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Alzheimers Dement ; 20(3): 1515-1526, 2024 Mar.
Article in English | MEDLINE | ID: mdl-38018380

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.


Subject(s)
Frontotemporal Dementia , Humans , Frontotemporal Dementia/genetics , Frontotemporal Dementia/diagnosis , Galectin 3/genetics , Galectin 3/metabolism , tau Proteins/cerebrospinal fluid , Brain/pathology , Biomarkers/cerebrospinal fluid , C9orf72 Protein/genetics , Mutation/genetics
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