001050016 001__ 1050016
001050016 005__ 20251219202235.0
001050016 0247_ $$2doi$$a10.1186/s13195-025-01885-6
001050016 0247_ $$2datacite_doi$$a10.34734/FZJ-2025-05730
001050016 037__ $$aFZJ-2025-05730
001050016 082__ $$a610
001050016 1001_ $$0P:(DE-Juel1)167565$$aRichter, Nils$$b0$$eCorresponding author$$ufzj
001050016 245__ $$aDetecting limbic predominant neurodegenerative co-pathologies in vivo in Alzheimer’s disease: magnetic resonance imaging markers, cognitive correlates, and prognosis
001050016 260__ $$aLondon$$bBioMed Central$$c2025
001050016 3367_ $$2DRIVER$$aarticle
001050016 3367_ $$2DataCite$$aOutput Types/Journal article
001050016 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1766153789_25560
001050016 3367_ $$2BibTeX$$aARTICLE
001050016 3367_ $$2ORCID$$aJOURNAL_ARTICLE
001050016 3367_ $$00$$2EndNote$$aJournal Article
001050016 500__ $$aOpen Access funding enabled and organized by Projekt DEAL. Datacollection and sharing for this project was funded by the Alzheimer'sDisease Neuroimaging Initiative (ADNI) (National Institutes of Health GrantU01 AG024904) and DOD ADNI (Department of Defense award numberW81XWH-12-2-0012). ADNI is funded by the National Institute on Aging, theNational Institute of Biomedical Imaging and Bioengineering, and throughgenerous contributions from the following: AbbVie, Alzheimer’s Association;Alzheimer’s Drug Discovery Foundation; Araclon Biotech; BioClinica, Inc.;Biogen; Bristol-Myers Squibb Company; CereSpir, Inc.; Cogstate; Eisai Inc.;Elan Pharmaceuticals, Inc.; Eli Lilly and Company; EuroImmun; F. Hoffmann-LaRoche Ltd and its affiliated company Genentech, Inc.; Fujirebio; GE Healthcare;IXICO Ltd.; Janssen Alzheimer Immunotherapy Research & Development,LLC.; Johnson & Johnson Pharmaceutical Research & Development LLC.;Lumosity; Lundbeck; Merck & Co., Inc.; Meso Scale Diagnostics, LLC.; NeuroRxResearch; Neurotrack Technologies; Novartis Pharmaceuticals Corporation;Pfizer Inc.; Piramal Imaging; Servier; Takeda Pharmaceutical Company;and Transition Therapeutics. The Canadian Institutes of Health Researchis providing funds to support ADNI clinical sites in Canada. Private sectorcontributions are facilitated by the Foundation for the National Institutes ofHealth (www.fnih.org). The grantee organization is the Northern CaliforniaInstitute for Research and Education, and the study is coordinated by theAlzheimer’s Therapeutic Research Institute at the University of SouthernCalifornia. ADNI data are disseminated by the Laboratory for Neuro Imagingat the University of Southern California.This work was supported by agrant from the Marga and Walter Boll Foundation (Nr. 210–08-13), Kerpen,Germany, to GRF and OO.Open access publication funded by the DeutscheForschungsgemeinschaft (DFG, German Research Foundation) – 491111487.
001050016 520__ $$aIn Alzheimer's disease (AD), limbic non-AD co-pathologies are common and contribute to memory impairment and accelerated clinical progression. To date, in vivo biomarkers of these co-pathologies are lacking. Here, we examined whether specific regional gray matter (GM) atrophy patterns on magnetic resonance imaging (MRI) allow distinguishing between patients with 'pure' AD pathology and those with AD pathology and limbic non-AD co-pathologies (AD+).Methods: Atrophy patterns based on ante-mortem MRI scans of histopathologically confirmed 'pure' AD (n = 36) and AD+, i.e., AD pathology with concomitant limbic TDP-43 pathology and argyrophilic grain disease (n = 39), were applied to classify an independent cohort of clinically diagnosed patients with mild cognitive impairment (MCI, n = 224) and dementia (n = 221). Furthermore, we examined the degree to which an MRI marker of cortical degeneration reflecting tau pathology could improve the estimation of clinical progression.Results: Histopathologically confirmed AD+ pathology was associated with more substantial hippocampal atrophy but less cortical degeneration in intermediate Braak stage regions than 'pure' AD pathology. Clinically diagnosed AD patients with an AD+-classified ratio of cortical-to-hippocampal GM exhibited significantly more memory impairment. At the stage of MCI, AD+-classified atrophy was also associated with speeded clinical decline. Furthermore, tau-associated cortical degeneration emerged as the primary predictor of clinical progression across groups and disease stages.Conclusions: The data suggest that in MCI due to AD, additional non-AD limbic co-pathologies are associated with greater hippocampal but less cortical atrophy and more rapid clinical decline. In contrast, in mild dementia due to AD, hippocampal GM was not associated with prognosis. Instead, cortical degeneration appeared to drive clinical progression.Keywords: Argyrophilic grain disease; Braak stages; Dementia; Limbic predominant age-related TDP-43 encephalopathy (LATE); Mild cognitive impairment; Tau-protein; Voxel-based morphometry.
001050016 536__ $$0G:(DE-HGF)POF4-5251$$a5251 - Multilevel Brain Organization and Variability (POF4-525)$$cPOF4-525$$fPOF IV$$x0
001050016 536__ $$0G:(GEPRIS)491111487$$aDFG project G:(GEPRIS)491111487 - Open-Access-Publikationskosten / 2025 - 2027 / Forschungszentrum Jülich (OAPKFZJ) (491111487)$$c491111487$$x1
001050016 588__ $$aDataset connected to DataCite
001050016 7001_ $$0P:(DE-HGF)0$$aOnur, Oezguer A.$$b1
001050016 7001_ $$0P:(DE-Juel1)131720$$aFink, Gereon R.$$b2$$ufzj
001050016 773__ $$0PERI:(DE-600)2506521-X$$a10.1186/s13195-025-01885-6$$gVol. 17, no. 1, p. 236$$n1$$p236$$tAlzheimer's research & therapy$$v17$$x1758-9193$$y2025
001050016 8564_ $$uhttps://juser.fz-juelich.de/record/1050016/files/PDF.pdf$$yOpenAccess
001050016 909CO $$ooai:juser.fz-juelich.de:1050016$$popenaire$$popen_access$$pVDB$$pdriver$$pdnbdelivery
001050016 9101_ $$0I:(DE-588b)5008462-8$$6P:(DE-Juel1)167565$$aForschungszentrum Jülich$$b0$$kFZJ
001050016 9101_ $$0I:(DE-588b)5008462-8$$6P:(DE-Juel1)131720$$aForschungszentrum Jülich$$b2$$kFZJ
001050016 9131_ $$0G:(DE-HGF)POF4-525$$1G:(DE-HGF)POF4-520$$2G:(DE-HGF)POF4-500$$3G:(DE-HGF)POF4$$4G:(DE-HGF)POF$$9G:(DE-HGF)POF4-5251$$aDE-HGF$$bKey Technologies$$lNatural, Artificial and Cognitive Information Processing$$vDecoding Brain Organization and Dysfunction$$x0
001050016 9141_ $$y2025
001050016 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS$$d2024-12-13
001050016 915__ $$0StatID:(DE-HGF)0160$$2StatID$$aDBCoverage$$bEssential Science Indicators$$d2024-12-13
001050016 915__ $$0LIC:(DE-HGF)CCBY4$$2HGFVOC$$aCreative Commons Attribution CC BY 4.0
001050016 915__ $$0StatID:(DE-HGF)0600$$2StatID$$aDBCoverage$$bEbsco Academic Search$$d2024-12-13
001050016 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bALZHEIMERS RES THER : 2022$$d2024-12-13
001050016 915__ $$0StatID:(DE-HGF)0501$$2StatID$$aDBCoverage$$bDOAJ Seal$$d2024-04-10T15:32:54Z
001050016 915__ $$0StatID:(DE-HGF)0500$$2StatID$$aDBCoverage$$bDOAJ$$d2024-04-10T15:32:54Z
001050016 915__ $$0StatID:(DE-HGF)0113$$2StatID$$aWoS$$bScience Citation Index Expanded$$d2024-12-13
001050016 915__ $$0StatID:(DE-HGF)0700$$2StatID$$aFees$$d2024-12-13
001050016 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection$$d2024-12-13
001050016 915__ $$0StatID:(DE-HGF)0510$$2StatID$$aOpenAccess
001050016 915__ $$0StatID:(DE-HGF)0030$$2StatID$$aPeer Review$$bASC$$d2024-12-13
001050016 915__ $$0StatID:(DE-HGF)0561$$2StatID$$aArticle Processing Charges$$d2024-12-13
001050016 915__ $$0StatID:(DE-HGF)9905$$2StatID$$aIF >= 5$$bALZHEIMERS RES THER : 2022$$d2024-12-13
001050016 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline$$d2024-12-13
001050016 915__ $$0StatID:(DE-HGF)1110$$2StatID$$aDBCoverage$$bCurrent Contents - Clinical Medicine$$d2024-12-13
001050016 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bClarivate Analytics Master Journal List$$d2024-12-13
001050016 920__ $$lyes
001050016 9201_ $$0I:(DE-Juel1)INM-3-20090406$$kINM-3$$lKognitive Neurowissenschaften$$x0
001050016 980__ $$ajournal
001050016 980__ $$aVDB
001050016 980__ $$aUNRESTRICTED
001050016 980__ $$aI:(DE-Juel1)INM-3-20090406
001050016 9801_ $$aFullTexts