Galectin-3 is upregulated in frontotemporal dementia patients with subtype specificity
(2023) In Alzheimer's and Dementia- 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... (More)
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.
(Less)
- author
- organization
- publishing date
- 2023
- type
- Contribution to journal
- publication status
- epub
- subject
- keywords
- C9orf72, CSF, frontotemporal dementia, galectin-3, GRN, MAPT, microglia, neuroinflammation
- in
- Alzheimer's and Dementia
- publisher
- Wiley
- external identifiers
-
- pmid:38018380
- scopus:85178237983
- ISSN
- 1552-5260
- DOI
- 10.1002/alz.13536
- language
- English
- LU publication?
- yes
- additional info
- 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.
- id
- 4654f386-0914-4ddd-8c71-cf4074c7e425
- date added to LUP
- 2024-01-04 09:55:47
- date last changed
- 2024-04-19 07:12:30
@article{4654f386-0914-4ddd-8c71-cf4074c7e425,
abstract = {{<p>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.</p>}},
author = {{Borrego-Ecija, Sergi and Pérez-Millan, Agnès and Antonell, Anna and Fort-Aznar, Laura and Kaya-Tilki, Elif and León-Halcón, Alberto and Lladó, Albert and Molina-Porcel, Laura and Balasa, Mircea and Juncà-Parella, Jordi and Vitorica, Javier and Venero, José L. and Deierborg, Tomas and Boza-Serrano, Antonio and Sánchez-Valle, Raquel}},
issn = {{1552-5260}},
keywords = {{C9orf72; CSF; frontotemporal dementia; galectin-3; GRN; MAPT; microglia; neuroinflammation}},
language = {{eng}},
publisher = {{Wiley}},
series = {{Alzheimer's and Dementia}},
title = {{Galectin-3 is upregulated in frontotemporal dementia patients with subtype specificity}},
url = {{http://dx.doi.org/10.1002/alz.13536}},
doi = {{10.1002/alz.13536}},
year = {{2023}},
}