# Galectin-3: a key player in microglia-mediated neuroinflammation and Alzheimer's disease

## TL;DR

This paper reviews the role of galectin-3 in microglia activation and Alzheimer's disease, highlighting its potential as a biomarker and therapeutic target.

## Contribution

The paper synthesizes recent findings on galectin-3's role in microglia-mediated neuroinflammation and Alzheimer's disease pathogenesis.

## Key findings

- Galectin-3 modulates microglial activation and affects amyloid-β deposition in Alzheimer's disease.
- Gal-3 is emerging as a potential biomarker for Alzheimer's and other neurodegenerative diseases.
- Understanding Gal-3's functions could lead to new diagnostic and therapeutic strategies for AD.

## Abstract

Alzheimer’s disease (AD) is the most common cause of dementia and is characterized by the deposition of extracellular aggregates of amyloid-β (Aβ), the formation of intraneuronal tau neurofibrillary tangles and microglial activation-mediated neuroinflammation. One of the key molecules involved in microglial activation is galectin-3 (Gal-3). In recent years, extensive studies have dissected the mechanisms by which Gal-3 modulates microglial activation, impacting Aβ deposition, in both animal models and human studies. In this review article, we focus on the emerging role of Gal-3 in biology and pathobiology, including its origin, its functions in regulating microglial activation and neuroinflammation, and its emergence as a biomarker in AD and other neurodegenerative diseases. These aspects are important to elucidate the involvement of Gal-3 in AD pathogenesis and may provide novel insights into the use of Gal-3 for AD diagnosis and therapy.