ArticleScience advances2025
l-Fucose is a candidate monosaccharide neuromodulator and mitigates Alzheimer's synaptic deficits.
Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- A perspective for alzheimer disease from gut microbiota-associated NMR-based fecal metabolomics: a study with 5XFAD mice.Metabolic brain disease · 2026Article
- Research progress of blood-brain barrier penetrating and brain diseases therapy by natural biopolymer - based nanomedicine delivery systems.Materials today. Bio · 2026Review
- L-fucose administration ameliorates chronic social defeat stress-induced depressive-like behaviors by restoring GDP-fucose biosynthetic activation and core fucosylation.Frontiers in immunology · 2026Article
- Pathway enrichment in genome-wide analysis of longitudinal Alzheimer's disease biomarker endophenotypes.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Fucosylation, a major glycan modification, has been shown to influence neuronal and microglial mechanisms, but whether unconjugated free l-fucose can affect brain function is unknown. l-Fucose can be transported into cells and metabolized by fucokinase (FCSK) via the poorly understood salvage pathway. Using mouse hippocampal slices, we showed that l-fucose enhanced excitatory neurotransmission and long-term potentiation (LTP) through regulation of presynaptic release. Such effects required l-fucose be metabolized through the FCSK-driven salvage pathway, suggesting a metabolic-signaling mechanism. Human Alzheimer's disease (AD) and 5xFAD mouse brains showed signs of fucose hypometabolism with impaired l-fucose signaling. Such abnormalities were corrected by exogenous l-fucose, exemplified by rectification of LTP deficits in 5xFAD hippocampus. A dietary l-fucose supplement, which increased cerebral free l-fucose levels and up-regulated FCSK to drive the salvage pathway, mitigated synaptic and behavioral deficits of 5xFAD mice. Our data suggest an unrecognized neuromodulatory function of free l-fucose and reveals its therapeutic potential for AD.
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Registered trials
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 Socratic graph.