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@INPROCEEDINGS{Kinton:283155,
      author       = {Kinton, Sofia and Dujardin, Simon and Levit, Mikhail and
                      Pao, Ping-Chieh and Sardi, Pablo and Zhang, Bailin and
                      Dodge, James and Krishnan, Rajaraman and Rizzo, Marianna and
                      Teunissen, Charlotte E and Zetterberg, Henrik and Blennow,
                      Kaj and Kollmorgen, Gwendlyn and Ramia, Nancy and Fernandes,
                      Sara B Gomes and Krüger, Rejko and Borejko, Olga and
                      Aarsland, Dag and Hu, Michele and Klockgether, Thomas and
                      Brockmann, Kathrin and Gasser, Thomas and Jessen, Frank and
                      Spottke, Annika and van der Flier, Wiesje M and Lemstra,
                      Afina W and Tijms, Betty M and Frisoni, Giovanni B and Hort,
                      Jakub and Nedelska, Zuzana and Chevalier, Claire and Visser,
                      Pieter Jelle and Vos, Stephanie J B},
      title        = {{P}roteomic {P}rofiling of {CSF} {R}eveals {I}nflammatory
                      {P}athways {A}ssociated with {T}au {N}europathology in
                      {A}lzheimer's {D}isease},
      journal      = {Alzheimer's and dementia},
      volume       = {21},
      number       = {S2},
      issn         = {1552-5260},
      reportid     = {DZNE-2026-00051},
      pages        = {e106780},
      year         = {2025},
      abstract     = {Aggregation of amyloid beta (Aβ) and tau proteins is a
                      hallmark of Alzheimer's disease (AD) and tauopathies. In AD,
                      extracellular deposition of Aβ peptide precedes tau
                      aggregation and the onset of neuroinflammatory processes.
                      Both neuroinflammation and tau deposition are associated
                      with synaptic loss, neurodegeneration, and cognitive
                      decline. However, the precise sequence of events from
                      amyloid deposition to tau aggregation, neuroinflammation,
                      and neurodegeneration remains unclear. A cross-sectional
                      analysis of tau and other proteins in the cerebrospinal
                      fluid (CSF) of AD patients can provide insight into the
                      inflammatory and degenerative processes. Tau levels may be
                      used as a proxy for disease progression, and we hypothesize
                      that the expression of neuroinflammatory markers will be
                      modulated in response to increasing tau aggregation.To
                      investigate this, we collaborated with the EPND-biomarker
                      consortium to analyze over 150 human CSF samples from AD and
                      control patients. We measured levels of Aβ1-40, Aβ1-42,
                      pTau181, and total tau, and conducted proteomic profiling
                      using the O-link and SomaScan platforms. Next, AD patients
                      were stratified into Aβ+Tau+ and Aβ+Tau- groups to
                      identify biomarkers associated with Aβ and/or tau
                      aggregation.As expected, inflammation markers were elevated
                      in AD CSF samples compared to controls. Interestingly, we
                      observed distinct correlations between these markers and
                      amyloid versus tau pathology biomarkers. Approximately
                      $10\%$ of the measured CSF proteins (∼250 proteins) showed
                      significant differences (p < 0.05) between AD and control
                      samples. CSF samples with elevated tau levels exhibited
                      altered levels of proteins involved in the complement
                      cascade, cytokine-cytokine receptor interactions, cell
                      adhesion, and vesicular transport.Increased inflammation
                      markers were observed in AD. Proteins linked to innate
                      immune response and synaptic loss were significantly altered
                      in relation to tau aggregation. These findings are crucial
                      for guiding therapeutic strategies for neurodegenerative
                      diseases and assessing their efficacy.},
      month         = {Jul},
      date          = {2025-07-27},
      organization  = {Alzheimer’s Association
                       International Conference, Toronto
                       (Canada), 27 Jul 2025 - 31 Jul 2025},
      keywords     = {Humans / Biomarkers: cerebrospinal fluid / Alzheimer
                      Disease: cerebrospinal fluid / tau Proteins: cerebrospinal
                      fluid / Amyloid beta-Peptides: cerebrospinal fluid / Female
                      / Male / Aged / Cross-Sectional Studies / Proteomics /
                      Middle Aged / Peptide Fragments: cerebrospinal fluid /
                      Biomarkers (NLM Chemicals) / tau Proteins (NLM Chemicals) /
                      Amyloid beta-Peptides (NLM Chemicals) / Peptide Fragments
                      (NLM Chemicals)},
      cin          = {Patient Studies (Bonn) / AG Gasser / AG Jessen},
      ddc          = {610},
      cid          = {I:(DE-2719)1011101 / I:(DE-2719)1210000 /
                      I:(DE-2719)1011102},
      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:41505027},
      doi          = {10.1002/alz70856_106780},
      url          = {https://pub.dzne.de/record/283155},
}