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Alzheimers Dement ; 20(3): 1515-1526, 2024 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-38018380

RESUMO

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.


Assuntos
Demência Frontotemporal , Humanos , Demência Frontotemporal/genética , Demência Frontotemporal/diagnóstico , Galectina 3/genética , Galectina 3/metabolismo , Proteínas tau/líquido cefalorraquidiano , Encéfalo/patologia , Biomarcadores/líquido cefalorraquidiano , Proteína C9orf72/genética , Mutação/genética
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