Background: The most common type of dementia, Alzheimer's disease (AD), is marked by the formation of extracellular amyloid beta (Aβ) plaques. The impairments of axons and synapses appear in the process of Aβ plaques formation, and this ...
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https://www.riss.kr/link?id=A108591164
Sujin Kim (Konyang University) ; Yunkwon Nam (Konyang University) ; Min-jeong Kim (Konyang University) ; Seung-hyun Kwon (Veterans Health Service Medical Center) ; Junhyeok Jeon (Korea Advanced Institute of Science and Technology (KAIST)) ; Soo Jung Shin (Konyang University) ; Soyoon Park (College of Biological Sciences, University of California) ; Sungjae Chang (Konyang University) ; Hyun Uk Kim (Korea Advanced Institute of Science and Technology) ; Yong Yook Lee (Korea Ginseng Corporation) ; Hak Su Kim (Veterans Health Service Medical Center) ; Minho Moon (Konyang University)
2023
English
SCIE,SCOPUS,KCI등재
학술저널
302-310(9쪽)
0
상세조회0
다운로드다국어 초록 (Multilingual Abstract)
Background: The most common type of dementia, Alzheimer's disease (AD), is marked by the formation of extracellular amyloid beta (Aβ) plaques. The impairments of axons and synapses appear in the process of Aβ plaques formation, and this ...
Background: The most common type of dementia, Alzheimer's disease (AD), is marked by the formation of extracellular amyloid beta (Aβ) plaques. The impairments of axons and synapses appear in the process of Aβ plaques formation, and this damage could cause neurodegeneration. We previously reported that non-saponin fraction with rich polysaccharide (NFP) from Korean Red Ginseng (KRG) showed neuroprotective effects in AD. However, precise molecular mechanism of the therapeutic effects of NFP from KRG in AD still remains elusive. Methods: To investigate the therapeutic mechanisms of NFP from KRG on AD, we conducted proteomic analysis for frontal cortex from vehicle-treated wild-type, vehicle-treated 5XFAD mice, and NFP-treated 5XFAD mice by using nano-LC-ESI-MS/MS. Metabolic network analysis was additionally performed as the effects of NFP appeared to be associated with metabolism according to the proteome analysis. Results: Starting from 5,470 proteins, 2,636 proteins were selected for hierarchical clustering analysis, and finally 111 proteins were further selected for protein-protein interaction network analysis. A series of these analyses revealed that proteins associated with synapse and mitochondria might be linked to the therapeutic mechanism of NFP. Subsequent metabolic network analysis via genome-scale metabolic models that represent the three mouse groups showed that there were significant changes in metabolic fluxes of mitochondrial carnitine shuttle pathway and mitochondrial beta-oxidation of polyunsaturated fatty acids. Conclusion: Our results suggested that the therapeutic effects of NFP on AD were associated with synaptic- and mitochondrial-related pathways, and they provided targets for further rigorous studies on precise understanding of the molecular mechanism of NFP.
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