دورية أكاديمية
أعرض في EDS

Advanced structural brain aging in preclinical autosomal dominant Alzheimer disease.

التفاصيل البيبلوغرافية
العنوان: Advanced structural brain aging in preclinical autosomal dominant Alzheimer disease.
المؤلفون: Millar PR; Department of Neurology, Washington University in St. Louis, St. Louis, MO, USA. pmillar@wustl.edu., Gordon BA; Mallinckrodt Institute of Radiology, Washington University in St. Louis, St. Louis, MO, USA., Wisch JK; Department of Neurology, Washington University in St. Louis, St. Louis, MO, USA., Schultz SA; Department of Neurology, Harvard Medical School, Boston, MA, USA.; Department of Neurology, Massachusetts General Hospital, Boston, MA, USA., Benzinger TL; Mallinckrodt Institute of Radiology, Washington University in St. Louis, St. Louis, MO, USA., Cruchaga C; Department of Psychiatry, Washington University in St. Louis, St. Louis, MO, USA., Hassenstab JJ; Department of Neurology, Washington University in St. Louis, St. Louis, MO, USA., Ibanez L; Department of Neurology, Washington University in St. Louis, St. Louis, MO, USA.; Department of Psychiatry, Washington University in St. Louis, St. Louis, MO, USA.; NeuroGenomics & Informatics Center, Washington University in St. Louis, St. Louis, MO, USA., Karch C; Department of Psychiatry, Washington University in St. Louis, St. Louis, MO, USA., Llibre-Guerra JJ; Department of Neurology, Washington University in St. Louis, St. Louis, MO, USA., Morris JC; Department of Neurology, Washington University in St. Louis, St. Louis, MO, USA., Perrin RJ; Department of Neurology, Washington University in St. Louis, St. Louis, MO, USA.; Department of Pathology & Immunology, Washington University in St. Louis, St. Louis, MO, USA., Supnet-Bell C; Department of Neurology, Washington University in St. Louis, St. Louis, MO, USA., Xiong C; Department of Biostatistics, Washington University in St. Louis, St. Louis, MO, USA., Allegri RF; Instituto Neurológico Fleni, Buenos Aires, Argentina., Berman SB; Department of Neurology, University of Pittsburgh, Pittsburgh, PA, USA., Chhatwal JP; Department of Neurology, Harvard Medical School, Boston, MA, USA.; Department of Neurology, Massachusetts General Hospital, Boston, MA, USA., Chrem Mendez PA; Instituto Neurológico Fleni, Buenos Aires, Argentina., Day GS; Department of Neurology, Mayo Clinic, Jacksonville, FL, USA., Hofmann A; German Center for Neurodegenerative Diseases (DZNE), 72076, Tübingen, Germany.; Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tübingen, 72076, Tübingen, Germany., Ikeuchi T; Department of Molecular Genetics, Brain Research Institute, Niigata University, Niigata, Japan., Jucker M; German Center for Neurodegenerative Diseases (DZNE), 72076, Tübingen, Germany.; Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tübingen, 72076, Tübingen, Germany., Lee JH; Department of Neurology, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Republic of Korea., Levin J; Department of Neurology, Ludwig-Maximilians-Universität München, Munich, Germany.; German Center for Neurodegenerative Diseases, Munich, Germany.; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany., Lopera F; Universidad de Antioquia, Medellín, Colombia., Niimi Y; Unit for Early and Exploratory Clinical Development, The University of Tokyo Hospital, Bunkyo-Ku, Tokyo, Japan., Sánchez-González VJ; Departamento de Clínicas, CUALTOS, Universidad de Guadalajara, Tepatitlán de Morelos, Jalisco, México., Schofield PR; Neuroscience Research Australia, Sydney, NSW, Australia.; School of Biomedical Sciences, University of New South Wales, Sydney, NSW, Australia., Sosa-Ortiz AL; Instituto Nacional de Neurologia y Neurocirugía MVS, CDMX, Ciudad de México, Mexico., Vöglein J; Department of Neurology, Ludwig-Maximilians-Universität München, Munich, Germany.; German Center for Neurodegenerative Diseases, Munich, Germany., Bateman RJ; Department of Neurology, Washington University in St. Louis, St. Louis, MO, USA., Ances BM; Department of Neurology, Washington University in St. Louis, St. Louis, MO, USA.; Mallinckrodt Institute of Radiology, Washington University in St. Louis, St. Louis, MO, USA., McDade EM; Department of Neurology, Washington University in St. Louis, St. Louis, MO, USA.
مؤلفون مشاركون: Dominantly Inherited Alzheimer Network
المصدر: Molecular neurodegeneration [Mol Neurodegener] 2023 Dec 19; Vol. 18 (1), pp. 98. Date of Electronic Publication: 2023 Dec 19.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: BioMed Central Country of Publication: England NLM ID: 101266600 Publication Model: Electronic Cited Medium: Internet ISSN: 1750-1326 (Electronic) Linking ISSN: 17501326 NLM ISO Abbreviation: Mol Neurodegener Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [London] : BioMed Central, 2006-
مواضيع طبية MeSH: Alzheimer Disease*, Humans ; Amyloid beta-Peptides/metabolism ; Brain/metabolism ; Amyloid ; Aging ; Biomarkers ; Positron-Emission Tomography ; tau Proteins/genetics ; tau Proteins/metabolism
مستخلص: Background: "Brain-predicted age" estimates biological age from complex, nonlinear features in neuroimaging scans. The brain age gap (BAG) between predicted and chronological age is elevated in sporadic Alzheimer disease (AD), but is underexplored in autosomal dominant AD (ADAD), in which AD progression is highly predictable with minimal confounding age-related co-pathology.
Methods: We modeled BAG in 257 deeply-phenotyped ADAD mutation-carriers and 179 non-carriers from the Dominantly Inherited Alzheimer Network using minimally-processed structural MRI scans. We then tested whether BAG differed as a function of mutation and cognitive status, or estimated years until symptom onset, and whether it was associated with established markers of amyloid (PiB PET, CSF amyloid-β-42/40), phosphorylated tau (CSF and plasma pTau-181), neurodegeneration (CSF and plasma neurofilament-light-chain [NfL]), and cognition (global neuropsychological composite and CDR-sum of boxes). We compared BAG to other MRI measures, and examined heterogeneity in BAG as a function of ADAD mutation variants, APOE ε4 carrier status, sex, and education.
Results: Advanced brain aging was observed in mutation-carriers approximately 7 years before expected symptom onset, in line with other established structural indicators of atrophy. BAG was moderately associated with amyloid PET and strongly associated with pTau-181, NfL, and cognition in mutation-carriers. Mutation variants, sex, and years of education contributed to variability in BAG.
Conclusions: We extend prior work using BAG from sporadic AD to ADAD, noting consistent results. BAG associates well with markers of pTau, neurodegeneration, and cognition, but to a lesser extent, amyloid, in ADAD. BAG may capture similar signal to established MRI measures. However, BAG offers unique benefits in simplicity of data processing and interpretation. Thus, results in this unique ADAD cohort with few age-related confounds suggest that brain aging attributable to AD neuropathology can be accurately quantified from minimally-processed MRI.
(© 2023. The Author(s).)
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معلومات مُعتمدة: P30 AG066444 United States AG NIA NIH HHS; P01-AG026276 United States AG NIA NIH HHS; SG-20-690363-DIAN United States ALZ Alzheimer's Association; 5-R01-AG052550 United States AG NIA NIH HHS; U19-AG032438 United States AG NIA NIH HHS; U19 AG032438 United States AG NIA NIH HHS; P01 AG003991 United States AG NIA NIH HHS; P30-AG066444 United States AG NIA NIH HHS; P01 AG026276 United States AG NIA NIH HHS; P01-AG03991 United States AG NIA NIH HHS; S10 OD025214 United States OD NIH HHS; R01 AG052550 United States AG NIA NIH HHS
فهرسة مساهمة: Keywords: Alzheimer disease; Brain aging; Machine learning; Structural MRI
المشرفين على المادة: 0 (Amyloid beta-Peptides)
0 (Amyloid)
0 (Biomarkers)
0 (tau Proteins)
تواريخ الأحداث: Date Created: 20231219 Date Completed: 20231220 Latest Revision: 20240210
رمز التحديث: 20240210
مُعرف محوري في PubMed: PMC10729487
DOI: 10.1186/s13024-023-00688-3
PMID: 38111006
قاعدة البيانات: MEDLINE
الوصف
تدمد:1750-1326
DOI:10.1186/s13024-023-00688-3