% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Richter:1050016,
      author       = {Richter, Nils and Onur, Oezguer A. and Fink, Gereon R.},
      title        = {{D}etecting limbic predominant neurodegenerative
                      co-pathologies in vivo in {A}lzheimer’s disease: magnetic
                      resonance imaging markers, cognitive correlates, and
                      prognosis},
      journal      = {Alzheimer's research $\&$ therapy},
      volume       = {17},
      number       = {1},
      issn         = {1758-9193},
      address      = {London},
      publisher    = {BioMed Central},
      reportid     = {FZJ-2025-05730},
      pages        = {236},
      year         = {2025},
      note         = {Open 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.},
      abstract     = {In 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.},
      cin          = {INM-3},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-3-20090406},
      pnm          = {5251 - Multilevel Brain Organization and Variability
                      (POF4-525) / DFG project G:(GEPRIS)491111487 -
                      Open-Access-Publikationskosten / 2025 - 2027 /
                      Forschungszentrum Jülich (OAPKFZJ) (491111487)},
      pid          = {G:(DE-HGF)POF4-5251 / G:(GEPRIS)491111487},
      typ          = {PUB:(DE-HGF)16},
      doi          = {10.1186/s13195-025-01885-6},
      url          = {https://juser.fz-juelich.de/record/1050016},
}