Mechanism of membrane depolarization caused by the Alzheimer Aβ1-42 peptide

Biochemical and Biophysical Research Communications

Volumn 293, Issue 4, 2002, Pages 1197-1203

  Blanchard, Barbara J ^a   Thomas, Veena L ^a   Ingram, Vernon M ^a  

^a MASSACHUSETTS INSTITUTE OF TECHNOLOGY   (United States)

Author keywords

Alzheimer's disease; A 1 42 peptide; hNT Cells; Membrane depolarization; mGlu Receptors; PC12 cells; Voltage sensitive dye; Sheet formation

Indexed keywords

1 AMINO 1,5 INDANDICARBOXYLIC ACID; 2 AMINO 2 (2 CARBOXYCYCLOPROPYL) 3 (XANTHEN 9 YL)PROPIONIC ACID; 2 METHYL 6 (PHENYLETHYNYL)PYRIDINE; 4 CARBOXY 2 METHYLPHENYLGLYCINE; 6 METHYL 2 PHENYLAZO 3 PYRIDINOL; AMYLOID BETA PROTEIN; CALCIUM ION; CHOLERA TOXIN; GLUTAMIC ACID; GUANINE NUCLEOTIDE BINDING PROTEIN; METABOTROPIC RECEPTOR; METABOTROPIC RECEPTOR AGONIST; METABOTROPIC RECEPTOR ANTAGONIST; PERTUSSIS TOXIN;

ALZHEIMER DISEASE; ANIMAL CELL; ARTICLE; CALCIUM TRANSPORT; CANCER CELL CULTURE; CELL MEMBRANE DEPOLARIZATION; CONCENTRATION RESPONSE; CONTROLLED STUDY; HUMAN; HUMAN CELL; MOLECULAR MIMICRY; NERVE CELL EXCITABILITY; NERVE CELL MEMBRANE POTENTIAL; NEUROTOXICITY; NONHUMAN; PHEOCHROMOCYTOMA CELL; PRIORITY JOURNAL; RAT; TERATOCARCINOMA;

AMYLOID BETA-PROTEIN; ANIMALS; CALCIUM; CALIBRATION; CELL LINE; CELL MEMBRANE; CHOLERA TOXIN; DIMERIZATION; DOSE-RESPONSE RELATIONSHIP, DRUG; GTP-BINDING PROTEINS; HUMANS; ION CHANNELS; KINETICS; NEURONS; PC12 CELLS; PEPTIDE FRAGMENTS; PROTEIN CONFORMATION; PROTEIN STRUCTURE, SECONDARY; PROTEIN STRUCTURE, TERTIARY; RATS; RECEPTORS, AMPA; TIME FACTORS; VIRULENCE FACTORS, BORDETELLA;

RODENTIA;

EID: 0036075751     PISSN: 0006291X     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0006-291X(02)00346-7     Document Type: Article

References (21)

1. Clearing the brain's amyloid cobwebs
2. Structural model for the beta-amyloid fibril based on interstrand alignment of an antiparallel-sheet comprising a C-terminal peptide
3. Mechanism and prevention of neurotoxicity caused by beta-amyloid peptides: Relation to Alzheimer's disease
4. Elimination of β-amyloid neurotoxicity
5. The toxicity in vitro of β-amyloidprotein
6. Beta-amyloid peptides destabilize calcium homeostasis and render human cortical neurons vulnerable to excitotoxicity
7. 2+ homeostasis in Alzheimer's disease
8. Calcium-destabilizing and neurodegenerative effects of aggregated beta-amyloid peptide are attenuated by basic FGF
9. Attenuation of beta-amyloid neurotoxicity in vitro by potassium-induced depolarization
10. Compromised mitochondrial function leads to increased cytosolic calcium and to activation of MAP kinases
11. An anion binding site that regulates the glutamate transporter of synaptic vesicles
12. Use of oxonol V as a probe of membrane potential in proteoliposomes containing cytochrome oxidase in the submitochondrial orientation
13. + channel openers and glucose deprivation
14. An improved method of preparing the amyloid beta-protein for fibrillogenesis and neurotoxicity experiments
15. Comparative measurements of membrane potentials with microelectrodes and voltage-sensitive dyes
16. Protein tyrosine kinase is required for the induction of long-term potentiation in the rat hippocampus
17. Long-term potentiation in the hippocampus is blocked by tyrosine kinase inhibitors
18. Genistein inhibits protein histidine kinase
19. Selective platelet-derived growth factor receptor kinase blockers reverse sis-transformation
20. Epidermal-growth-factor-dependent activation of the src-family kinases
21. Eliminating membrane depolarization caused by the Alzheimer peptide Aβ(1-42, aggr.)