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• W2142974145 abstract "The accumulation of intracellular β amyloid (Aβ) may be one of the factors leading to neuronal cell death in Alzheimer's disease (AD). Using a pyrazole called CNB-001, which was selected for its ability to reduce intracellular Aβ, we show that the activation of the eIF2α/ATF4 arm of the unfolded protein response is sufficient to degrade aggregated intracellular Aβ. CNB-001 is a potent inhibitor of 5-lipoxygenase (5-LOX), decreases 5-LOX expression, and increases proteasome activity. 5-LOX inhibition induces eIF2α and PERK (protein kinase R-like extracellular signal-regulated kinase) phosphorylation, and HSP90 and ATF4 levels. When fed to AD transgenic mice, CNB-001 also increases eIF2α phosphorylation and HSP90 and ATF4 levels, and limits the accumulation of soluble Aβ and ubiquitinated aggregated proteins. Finally, CNB-001 maintains the expression of synapse-associated proteins and improves memory. Therefore, 5-LOX metabolism is a key element in the promotion of endoplasmic reticulum dysfunction, and its inhibition under conditions of stress is sufficient to reduce proteotoxicity both in vivo and in vitro." @default.
• W2142974145 created "2016-06-24" @default.
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• W2142974145 date "2013-06-19" @default.
• W2142974145 modified "2023-10-18" @default.
• W2142974145 title "Modulation of 5-Lipoxygenase in Proteotoxicity and Alzheimer's Disease" @default.
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• W2142974145 doi "https://doi.org/10.1523/jneurosci.5183-12.2013" @default.
• W2142974145 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3685841" @default.
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