Formation and stabilization model of the 42-mer Abeta radical: implications for the long-lasting oxidative stress in Alzheimer's disease.
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Site-specific inhibitory mechanism for amyloid β42 aggregation by catechol-type flavonoids targeting the Lys residues.C-terminal peptides coassemble into Abeta42 oligomers and protect neurons against Abeta42-induced neurotoxicity.Efavirenz promotes β-secretase expression and increased Aβ1-40,42 via oxidative stress and reduced microglial phagocytosis: implications for HIV associated neurocognitive disorders (HAND).The turn formation at positions 22 and 23 in the 42-mer amyloid beta peptide: the emerging role in the pathogenesis of Alzheimer's disease.In vivo and in vitro effects of an apolipoprotein e mimetic peptide on amyloid-β pathologyAspirin: a review of its neurobiological properties and therapeutic potential for mental illnessAmyloid beta-protein assembly and Alzheimer disease.Structural basis for Aβ1–42 toxicity inhibition by Aβ C-terminal fragments: discrete molecular dynamics study.New approaches to treating Alzheimer's diseaseGeneric hydrophobic residues are sufficient to promote aggregation of the Alzheimer's Abeta42 peptide.SOD1 (copper/zinc superoxide dismutase) deficiency drives amyloid β protein oligomerization and memory loss in mouse model of Alzheimer diseaseVanda roxburghii chloroform extract as a potential source of polyphenols with antioxidant and cholinesterase inhibitory activities: identification of a strong phenolic antioxidantMonoclonal antibody against the turn of the 42-residue amyloid β-protein at positions 22 and 23EVALUATION OF HOW CIGARETTE SMOKE IS A DIRECT RISK FACTOR FOR ALZHEIMER'S DISEASE.Toxicity in rat primary neurons through the cellular oxidative stress induced by the turn formation at positions 22 and 23 of Aβ42.Oxidative stress activates a positive feedback between the gamma- and beta-secretase cleavages of the beta-amyloid precursor proteinC-terminal turn stability determines assembly differences between Aβ40 and Aβ42Nanoprobing of the effect of Cu(2+) cations on misfolding, interaction and aggregation of amyloid β peptide.Discrete molecular dynamics study of oligomer formation by N-terminally truncated amyloid β-protein.Amino acid position-specific contributions to amyloid beta-protein oligomerization.Small molecule inhibitors of amyloid β peptide aggregation as a potential therapeutic strategy for Alzheimer's disease.Amyloid-β production: major link between oxidative stress and BACE1.Formation of the 42-mer Amyloid β Radical and the Therapeutic Role of Superoxide Dismutase in Alzheimer's Disease.Conformation-specific antibodies to target amyloid β oligomers and their application to immunotherapy for Alzheimer's disease.Neuroprotective effects of resveratrol in Alzheimer disease pathology.Aβ42 and Aβ40: similarities and differences.Perspectives on Inhibiting β-Amyloid Aggregation through Structure-Based Drug Design.Comparison of neurotoxicity of different aggregated forms of Aβ40, Aβ42 and Aβ43 in cell cultures.Energetic contributions of residues to the formation of early amyloid-β oligomers.Preventing expression of the nicotinic receptor subunit α7 in SH-SY5Y cells with interference RNA indicates that this receptor may protect against the neurotoxicity of Aβ.Protective effects of decursin and decursinol angelate against amyloid β-protein-induced oxidative stress in the PC12 cell line: the role of Nrf2 and antioxidant enzymes.Flavonoid-mediated presenilin-1 phosphorylation reduces Alzheimer's disease beta-amyloid production.Oxidative stress mediates the pathogenic effect of different Alzheimer's disease risk factors.A Toxic Conformer of Aβ42 with a Turn at 22-23 is a Novel Therapeutic Target for Alzheimer's DiseaseAβ-40 Y10F increases βfibrils formation but attenuates the neurotoxicity of amyloid-β peptide.E22Δ Mutation in Amyloid β-Protein Promotes β-Sheet Transformation, Radical Production, and Synaptotoxicity, But Not Neurotoxicity.Identification of key regions and residues controlling Aβ folding and assembly.Diosmin reduces cerebral Aβ levels, tau hyperphosphorylation, neuroinflammation, and cognitive impairment in the 3xTg-AD mice.Cytoplasmic superoxide radical: a possible contributing factor to intracellular Aβ oligomerization in Alzheimer disease.Synthesis and Purification of Highly Hydrophobic Peptides Derived from the C-Terminus of Amyloid β-Protein.
P2860
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P2860
Formation and stabilization model of the 42-mer Abeta radical: implications for the long-lasting oxidative stress in Alzheimer's disease.
description
2005 nî lūn-bûn
@nan
2005年の論文
@ja
2005年学术文章
@wuu
2005年学术文章
@zh-cn
2005年学术文章
@zh-hans
2005年学术文章
@zh-my
2005年学术文章
@zh-sg
2005年學術文章
@yue
2005年學術文章
@zh
2005年學術文章
@zh-hant
name
Formation and stabilization mo ...... stress in Alzheimer's disease.
@en
Formation and stabilization mo ...... stress in Alzheimer's disease.
@nl
type
label
Formation and stabilization mo ...... stress in Alzheimer's disease.
@en
Formation and stabilization mo ...... stress in Alzheimer's disease.
@nl
prefLabel
Formation and stabilization mo ...... stress in Alzheimer's disease.
@en
Formation and stabilization mo ...... stress in Alzheimer's disease.
@nl
P2093
P356
P1476
Formation and stabilization mo ...... stress in Alzheimer's disease.
@en
P2093
Hajime Ohigashi
Hideyuki Hara
Kazuma Murakami
Masaya Nagao
Takahiko Shimizu
Takuji Shirasawa
P304
15168-15174
P356
10.1021/JA054041C
P407
P577
2005-11-01T00:00:00Z