ACTA NEUROPATHOLOGICA,142,(4)
MLA：
Chen Charles D,et al."Comparing amyloid-β plaque burden with antemortem PiB PET in autosomal dominant and late-onset Alzheimer disease.".ACTA NEUROPATHOLOGICA 142..4(2021):689-706

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