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@INPROCEEDINGS{Rizzo:283058,
      author       = {Rizzo, Marianna and Teunissen, Charlotte E and Brosseron,
                      Frederic and Kuhs, Sandra and Kollmorgen, Gwendlyn and
                      Zetterberg, Henrik and Blennow, Kaj and Krüger, Rejko and
                      Fernandes, Sara B Gomes and Aarsland, Dag and Borejko, Olga
                      and Chokoshvili, Davit and van der Flier, Wiesje M and
                      Lemstra, Afina W and Tijms, Betty M and Petzold, Gabor C and
                      Spottke, Annika and Frisoni, Giovanni B and Brockmann,
                      Kathrin and Gasser, Thomas and Fladby, Tormod and
                      Wettergreen, Marianne and Jessen, Frank and Düzel, Emrah
                      and Höglinger, Günter U and Chevalier, Claire and
                      Krishnan, Rajaraman and Visser, Pieter Jelle and Vos,
                      Stephanie J B},
      collaboration = {consortium, IMI EPND},
      title        = {{A}ssociations between {CSF} complement factors and
                      biomarkers of amyloid, tau, neurofilament light chain, and
                      α‐synuclein in {AD}, {DLB}, and {PD}},
      journal      = {Alzheimer's and dementia},
      volume       = {21},
      number       = {Suppl 2},
      issn         = {1552-5260},
      reportid     = {DZNE-2025-01465},
      pages        = {e104363},
      year         = {2025},
      abstract     = {While evidence suggests complement system involvement in
                      Alzheimer's disease (AD), dementia with Lewy bodies (DLB),
                      and Parkinson's disease (PD), its association with disease
                      biomarkers remains unclear. We investigated the relationship
                      of complement factors with amyloid, tau, NfL, and
                      α-synuclein in CSF in AD, DLB, PD, and controls.We included
                      321 individuals with AD, DLB, PD, and controls from 6
                      centers of the EPND study. CSF Aβ42/40, p-tau181, NfL, and
                      α-syn were centrally measured using NeuroToolKit (Roche
                      Diagnostics), and 14 CSF complement factors using Milliplex
                      (Merck KGaA). Controls were defined as normal cognition and
                      normal Aβ42/40, whereas AD as abnormal Aβ42/40 without
                      meeting clinical criteria of DLB or PD. Linear regression
                      models adjusted for age and sex were used. Associations were
                      post-hoc compared between individuals with low(≤23),
                      intermediate(24-27), and high(≥28) MMSE scores.Sample
                      characteristics are presented in Table 1. Lower Aβ42/40
                      levels were associated with lower levels of 7 complement
                      factors in controls and with higher C1q and C2 levels
                      specifically in AD (Figure 1, Figure 2). No associations of
                      Aβ42/40 with complement were found in DLB and PD. Higher
                      p-tau181 levels were associated with increased levels of 7
                      complement factors in controls and 6 in AD, and showed fewer
                      associations in DLB and PD. The strength of p-tau181
                      associations with complement was similar across groups.
                      Higher NfL levels were widely associated with higher
                      complement factor levels in controls (13) and AD (12), and
                      less in PD (6) and DLB (4). Higher α-syn levels were
                      broadly associated with higher complement factor levels in
                      AD (13), controls (12), and DLB (12), but only minimally in
                      PD (1). The strength of these NfL and α-syn associations
                      with complement was not disease-specific. Conversely,
                      compared to all groups, in PD higher α-syn levels were
                      associated with lower C5, C5a, C9, factor-I and properdin
                      levels. Individuals with intermediate MMSE scores largely
                      drove the associations of α-syn with complement in AD. MMSE
                      level did not clearly impact other associations.CSF
                      complement factors were associated with amyloid, tau, NfL,
                      and α-synuclein, suggesting complement system involvement
                      in several neurodegenerative diseases. Complement showed
                      disease-specific associations with amyloid in AD and
                      α-synuclein in PD.},
      month         = {Jul},
      date          = {2025-07-27},
      organization  = {Alzheimer’s Association
                       International Conference, Toronto
                       (Canada), 27 Jul 2025 - 31 Jul 2025},
      keywords     = {Humans / Female / Male / Biomarkers: cerebrospinal fluid /
                      Alzheimer Disease: cerebrospinal fluid / Aged / Amyloid
                      beta-Peptides: cerebrospinal fluid / Parkinson Disease:
                      cerebrospinal fluid / tau Proteins: cerebrospinal fluid /
                      alpha-Synuclein: cerebrospinal fluid / Lewy Body Disease:
                      cerebrospinal fluid / Peptide Fragments: cerebrospinal fluid
                      / Neurofilament Proteins: cerebrospinal fluid / Aged, 80 and
                      over / Middle Aged / Complement System Proteins:
                      cerebrospinal fluid / Biomarkers (NLM Chemicals) / Amyloid
                      beta-Peptides (NLM Chemicals) / tau Proteins (NLM Chemicals)
                      / alpha-Synuclein (NLM Chemicals) / Peptide Fragments (NLM
                      Chemicals) / Neurofilament Proteins (NLM Chemicals) /
                      neurofilament protein L (NLM Chemicals) / amyloid
                      beta-protein (1-42) (NLM Chemicals) / Complement System
                      Proteins (NLM Chemicals)},
      cin          = {AG Heneka / AG Spottke / AG Petzold / AG Gasser / AG Jessen
                      / AG Düzel / Clinical Research (Munich)},
      ddc          = {610},
      cid          = {I:(DE-2719)1011303 / I:(DE-2719)1011103 /
                      I:(DE-2719)1013020 / I:(DE-2719)1210000 / I:(DE-2719)1011102
                      / I:(DE-2719)5000006 / I:(DE-2719)1111015},
      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:41453027},
      pmc          = {pmc:PMC12742826},
      doi          = {10.1002/alz70856_104363},
      url          = {https://pub.dzne.de/record/283058},
}