The redox chemistry of the Alzheimer's disease amyloid beta peptide.
about
Towards a unifying, systems biology understanding of large-scale cellular death and destruction caused by poorly liganded iron: Parkinson's, Huntington's, Alzheimer's, prions, bactericides, chemical toxicology and others as examplesThe role of oxidative stress in Parkinson's diseaseA partially folded structure of amyloid-beta(1-40) in an aqueous environmentNavigating the Chemical Space of Multitarget-Directed Ligands: From Hybrids to Fragments in Alzheimer's DiseaseOxidative Stress and Antioxidant Defense in Endometriosis and Its Malignant TransformationThe 5-lipoxygenase pathway: oxidative and inflammatory contributions to the Alzheimer's disease phenotypeAmyloid beta: multiple mechanisms of toxicity and only some protective effects?Ceramides in Alzheimer's Disease: Key Mediators of Neuronal Apoptosis Induced by Oxidative Stress and Aβ AccumulationResveratrol acts not through anti-aggregative pathways but mainly via its scavenging properties against Aβ and Aβ-metal complexes toxicityAmyloid-beta (Aβ) D7H mutation increases oligomeric Aβ42 and alters properties of Aβ-zinc/copper assembliesA Bacterial Component to Alzheimer’s-Type Dementia Seen via a Systems Biology Approach that Links Iron Dysregulation and Inflammagen Shedding to DiseaseCopper promotes the trafficking of the amyloid precursor proteinInvolvement of brain oxidation in the cognitive impairment in a triple transgenic mouse model of Alzheimer's disease: noninvasive measurement of the brain redox state by magnetic resonance imaging.Texture analyses of quantitative susceptibility maps to differentiate Alzheimer's disease from cognitive normal and mild cognitive impairment.Amyloid seeds formed by cellular uptake, concentration, and aggregation of the amyloid-beta peptide.Multifunctional antioxidants for the treatment of age-related diseasesMolecular basis for increased risk for late-onset Alzheimer disease due to the naturally occurring L28P mutation in apolipoprotein E4.Mechanisms of brain iron transport: insight into neurodegeneration and CNS disorders.Effect of metals on kinetic pathways of amyloid-β aggregationVascular endothelial barrier dysfunction mediated by amyloid-beta proteins.Chronic treatment with a smart antioxidative nanoparticle for inhibition of amyloid plaque propagation in Tg2576 mouse model of Alzheimer's disease.Redox control of prion and disease pathogenesis.Tissue plasminogen activator alters intracellular sequestration of zinc through interaction with the transporter ZIP4Evidence for copper-dioxygen reactivity during alpha-synuclein fibril formation.APE1/Ref-1 as an emerging therapeutic target for various human diseases: phytochemical modulation of its functionsA molecular dynamics study of the early stages of amyloid-beta(1-42) oligomerization: the role of lipid membranes.An apolipoprotein E4 fragment can promote intracellular accumulation of amyloid peptide beta 42Copper binding to the Alzheimer's disease amyloid precursor proteinToward understanding transverse relaxation in human brain through its field dependence.Reevaluation of copper(I) affinity for amyloid-β peptides by competition with ferrozine--an unusual copper(I) indicator.Lipocalin-type prostaglandin D synthase protects against oxidative stress-induced neuronal cell death.Electrochemical and homogeneous electron transfers to the Alzheimer amyloid-beta copper complex follow a preorganization mechanism.Metal chaperones: a holistic approach to the treatment of Alzheimer's diseaseHydralazine modifies Aβ fibril formation and prevents modification by lipids in vitro.Amyloid beta dimers/trimers potently induce cofilin-actin rods that are inhibited by maintaining cofilin-phosphorylationIron promotes the toxicity of amyloid beta peptide by impeding its ordered aggregation.Potential therapeutic effects of curcumin, the anti-inflammatory agent, against neurodegenerative, cardiovascular, pulmonary, metabolic, autoimmune and neoplastic diseasesAlzheimer's disease & metals: therapeutic opportunities.Elevation in sphingomyelin synthase activity is associated with increases in amyloid-beta peptide generation.PARP-1 modulates amyloid beta peptide-induced neuronal damage.
P2860
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P2860
The redox chemistry of the Alzheimer's disease amyloid beta peptide.
description
2007 nî lūn-bûn
@nan
2007年の論文
@ja
2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
2007年论文
@zh
2007年论文
@zh-cn
name
The redox chemistry of the Alzheimer's disease amyloid beta peptide.
@ast
The redox chemistry of the Alzheimer's disease amyloid beta peptide.
@en
type
label
The redox chemistry of the Alzheimer's disease amyloid beta peptide.
@ast
The redox chemistry of the Alzheimer's disease amyloid beta peptide.
@en
prefLabel
The redox chemistry of the Alzheimer's disease amyloid beta peptide.
@ast
The redox chemistry of the Alzheimer's disease amyloid beta peptide.
@en
P1476
The redox chemistry of the Alzheimer's disease amyloid beta peptide
@en
P2093
Danielle G Smith
Kevin J Barnham
P304
P356
10.1016/J.BBAMEM.2007.02.002
P407
P577
2007-02-09T00:00:00Z