TY  - CONF
AU  - Kinton, Sofia
AU  - Dujardin, Simon
AU  - Levit, Mikhail
AU  - Pao, Ping-Chieh
AU  - Sardi, Pablo
AU  - Zhang, Bailin
AU  - Dodge, James
AU  - Krishnan, Rajaraman
AU  - Rizzo, Marianna
AU  - Teunissen, Charlotte E
AU  - Zetterberg, Henrik
AU  - Blennow, Kaj
AU  - Kollmorgen, Gwendlyn
AU  - Ramia, Nancy
AU  - Fernandes, Sara B Gomes
AU  - Krüger, Rejko
AU  - Borejko, Olga
AU  - Aarsland, Dag
AU  - Hu, Michele
AU  - Klockgether, Thomas
AU  - Brockmann, Kathrin
AU  - Gasser, Thomas
AU  - Jessen, Frank
AU  - Spottke, Annika
AU  - van der Flier, Wiesje M
AU  - Lemstra, Afina W
AU  - Tijms, Betty M
AU  - Frisoni, Giovanni B
AU  - Hort, Jakub
AU  - Nedelska, Zuzana
AU  - Chevalier, Claire
AU  - Visser, Pieter Jelle
AU  - Vos, Stephanie J B
TI  - Proteomic Profiling of CSF Reveals Inflammatory Pathways Associated with Tau Neuropathology in Alzheimer's Disease
JO  - Alzheimer's and dementia
VL  - 21
IS  - S2
SN  - 1552-5260
M1  - DZNE-2026-00051
SP  - e106780
PY  - 2025
AB  - 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
T2  - Alzheimer’s Association International Conference
CY  - 27 Jul 2025 - 31 Jul 2025, Toronto (Canada)
Y2  - 27 Jul 2025 - 31 Jul 2025
M2  - Toronto, Canada
KW  - Humans
KW  - Biomarkers: cerebrospinal fluid
KW  - Alzheimer Disease: cerebrospinal fluid
KW  - tau Proteins: cerebrospinal fluid
KW  - Amyloid beta-Peptides: cerebrospinal fluid
KW  - Female
KW  - Male
KW  - Aged
KW  - Cross-Sectional Studies
KW  - Proteomics
KW  - Middle Aged
KW  - Peptide Fragments: cerebrospinal fluid
KW  - Biomarkers (NLM Chemicals)
KW  - tau Proteins (NLM Chemicals)
KW  - Amyloid beta-Peptides (NLM Chemicals)
KW  - Peptide Fragments (NLM Chemicals)
LB  - PUB:(DE-HGF)1 ; PUB:(DE-HGF)16
C6  - pmid:41505027
DO  - DOI:10.1002/alz70856_106780
UR  - https://pub.dzne.de/record/283155
ER  -