여름정기학술대회
2022여름초록
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Brief Oral Presentation 발표신청 |
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공동저자
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접수자
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Alzheimer’s disease (AD) is the most devastating neurodegenerative disease that destroys memory and cognitive function. Risk factors for sporadic AD include age, genotype, diet type, environment stress, lifestyle, and interactions. Although the mediators of AD etiology are multifactorial, the detailed molecular mechanism underlying the link between multi-risk factors and AD is still ambiguous.
Here, we aimed to investigate metabolic regulation by aging, Alzheimer-related gene, and a high-fat diet in addition to ultrafine particle (UFP) exposure. We applied an untargeted metabolomics strategy based on gas chromatography time-of-flight mass spectrometry (GC-TOF-MS) and liquid-chromatography Orbitrap mass spectrometry (LC-Orbitrap MS). We presented a comprehensive data analysis of metabolomes of the mouse brain, blood, and human blood.
The differential metabolic phenotype was primarily characterized by regional brain specificity, followed by multi-risk factors. The key metabolic modules according to age, genotype, and diet were identified as histidine metabolism, methionine metabolism, and galactose metabolism, respectively. The significant metabolic alterations by UFP exposure were in the methionine salvage pathway and cysteine-glutathione metabolism, which suggested a potential redox imbalance associated with oxidative stress. The results may help in understanding putative linkages of AD to multi-risk factors and suggest a plausible treatment target for alleviating AD pathology.
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