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@INPROCEEDINGS{Erszl:283177,
      author       = {Ersözlü, Ersin and Hellmann-Regen, Julian},
      title        = {{A}n explorative analyses of in vivo plasma marker
                      alterations in relation to imaging and neuropathological
                      indicators of cerebral amyloid angiopathy},
      journal      = {Alzheimer's and dementia},
      volume       = {21 Suppl 2},
      number       = {Suppl 2},
      issn         = {1552-5260},
      reportid     = {DZNE-2026-00056},
      pages        = {e105585},
      year         = {2025},
      abstract     = {Alzheimer's disease (AD) is one of the most prevalent
                      causes of dementia, while concomitant diseases such as
                      cerebral amyloid angiopathy (CAA) has a substantial impact
                      on clinical trajectories and therapy, i.e. risk factor for
                      imaging abnormalities under anti-amyloid antibodies. As
                      there are no established biomarkers to identify individual
                      with CAA, we aim to explore potential plasma biomarkers for
                      mechanisms related to CAA in participants in continuum of
                      AD.We included a total of 47 participants from the AD
                      Neuroimaging Initiative study with available plasma
                      biomarkers from a multiplex immunoassay panel (n = 145
                      analytes from 'Biomarkers Consortium MRM data', consisting
                      of proteins related to cancer, cardiovascular disease,
                      metabolic disorders, inflammation, and AD). We stratified
                      the cohort into participants with either T2*-GRE magnetic
                      resonance images (MRI) (n = 21) at baseline or postmortem
                      neuropathological assessment (n = 26). The numbers of
                      definite lobar microbleeds were obtained from central visual
                      readings (Mayo Clinic, Jack Lab), while central
                      neuropathological severity scales for AD (AD neuropathologic
                      change) and CAA (overall neocortical amyloid angiopathy)
                      were included. We defined CAA status as at least two lobar
                      microbleeds in orientation to the Boston criteria and at
                      least moderate density in neuropathology. Plasma analytes
                      were measured twice with a one-year time difference with a
                      maximum of 6.6 years prior to either first MRI or time of
                      death. Non-parametric receiver operating characteristic
                      curves and area under the curve (AUC) values of analytes in
                      differentiation of CAA status.In both cohorts with imaging
                      and NP data, most of the participants exhibited cognitive
                      symptoms and revealed in vivo or neuropathological changes
                      regarding AD (Table-1). Using the imaging, various markers
                      related to inflammation, lipid metabolism, cell adhesion,
                      and sex steroids are found to show a constant increase in
                      CAA (Table-2, Figure 1). Moreover, we identified increases
                      in Clusterin and Complement Factor H levels as well as
                      reduced Alpha-Fetoprotein, characterizing the
                      neuropathological definition of CAA (Table-2, Figure
                      1).Using both ante-mortem and post-mortem indicators of CAA,
                      several candidate plasma biomarkers of CAA have been found,
                      whereas replications in bigger samples with multiple
                      measurements are crucial to address confounder factors and
                      temporal relationships.},
      month         = {Jul},
      date          = {2025-07-27},
      organization  = {Alzheimer’s Association
                       International Conference, Toronto
                       (Canada), 27 Jul 2025 - 31 Jul 2025},
      keywords     = {Humans / Biomarkers: blood / Male / Female / Alzheimer
                      Disease: blood / Alzheimer Disease: pathology / Alzheimer
                      Disease: diagnostic imaging / Aged / Magnetic Resonance
                      Imaging / Cerebral Amyloid Angiopathy: blood / Cerebral
                      Amyloid Angiopathy: pathology / Cerebral Amyloid Angiopathy:
                      diagnostic imaging / Aged, 80 and over / Cohort Studies /
                      Brain: pathology / Brain: diagnostic imaging / Biomarkers
                      (NLM Chemicals)},
      cin          = {AG Endres},
      ddc          = {610},
      cid          = {I:(DE-2719)1811005},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)1 / PUB:(DE-HGF)16},
      pubmed       = {pmid:41512227},
      pmc          = {pmc:PMC12788821},
      doi          = {10.1002/alz70856_105585},
      url          = {https://pub.dzne.de/record/283177},
}