Amyloid β protein inhibits cellular MTT reduction not by suppression of mitochondrial succinate dehydrogenase but by acceleration of MTT formazan exocytosis in cultured rat cortical astrocytes

[1]  D. Schubert,et al.  Cytotoxic Amyloid Peptides Inhibit Cellular 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐Diphenyltetrazolium Bromide (MTT) Reduction by Enhancing MTT Formazan Exocytosis , 1997, Journal of neurochemistry.

[2]  H. Saito,et al.  Congo red reverses amyloid β protein-induced cellular stress in astrocytes , 1997, Neuroscience Research.

[3]  D. Peterson,et al.  Mechanism of Cellular 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐Diphenyltetrazolium Bromide (MTT) Reduction , 1997, Journal of neurochemistry.

[4]  K. Abe,et al.  Human amylin mimicks amyloid β protein-induced reactive gliosis and inhibition of cellular redox activity in cultured astrocytes , 1997, Brain Research.

[5]  J. Geddes,et al.  Mechanisms of Cell Death Induced by the Mitochondrial Toxin 3-Nitropropionic Acid: Acute Excitotoxic Necrosis and Delayed Apoptosis , 1997, The Journal of Neuroscience.

[6]  K. Abe,et al.  Nanomolar Amyloid β Protein‐Induced Inhibition of Cellular Redox Activity in Cultured Astrocytes , 1997, Journal of neurochemistry.

[7]  K. Abe,et al.  Menadione toxicity in cultured rat cortical astrocytes. , 1996, Japanese journal of pharmacology.

[8]  H. Kimura,et al.  Amyloid β Toxicity Consists of a Ca2+‐Independent Early Phase and a Ca2+‐Dependent Late Phase , 1996 .

[9]  X. Chen,et al.  RAGE and amyloid-β peptide neurotoxicity in Alzheimer's disease , 1996, Nature.

[10]  A. Patel,et al.  beta-Amyloid-mediated inhibition of redox activity (MTT reduction) is not an indicator of astroglial degeneration. , 1996, Neuroreport.

[11]  J. Kemp,et al.  β‐Amyloid‐Induced Cell Toxicity: Enhancement of 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐Diphenyltetrazolium Bromide‐Dependent Cell Death , 1996, Journal of neurochemistry.

[12]  J. Glowinski,et al.  Astrocytes protect neurons from hydrogen peroxide toxicity , 1996, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[13]  I. Kaneko,et al.  Suppression of Mitochondrial Succinate Dehydrogenase, a Primary Target of β‐Amyloid, and Its Derivative Racemized at Ser Residue , 1995, Journal of neurochemistry.

[14]  M. Shearman,et al.  The Intracellular Component of Cellular 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐Diphenyltetrazolium Bromide (MTT) Reduction Is Specifically Inhibited by β‐Amyloid Peptides , 1995 .

[15]  M. Behrens,et al.  3-Nitropropionic acid induces apoptosis in cultured striatal and cortical neurons. , 1995, Neuroreport.

[16]  B. Yankner,et al.  Beta-amyloid neurotoxicity requires fibril formation and is inhibited by congo red. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[17]  Brian J Cummings,et al.  β-Amyloid-induced changes in cultured astrocytes parallel reactive astrocytosis associated with senile plaques in Alzheimer's disease , 1994, Neuroscience.

[18]  C. Behl,et al.  Hydrogen peroxide mediates amyloid β protein toxicity , 1994, Cell.

[19]  L. Hertz,et al.  Cell death in primary cultures of mouse neurons and astrocytes during exposure to and ‘recovery’ from hypoxia, substrate deprivation and simulated ischemia , 1994, Brain Research.

[20]  L. Iversen,et al.  Inhibition of PC12 cell redox activity is a specific, early indicator of the mechanism of beta-amyloid-mediated cell death. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[21]  P. May,et al.  Neurotoxicity of Human Amylin in Rat Primary Hippocampal Cultures: Similarity to Alzheimer's Disease Amyloid‐β Neurotoxicity , 1993, Journal of neurochemistry.

[22]  J. Silver,et al.  β-Amyloid of Alzheimer's Disease Induces Reactive Gliosis That Inhibits Axonal Outgrowth , 1993, Experimental Neurology.

[23]  M. Mattson,et al.  Calcium-destabilizing and neurodegenerative effects of aggregated β-amyloid peptide are attenuated by basic FGF , 1993, Brain Research.

[24]  Carl W. Cotman,et al.  In vitro aging of ß-amyloid protein causes peptide aggregation and neurotoxicity , 1991, Brain Research.

[25]  V. Renugopalakrishnan,et al.  Syntheses, structures and anorectic effects of human and rat amylin , 1991, Peptides.

[26]  D. Kirschner,et al.  Neurotrophic and neurotoxic effects of amyloid beta protein: reversal by tachykinin neuropeptides. , 1990, Science.

[27]  C. Betsholtz,et al.  Islet amyloid polypeptide: pinpointing amino acid residues linked to amyloid fibril formation. , 1990, Proceedings of the National Academy of Sciences of the United States of America.

[28]  T. Mandybur,et al.  Astrocytes and the plaques of Alzheimer's disease , 1990, Neurology.

[29]  W. Walz.  Role of glial cells in the regulation of the brain ion microenvironment , 1989, Progress in Neurobiology.

[30]  M. Nakazato,et al.  Isolation and sequence determination of ratislet amyloid polypeptide , 1989 .

[31]  A. Yu,et al.  Hypoxia-Induced Dysfunctions and Injury of Astrocytes in Primary Cell Cultures , 1989, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[32]  C. Mason,et al.  The extending astroglial process: development of glial cell shape, the growing tip, and interactions with neurons , 1988, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[33]  D. Dickson,et al.  Alzheimer's disease. A double-labeling immunohistochemical study of senile plaques. , 1988, The American journal of pathology.

[34]  M. Hatten,et al.  In vitro neurite extension by granule neurons is dependent upon astroglial-derived fibroblast growth factor. , 1988, Developmental biology.

[35]  R. Turner,et al.  Purification and characterization of a peptide from amyloid-rich pancreases of type 2 diabetic patients. , 1987, Proceedings of the National Academy of Sciences of the United States of America.

[36]  R. Busto,et al.  Astrocytes protect cultured neurons from degeneration induced by anoxia , 1987, Brain Research.

[37]  D. W. Hayden,et al.  Amyloid fibrils in human insulinoma and islets of Langerhans of the diabetic cat are derived from a neuropeptide-like protein also present in normal islet cells. , 1987, Proceedings of the National Academy of Sciences of the United States of America.

[38]  S. Furukawa,et al.  Synthesis and secretion of nerve growth factor by mouse astroglial cells in culture. , 1986, Biochemical and biophysical research communications.

[39]  M. Rapport,et al.  Glial fibrillary acidic protein and Alzheimer‐type senile dementia , 1980, Neurology.

[40]  P. Rakić,et al.  Neuron‐glia relationship during granule cell migration in developing cerebellar cortex. A Golgi and electonmicroscopic study in Macacus rhesus , 1971, The Journal of comparative neurology.

[41]  T. Slater,et al.  STUDIES ON SUCCINATE-TETRAZOLIUM REDUCTASE SYSTEMS. III. POINTS OF COUPLING OF FOUR DIFFERENT TETRAZOLIUM SALTS. , 1963, Biochimica et biophysica acta.

[42]  S. J. Smith,et al.  Do astrocytes process neural information? , 1992, Progress in brain research.