Direct evidence of oxidative injury produced by the Alzheimer's β-Amyloid peptide (1-40) in cultured hippocampal neurons

Experimental Neurology

Volumn 131, Issue 2, 1995, Pages 193-202

  Harris, Marni E ^a   Hensley, Kenneth ^b   Butterfield, D Allan ^b   Leedle, Robert A ^c   Carney, John M ^a  

^a UNIVERSITY OF KENTUCKY   (United States)

^b UNIVERSITY OF KENTUCKY   (United States)

^c KANSAS STATE UNIVERSITY   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

AMYLOID BETA PROTEIN; DICHLOROFLUORESCEIN; FREE RADICAL; N TERT BUTYL ALPHA PHENYLNITRONE; UNCLASSIFIED DRUG;

ALZHEIMER DISEASE; ANIMAL CELL; ARTICLE; CALCIUM CELL LEVEL; CELL CULTURE; CONTROLLED STUDY; ELECTRON SPIN RESONANCE; EMBRYO; HIPPOCAMPUS; NONHUMAN; OXIDATIVE STRESS; PRIORITY JOURNAL; RAT;

AMYLOID BETA-PROTEIN; ANIMAL; BIOTIN; CALCIUM; CELL DEATH; CELLS, CULTURED; ELECTRON SPIN RESONANCE SPECTROSCOPY; FLUORESCEINS; FLUORESCENT DYES; FREE RADICALS; GLUTAMATE-AMMONIA LIGASE; HIPPOCAMPUS; MICROSCOPY, CONFOCAL; MICROSCOPY, FLUORESCENCE; NERVE TISSUE PROTEINS; NEURONS; OXIDATIVE STRESS; PEPTIDE FRAGMENTS; RATS; RATS, SPRAGUE-DAWLEY; SPIN LABELS; SUPPORT, U.S. GOV'T, NON-P.H.S.; SUPPORT, U.S. GOV'T, P.H.S.;

EID: 0028908516     PISSN: 00144886     EISSN: 10902430     Source Type: Journal    
DOI: 10.1016/0014-4886(95)90041-1     Document Type: Article

References (53)

1. β-Amyloid stimulates glial cells in vitro to produce growth factors that accumulate in senile plaques in alzheimer's disease
2. Alzheimer disease amyloid β protein forms calcium channels in bilayer membranes: Blockade by tromethamine and aluminum
3. Does impairment of energy metabolism result in excitotoxic neuronal death in neurodegenerative illnesses?
4. Vitamin E protects nerve cells from amyloid β protein toxicity
5. Hydrogen peroxide mediates amyloid B protein toxicity
6. Oxidative stress induced by glutamate receptor agonists
7. Assembly and aggregation properties of synthetic Alzheimer's A4/β amyloid peptide analogues
8. Methodological variables in the assessment of beta amyloid neurotoxicity
9. β-Amyloid peptide free radical fragments initiate synaptosomal lipoperoxidation in an sequence-specific fashion: Implications to Alzheimer's disease
10. Microglia
11. Amyloidogenicity of βA4 and βA4-bearing amyloid protein precursor fragments by metal-catalyzed oxidation
12. Use of salicylate with high performance liquid chromatography and electrochemical detection (LCED) as a sensitive measure of hydroxyl free radicals in adriamycin treated rats
13. Astroglia in Alzheimer's disease
14. Inactivation of key metabolic enzymes by mixed-function oxidation reactions: Possible implications in protein turnover and ageing
15. Regional specificity of membrane instability in Alzheimer's disease brain
16. Similarities between β amyloid peptides 1–40 and 40-1: Effects on aggregation, toxicity in vitro, and injection in young and aged rats
17. Secreted forms of β-amyloid precursor protein protect hippocampal neurons against amyloid β-peptide toxicity and oxidative injury
18. Detection of Oxidation Products in Individual Neurons by Fluorescence Microscopy
19. A model for β-amyloid aggregation and neurotoxicity based on free radical generation by the peptide: Relevance to Alzheimer disease
20. Relationship of microglia and astrocytes to amyloid deposits in Alzheimer's disease
21. Seeding “one-dimensional crystallization” of amyloid: A pathogenic mechanism in Alzheimer's disease and scrapie?
22. β-Amyloid protein increases the vulnerability of cultured cortical neurons to excitotoxic damage
23. Oxygen radicals in CNS damage
24. Oxidation products in endothelial cells: A fluorescence microscopic method for visualizing carbonyls in situ
25. Increased cerebral glucose-6-phosphate dehydrogenase activity in Alzheimer's disease may reflect oxidative stress
26. Outgrowthregulating actions of glutamate in isolated hippocampal pyramidal neurons
27. Isolated hippocampal neurons in cryopreserved long term culture: Development of neuroarchitecture and sensitivity to NMDA
28. β-Amyloid peptides destabilize calcium homeostasis and render human cortical neurons vulnerable to excitotoxicity
29. β-Amyloid precursor protein metabolites and loss of neuronal Ca2+ homeostasis in Alzheimer's disease
30. Calcium-destabilizing and neurodegenerative effects of aggregated β-amyloid peptide are attenuated by basic FGF
31. B-Amyloid peptide in vitro toxicity: Lot-to-lot variability
32. Aβ role of mixed-function oxidation reactions in the accumulation of altered enzyme forms during aging
33. Role of Ca2+ in toxic cell killing
34. Release of arachidonic acid by NMDA-receptor activation in the rat hippocampus
35. Aggregation-related toxicity of synthetic β-amyloid protein in hippocampal cultures
36. In vitro aging of B-amyloid protein causes peptide aggregation and neurotoxicity
37. β-Amyloid induces neuritic dystrophy in vitro: similarities with Alzheimer pathology
38. Neurodegeneration induced by β-amyloid peptides in vitro: the role of peptide assemble state
39. The involvement of astrocytes and an acute phase response in the amyloid deposition of Alzheimer's disease
40. Aβ special type of senile plaque possibly an initial stage
41. Glutamine Synthetase (Sheep Brain)
42. Biochemistry of altered brain proteins in Alzheimer's disease
43. The molecular pathology of Alzheimer's disease
44. Secondary structure of amyloid β peptide correlates with neurotoxic activity in vitro
45. Amyloid β peptides act directly on single neurons
46. Excess brain protein oxidation and enzyme dysfunction in normal aging and in Alzheimer disease
47. Metal ion catalyzed oxidation of proteins: biochemical mechanism and biological consequences
48. Autopsy samples of Alzheimer's cortex show increased peroxidation in vitro
49. Kinetics of aggregation of synthetic β-Amyloid peptide
50. Involvement of free radicals in dementia of the Alzheimer type: A hypothesis
51. Ca2+ channel blockers attenuate β-amyloid peptide toxicity to cortical neurons in culture
52. Superoxide dismutase activity in Alzheimer's disease: possible mechanism for paired helical filament formation
53. Basic FGF, NGF, and IGFs protect hippocampal and cortical neurons against iron-induced degeneration