Synaptic dysfunction and glial activation markers throughout aging and early neurodegeneration: a longitudinal CSF biomarker-based study

Synaptic dysfunction markers at baseline influence the longitudinal dynamics of CSF sTREM2 independently of AD-pathology related biomarkers throughout aging and earliest stages of neurodegeneration. In turn, higher baseline sTREM2 is associated with more stable neurogranin levels over time. These results suggest an independent interaction between synaptic dysfunction and TREM2-dependent microglial activation throughout aging and early neurodegeneration beyond AD pathology.

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Publication Details

Journal
Molecular Neurodegeneration
Published
2025-10-16
DOI
https://doi.org/10.1186/s13024-025-00901-5
Citations
2
Primary Topic
Neuroinflammation and Neurodegeneration Mechanisms
Type
article
Field-Weighted Citation Impact
1.68
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article

Synaptic dysfunction and glial activation markers throughout aging and early neurodegeneration: a longitudinal CSF biomarker-based study

Barbara B. Bendlin, Kaj Blennow, Alberto Villarejo‐Galende, Mariana I. Muñoz-García et al.
2 citations
Molecular Neurodegeneration
Neuroinflammation and Neurodegeneration Mechanisms
1.68
article

Synaptic dysfunction and glial activation markers throughout aging and early neurodegeneration: a longitudinal CSF biomarker-based study

Barbara B. Bendlin, Kaj Blennow, Alberto Villarejo‐Galende, Mariana I. Muñoz-García, David A. Pérez-Martínez, Estrella Morenas‐Rodríguez, Yuetiva Deming, Gwendlyn Kollmorgen, Henrik Zetterberg, Sterling C. Johnson, Marc Suárez‐Calvet, Cynthia M. Carlsson, Clara Quijano‐Rubio, Ozioma C. Okonkwo, Sanjay Asthana, Ferran Lugo-Hernández
article en
2 citations

Abstract

Synaptic dysfunction markers at baseline influence the longitudinal dynamics of CSF sTREM2 independently of AD-pathology related biomarkers throughout aging and earliest stages of neurodegeneration. In turn, higher baseline sTREM2 is associated with more stable neurogranin levels over time. These results suggest an independent interaction between synaptic dysfunction and TREM2-dependent microglial activation throughout aging and early neurodegeneration beyond AD pathology.

Molecular NeurodegenerationVol. 20(1)
Roche (Switzerland) (CH), University of Wisconsin–Madison (US), Sahlgrenska University Hospital (SE), Research Institute Hospital 12 de Octubre (ES), Roche Pharma AG (Germany) (DE), Hospital Universitario 12 De Octubre (ES), Pasqual Maragall Foundation (ES), UK Dementia Research Institute (GB), Hospital Del Mar (ES), National Hospital for Neurology and Neurosurgery (GB), University College London (GB), Indian Institute of Science Bangalore (IN), University of Gothenburg (SE)
Openalex Percentile: Top 13%
Neuroinflammation and Neurodegeneration Mechanisms
1.68
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