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Volumn 76, Issue 4, 2001, Pages 1050-1056
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Neurotoxic Aβ peptides increase oxidative stress in vivo through NMDA-receptor and nitric-oxide-synthase mechanisms, and inhibit complex IV activity and induce a mitochondrial permeability transition in vitro
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Author keywords
Alzheimer's disease; Beta amyloid; Complex IV; Mitochondrial permeability transition; Neurotoxicity; Oxidative stress
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Indexed keywords
AMYLOID BETA PROTEIN;
CHLORPROMAZINE;
CYCLOSPORIN A;
CYTOCHROME C OXIDASE;
N METHYL DEXTRO ASPARTIC ACID RECEPTOR;
OXYGEN RADICAL;
RUTHENIUM RED;
AMYLOID BETA PROTEIN (1 28);
AMYLOID BETA PROTEIN (25 35);
AMYLOID BETA PROTEIN (35 25);
AMYLOID BETA PROTEIN[1-40];
AMYLOID BETA-PROTEIN (1-28);
AMYLOID BETA-PROTEIN (25-35);
AMYLOID BETA-PROTEIN (35-25);
CYCLOSPORIN;
NITRIC OXIDE SYNTHASE;
PEPTIDE FRAGMENT;
REACTIVE OXYGEN METABOLITE;
ALZHEIMER DISEASE;
ANIMAL CELL;
ARTICLE;
CONTROLLED STUDY;
ELECTRON MICROSCOPY;
ENZYME ACTIVITY;
IN VIVO STUDY;
MICRODIALYSIS;
MITOCHONDRION;
MOUSE;
NEUROTOXICITY;
NONHUMAN;
OXIDATIVE STRESS;
PRIORITY JOURNAL;
ANIMAL;
CORPUS STRIATUM;
DRUG ANTAGONISM;
DRUG EFFECT;
IN VITRO STUDY;
INTRACELLULAR MEMBRANE;
LIVER MITOCHONDRION;
MALE;
METABOLISM;
PERMEABILITY;
RAT;
SPRAGUE DAWLEY RAT;
ULTRASTRUCTURE;
WAKEFULNESS;
ANIMALIA;
AMYLOID BETA-PROTEIN;
ANIMALS;
CORPUS STRIATUM;
CYCLOSPORINE;
ELECTRON TRANSPORT COMPLEX IV;
INTRACELLULAR MEMBRANES;
MALE;
MICRODIALYSIS;
MITOCHONDRIA, LIVER;
NITRIC OXIDE SYNTHASE;
PEPTIDE FRAGMENTS;
PERMEABILITY;
RATS;
RATS, SPRAGUE-DAWLEY;
REACTIVE OXYGEN SPECIES;
RECEPTORS, N-METHYL-D-ASPARTATE;
RUTHENIUM RED;
WAKEFULNESS;
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EID: 0034745636
PISSN: 00223042
EISSN: None
Source Type: Journal
DOI: 10.1046/j.1471-4159.2001.00112.x Document Type: Article |
Times cited : (191)
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References (37)
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