MassIVE MSV000092141

Partial Public

Uncover possible mechanism of sodium benzoate in treating patients with AD using label free quantitative serum proteomics

Description

AD is a progressive neurodegenerative disorder characterized by a decline in memory that ultimately leads to dementia. N-methyl-D-aspartate receptors are crucial components of brain function involved in memory and neurotransmission. Currently, targeting NMDARs with medication has shown potential in providing dementia-related benefits for AD patients. Sodium benzoate is a promising NMDAR enhancer that reduces oxidative stress, thereby offering neuroprotection. Sodium benzoate has been proved as a novel, safe and efficient therapy to patients with AD. However, in addition to the role as an NMDAR enhancer, other mechanism of sodium benzoate is still unclear. To uncover possible mechanism of sodium benzoate in treating patients with Alzheimer's disease, in this study, serum samples from AD patients with sodium benzoate treatment or a placebo were analyzed using label free quantitative proteomics. The serum proteins were separated into 24 fractions using immobilized pH gradient. Each subfraction was individually digested with trypsin and then subjected to nanoLC-MS/MS to analyze the proteome of all patients. There were 837 and 807 protein groups identified in the benzoate-treatment group and the placebo group, respectively. Our result shows that sodium benzoate had the most significant effect in the pathway of complement and coagulation cascades, disease-gene associations of amyloidosis, the biological process of immune responses, and lipid metabolic process. TTR, FGA, HP, ApoB, FGB APOE and ApoA1 were found to be the hub proteins of the protein-protein interaction networks. Our results showed that sodium benzoate could affect some important pathways which play key roles in the pathogenesis of AD. [doi:10.25345/C5S46HG8N] [dataset license: CC0 1.0 Universal (CC0 1.0)]

Keywords: label free quantitative ; serum proteomics ; sodium benzoate

Contact

Principal Investigators:
(in alphabetical order)
Chao-Jung Chen, China Medical University, Taiwan
Submitting User: cjchen_01
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