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 Vitorica, Jose Luis Venero, Tomas Deierborg, Antonio Boza‐Serrano, Raquel Sánchez‐Valle- Psychiatry and Mental health
- Cellular and Molecular Neuroscience
- Geriatrics and Gerontology
- Neurology (clinical)
- Developmental Neuroscience
- Health Policy
- Epidemiology
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.