ArticleNeuroSci2022
Sialic Acid Ameliorates Cognitive Deficits by Reducing Amyloid Deposition, Nerve Fiber Production, and Neuronal Apoptosis in a Mice Model of Alzheimer's Disease.
Article in NeuroSci, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed.
- Edible Bird's Nest as a Multi-Component Functional Food for Brain Aging: From Single-Bioactive Actions to Network-Regulatory Mechanisms.Nutrients · 2026Review
- Transcutaneous Auricular Vagus Nerve Stimulation Restores Cognitive Impairment in Morphine-Withdrawn Rats: Role of BDNF and Glial Cells in the Hippocampus.Addiction biology · 2025Article
- Neuraminidase as a novel therapeutic management strategy for Alzheimer's disease: evidenced through molecular docking, molecular dynamic simulation and gene expression analysis.Frontiers in chemistry · 2025Article
- Effects of extracts and manna ofResearch in pharmaceutical sciences · 2024Article
- Therapeutic potential to target sialylation and SIGLECs in neurodegenerative and psychiatric diseases.Frontiers in neurology · 2024Review
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
(1) Background: As a natural carbohydrate, sialic acid (SA) is helpful for brain development, cognitive ability, and the nervous system, but there are few reports about the effect of SA on Alzheimer's disease (AD). (2) Method: The present study evaluated the effect of SA on cognitive ability, neuronal activity, Aβ formation, and tau hyperphosphorylation in a double transgenic AD (2×Tg-AD) mice model. The 2×Tg-AD mice were randomly divided into four groups: the AD control group, 17 mg/kg SA-treated AD group, 84 mg/kg SA-treated AD group, and 420 mg/kg SA-treated AD group. Mice from all four groups were fed to 7 months of age for the behavioral test and to 9 months of age for the pathological factors investigation. (3) Results: In the Morris water maze, the escape latency significantly decreased on the fifth day in the SA-treated groups. The number of rearing and crossing times in the open field test also increased significantly, compared with the control group. SA treatment significantly reduced amyloid β-peptide (Aβ) and nerve fibers and increased the number of Nissl bodies in the brain of AD mice. (4) Conclusions: SA reduced the neuron damage by reducing Aβ and inhibited tau protein hyperphosphorylation, which improved the cognitive ability and mobility of AD mice.
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