Galectin-3 is upregulated in frontotemporal dementia patients with subtype specificity
Sergi Borrego-Écija1, Agnès Pérez-Millan1,2, Anna Antonell1
1Alzheimer's disease and other cognitive disorders Unit. Service of Neurology, Fundació Recerca Clínic Barcelona-IDIBAPS, Hospital Clínic de Barcelona, Barcelona, Spain.
Introduction:
Neuroinflammation is a major contributor to the progression of frontotemporal dementia (FTD). Galectin-3 (Gal-3), a microglial activation regulator, holds promise as a therapeutic target and potential biomarker. Our study aimed to investigate Gal-3 levels in patients with FTD and assess its diagnostic potential.
Methods:
We examined Gal-3 levels in brain, serum, and cerebrospinal fluid (CSF) samples of patients with FTD and controls. Multiple linear regressions between Gal-3 levels and other FTD markers were explored.
Results:
Gal-3 levels were increased significantly in patients with FTD, mainly across brain tissue and CSF, compared to controls. Remarkably, Gal-3 levels were higher in cases with tau pathology than TAR-DNA Binding Protein 43 (TDP-43) pathology. Only MAPT mutation carriers displayed increased Gal-3 levels in CSF samples, which correlated with total tau and 14-3-3.
Discussion:
Our findings underscore the potential of Gal-3 as a diagnostic marker for FTD, particularly in MAPT cases, and highlights the relation of Gal-3 with neuronal injury markers.
