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

• Published in: Cell & bioscience 2021-04, Vol.11 (1), p.78-78, Article 78
• Main Authors: Tan, Yinyin, Zheng, Yanqun, Xu, Daiwen, Sun, Zhanfang, Yang, Huan, Yin, Qingqing
• Format: Article
• Language: English
• Subjects: Advertising executives; Alzheimer's disease; Amino acids; Amyloid; Amyloid-β; Animal models; Antigens; Apoptosis; Autophagy; B cells; Binding sites; Carbohydrates; Cell adhesion & migration; Cell cycle; Cell growth; Cytoplasm; Dementia disorders; Development and progression; Galectin-3; Inflammation; Kinases; Ligands; Localization; Microglia; Neurodegenerative diseases; Neurofibrillary tangles; Neuroinflammation; Phosphorylation; Physiology; Proteins; Review; Tau protein; Thyroid gland; Transcription factors
• ISSN: 2045-3701; 2045-3701
• DOI: 10.1186/s13578-021-00592-7

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.