ArticleCNS neuroscience & therapeutics2024
Farnesylthiosalicylic Acid Through Inhibition of Galectin-3 Improves Neuroinflammation in Alzheimer Disease via Multiple Pathways.
Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The trial behind it
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Who cites it
6 citing papers in PubMed.
- Bellidifolin alleviates doxorubicin-induced hepatotoxicity: a study integrating network pharmacology, molecular docking, and experimental validation.Die Naturwissenschaften · 2026Article
- Neuroinflammation and RAMP1: the Role of the Peripheral and Central Nervous System in Tumor Progression.Cell biochemistry and biophysics · 2026Review
- Targeting Apolipoprotein E4 rescues photoreceptor degeneration by inhibiting the disease-associated microglia activation in experimental retinal detachment.Journal of neuroinflammation · 2026Article
- USP22 knockdown attenuatesFrontiers in neuroscience · 2026Article
- Pleiotropic regulatory mechanisms and targeted therapeutic prospects of Galectin-3 in aging-related diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Galectin-3 in acute myocardial infarction: from molecular mechanisms to clinical translation.Frontiers in molecular biosciences · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
aimsMany factors affect the neuroinflammatory response in patients with Alzheimer disease (AD). Galectin-3 (Gal-3) is closely related to microglial activation in the nervous system and can promote the aggregation of cancer cells in tumors. This study aimed to investigate the mechanism by which farnesylthiosalicylic acid (FTS) affects neuroinflammation in Aβ
methodsWe used the Morris water maze, reverse transcription-polymerase chain reaction (RT-PCR), Western blotting, enzyme-linked immunosorbent assay (ELISA), and immunofluorescence to conduct our study.
resultsFTS reduced the levels of proinflammatory factors and microglial activation in Aβ
conclusionFTS may through inhibiting Gal-3 reduce the expression of TLR4 and CD14 and alleviate Aβ pathology, downregulating Aβ-stimulated TLR2, TLR4, and CD14 expression, and thus alleviate neuroinflammation in Aβ
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Registered trials
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