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

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...

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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
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creator Tan, Yinyin
Zheng, Yanqun
Xu, Daiwen
Sun, Zhanfang
Yang, Huan
Yin, Qingqing
description 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.
doi_str_mv 10.1186/s13578-021-00592-7
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source Publicly Available Content (ProQuest); PubMed Central
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
title Galectin-3: a key player in microglia-mediated neuroinflammation and Alzheimer's disease
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