Galectin-3 is upregulated in frontotemporal dementia patients with subtype specificity

Sergi Borrego-Ecija, 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, José L. Venero, Tomas Deierborg, Antonio Boza-Serrano, Raquel Sánchez-Valle

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
JournalAlzheimer's and Dementia
Publication statusE-pub ahead of print - 2023

Bibliographical note

Funding Information:
The authors thank patients, their relatives, and healthy controls for participating in the research. This work was supported by Instituto de Salud Carlos III, Spain (grant no. PI20/0448 to Dr R. Sanchez‐Valle, Instituto de Salud Carlos III, Spain, co‐funded by the EU (FEDER) “Una manera de hacer Europa” and PI19/00449 to Dr Lladó) and Generalitat de Catalunya (SGR 2021‐01126). Dr S. Borrego‐Écija is a recipient of the Joan Rodés Josep Baselga grant from FBBVA. Antonio Boza‐Serrano, PhD is recipient of the Vetenskapsrådet grant, 2019‐0633, Kungliga Fysiografiska Sällskapet i Lund, 20191114ABS and 20211129ABS, Greta och Johan Kocks stiftelser, 20201201ABS, and Juan de la Cierva Incorporación—IJC2019‐040731‐I. Professor Jose Luis Venero is recipient of Spanish Ministerio de Ciencia e Innovación /FEDER/UE (PID2021‐124096OB‐I00). Professor Javier Vitorica is recipient of Instituto de Salud Carlos III, Union PI18/01556, PI21/00914. Professor Tomas Deierborg is recipient of: Swedish Demensfonden, The Strategic Research Area MultiPark (Multidisciplinary Research in neurodegenerative diseases) at Lund University, the Swedish Brain Foundation, Crafoord Foundation, Swedish Dementia Association, G&J Kock Foundation, Olle Engkvist Foundation, Gamla Tjänarinnor Foundation, the Swedish Medical Research Council, the Swedish Parkinson Foundation, the Swedish Parkinson Research Foundation, the A.E. Berger Foundation.

Publisher Copyright:
© 2023 The Authors. Alzheimer's & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer's Association.

Subject classification (UKÄ)

  • Neurosciences

Free keywords

  • C9orf72
  • CSF
  • frontotemporal dementia
  • galectin-3
  • GRN
  • MAPT
  • microglia
  • neuroinflammation


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