Galectin‐3 is upregulated in frontotemporal dementia patients with subtype specificity
Sergi Borrego‐Écija, Agnès Pérez‐Millan, Anna Antonell, Laura Fort‐Aznar, Elif Kaya Tilki, Alberto León‐Halcón, Albert Lladó, Laura Molina‐Porcel, Mircea Balasa, Jordi Juncà‐Parella, Javier Vitórica, José L. Venero, Tomas Deierborg, Antonio Boza‐Serrano, Raquel Sánchez‐Valle
Abstract
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.