DOI: 10.1101/477927Dec 4, 2018Paper

Galectin-3, A Novel Endogenous TREM2 Ligand, Regulates Inflammatory Response And Aβ Fibrilation In Alzheimer's Disease.

BioRxiv : the Preprint Server for Biology
Antonio Boza SerranoTomas Deierborg

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disease in which the formation of extracellular aggregates of amyloid beta peptide, intraneuronal tau neurofibrillary tangles and microglial activation are major pathological hallmarks. One of the key molecules involved in microglial activation is galectin-3 (gal3), and we demonstrate here for the first time a key role of gal3 in AD pathology. Gal3 was highly upregulated in the brains of AD patients and 5xFAD (familial Alzheimer's disease) mice, and found specifically expressed in microglia associated with Aβ plaques. Single nucleotide polymorphisms in the LGALS3 gene, which encodes gal3, were associated to an increased risk of AD. Gal3 deletion in 5xFAD mice attenuated microglia-associated immune responses, particularly those associated with TLR and TREM2/DAP12 signaling. In vitro data demonstrated the requirement of gal3 to fully activate microglia in response to fibrillar Aβ. Gal3 deletion decreased the Aβ burden in 5xFAD mice and improved cognitive behavior. Electron microscopy of gal3 in AD mice demonstrated i) a preferential expression of gal3 by plaque-associated microglia, ii) its presence in the extracellular space and iii) its association to Aβ plaques. Low c...Continue Reading

Related Concepts

Alzheimer's Disease
Brain
Extracellular Space
Fluorescent Antibody Technique
Gene Deletion
Ligands
Laboratory mice
Electron Microscopy
Nerve Degeneration
Pathologic Processes

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