KMID : 1100220170160040121
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Dementia and Neurocognitive Disorders 2017 Volume.16 No. 4 p.121 ~ p.127
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Neural Stem Cell Death Mechanisms Induced by Amyloid Beta
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Lee Jong-Min
Park Hyun-Hee Koh Seong-Ho Choi Ho-Jin
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Abstract
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Background and Purpose: Amyloid beta (A¥â) is the main component of amyloid plaques, which are deposited in the brains of patients with Alzheimer¡¯s disease (AD). Biochemical and animal studies support the central role of A¥â in AD pathogenesis. Despite several investigations focused on the pathogenic mechanisms of A¥â, it is still unclear how A¥â accumulates in the central nervous system and subsequently initiates the disease at the cellular level. In this study, we investigated the pathogenic mechanisms of A¥â using proteomics and antibody microarrays.
Methods: To evaluate the effect of A¥â on neural stem cells (NSCs), we treated primary cultured cortical NSCs with several doses of A¥â for 48 h. A 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide assay, trypan blue staining, and bromodeoxyuridine cell proliferation assay were performed. We detected several intracellular proteins that may be associated with A¥â by proteomics and Western blotting analysis.
Results: Various viability tests showed that A¥â decreased NSCs viability and cell proliferation in a concentration-dependent manner. A¥â treatment significantly decreased lactate dehydrogenase B, high-mobility group box 1, aldolase C, Ezrin, and survival signals including phosphorylated phosphoinositide 3-kinase, Akt, and glycogen synthase kinase-3¥â.
Conclusions: These results suggest that several factors determined by proteomics and Western blot hold the clue to A¥â pathogenesis. Further studies are required to investigate the role of these factors.
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KEYWORD
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amyloid beta, neural stem cells, proteomics
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