Evidence map›Paper›PMID 37988169›Full record

ArticleThe Journal of clinical investigation2024

Galectin-3 aggravates microglial activation and tau transmission in tauopathy.

Jian Jing Siew, Hui-Mei Chen, Feng-Lan Chiu, Chia-Wei Lee, Yao-Ming Chang, Hung-Lin Chen, Thi Ngoc Anh Nguyen, Hung-Ting Liao, Mengyu Liu, Hsiao-Tien Hagar and 12 more

Open access · goldAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.8field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  10. [Mediation analysis of plasma phosphorylated tau217 in the association between periodontitis and mild cognitive impairment].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2025
    Article
  11. Pleiotropic regulatory mechanisms and targeted therapeutic prospects of Galectin-3 in aging-related diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  12. Article
  13. Implications of Mucin-TypeMolecules (Basel, Switzerland) · 2025
    Review
  14. Improving vulnerable Calbindin1Translational neurodegeneration · 2025
    Article
  15. Article
  16. Review
  17. Article
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  19. Profiling the impact of different tau species on glial cell biology.Frontiers in cell and developmental biology · 2025
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

22 authors at 6 institutions in 4 countries.

Jian Jing SiewInstitute of Biomedical Sciences.
Hui-Mei ChenInstitute of Biomedical Sciences.
Feng-Lan ChiuInstitute of Cellular and Organismic Biology, Academia Sinica, Taipei, Taiwan.
Chia-Wei LeeInstitute of Biomedical Sciences.
Yao-Ming ChangInstitute of Biomedical Sciences.
Hung-Lin ChenInstitute of Biomedical Sciences.
Thi Ngoc Anh NguyenInstitute of Biomedical Sciences.
Hung-Ting LiaoInstitute of Biomedical Sciences.
Mengyu LiuDepartment of Biochemistry and Molecular Biology, Michigan State University, East Lansing, Michigan, USA.
Hsiao-Tien HagarDepartment of Biochemistry and Molecular Biology, Michigan State University, East Lansing, Michigan, USA.
Yung-Chen SunInstitute of Biochemistry and Molecular Biology, National Yang Ming Chiao Tung University, Taipei, Taiwan.
Hsing-Lin LaiInstitute of Biomedical Sciences.
Min-Hao KuoDepartment of Biochemistry and Molecular Biology, Michigan State University, East Lansing, Michigan, USA.
David BlumUniv. Lille, Inserm, CHU Lille, U1172 - LilNCog - Lille Neuroscience & Cognition, Lille, France.
Luc BuéeUniv. Lille, Inserm, CHU Lille, U1172 - LilNCog - Lille Neuroscience & Cognition, Lille, France.
Lee-Way JinDepartment of Pathology and Laboratory Medicine, University of California Davis, Sacramento, California, USA.
Shih-Yu ChenInstitute of Biomedical Sciences.
Tai-Ming KoInstitute of Biomedical Sciences.
Jie-Rong HuangInstitute of Biochemistry and Molecular Biology, National Yang Ming Chiao Tung University, Taipei, Taiwan.
Hung-Chih KuoInstitute of Cellular and Organismic Biology, Academia Sinica, Taipei, Taiwan.
Fu-Tong LiuInstitute of Biomedical Sciences.
Yijuang ChernInstitute of Biomedical Sciences.
Institute of Biomedical Sciences, Academia Sinica · TWMichigan State University · USNational Yang Ming Chiao Tung University · TWInserm · FRInstitute of Cellular and Organismic Biology, Academia Sinica · TWUniversity of California Davis Medical Center · US

Funding

UC Davis Alzheimer's Disease Core CenterP30AG010129 · NIA · UNIVERSITY OF CALIFORNIA DAVIS · PI DECARLI, CHARLES · 1991 to 2020
$28.3M
UC Davis Alzheimer's Disease Research CenterP30AG072972 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Charles DeCarli, Rachel A Whitmer · 2021 to 2026
$25.2M
Hyperphosphorylated tau aggregation-based Alzheimer’s disease early drug discoveryR01AG062435 · NIA · MICHIGAN STATE UNIVERSITY · PI KUO, MIN-HAO · 2019 to 2021
$1.3M
Hyperphosphorylated tau aggregation kit to identify tauopathy risk factorR41AG057274 · NIA · CAYMAN CHEMICAL COMPANY, INC. · PI BOCHAR, DANIEL · 2017 to 2017
$225k
NIA NIH HHS P30 AG010129NIA NIH HHS P30 AG072972NIA NIH HHS R01 AG062435NIA NIH HHS R41 AG057274
6 · The paper itself

Abstract

Alzheimer's disease is characterized by the accumulation of amyloid-β plaques, aggregation of hyperphosphorylated tau (pTau), and microglia activation. Galectin-3 (Gal3) is a β-galactoside-binding protein that has been implicated in amyloid pathology. Its role in tauopathy remains enigmatic. Here, we showed that Gal3 was upregulated in the microglia of humans and mice with tauopathy. pTau triggered the release of Gal3 from human induced pluripotent stem cell-derived microglia in both its free and extracellular vesicular-associated (EV-associated) forms. Both forms of Gal3 increased the accumulation of pathogenic tau in recipient cells. Binding of Gal3 to pTau greatly enhanced tau fibrillation. Besides Gal3, pTau was sorted into EVs for transmission. Moreover, pTau markedly enhanced the number of EVs released by iMGL in a Gal3-dependent manner, suggesting a role of Gal3 in biogenesis of EVs. Single-cell RNA-Seq analysis of the hippocampus of a mouse model of tauopathy (THY-Tau22) revealed a group of pathogenic tau-evoked, Gal3-associated microglia with altered cellular machineries implicated in neurodegeneration, including enhanced immune and inflammatory responses. Genetic removal of Gal3 in THY-Tau22 mice suppressed microglia activation, reduced the level of pTau and synaptic loss in neurons, and rescued memory impairment. Collectively, Gal3 is a potential therapeutic target for tauopathy.

Indexed as

Galectin 3Tauopathiestau ProteinsAlzheimer DiseaseAnimalsBlood ProteinsDisease Models, AnimalGalectinsHumansInduced Pluripotent Stem CellsMiceMice, TransgenicMicrogliaBlood ProteinsGalectin 3GalectinsLGALS3 protein, humantau ProteinsAlzheimer diseaseiPS cellsNeurodegenerationNeuroscience

Identifiers

PMID37988169
PMCPMC10786694
OpenAlexW4388867076

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.