Access the full text.
Sign up today, get DeepDyve free for 14 days.
E. Uemura, H. Greenlee (2001)
Amyloid beta-peptide inhibits neuronal glucose uptake by preventing exocytosis.Experimental neurology, 170 2
C. Alano, W. Ying, R. Swanson (2004)
Poly(ADP-ribose) Polymerase-1-mediated Cell Death in Astrocytes Requires NAD+ Depletion and Mitochondrial Permeability Transition*Journal of Biological Chemistry, 279
F. Moroni (2008)
Poly(ADP-ribose)polymerase 1 (PARP-1) and postischemic brain damage.Current opinion in pharmacology, 8 1
C. Cecchi, C. Fiorillo, S. Sorbi, S. Latorraca, B. Nacmias, S. Bagnoli, P. Nassi, G. Liguri (2002)
Oxidative stress and reduced antioxidant defenses in peripheral cells from familial Alzheimer's patients.Free radical biology & medicine, 33 10
D. Howlett, J. Richardson, Angela Austin, A. Parsons, S. Bate, D. Davies, M. González (2004)
Cognitive correlates of Aβ deposition in male and female mice bearing amyloid precursor protein and presenilin-1 mutant transgenesBrain Research, 1017
J. Blass, G. Gibson (1991)
The role of oxidative abnormalities in the pathophysiology of Alzheimer's disease.Revue neurologique, 147 6-7
S. Andreoli, J. Mcateer, S. Seifert, S. Kempson (1993)
Oxidant-induced alterations in glucose and phosphate transport in LLC-PK1 cells: mechanisms of injury.The American journal of physiology, 265 3 Pt 2
A. Abramov, L. Canevari, M. Duchen (2004)
β-Amyloid Peptides Induce Mitochondrial Dysfunction and Oxidative Stress in Astrocytes and Death of Neurons through Activation of NADPH OxidaseThe Journal of Neuroscience, 24
J. Diefenbach, A. Bürkle (2005)
Introduction to poly(ADP-ribose) metabolism.Cellular and molecular life sciences : CMLS, 62 7-8
S. Pelech (1995)
Networking with proline-directed protein kinases implicated in Tau phosphorylationNeurobiology of Aging, 16
B. Ovbiagele, C. Kidwell, J. Saver (2005)
A Quantitative Study
E. Uemura, H. Greenlee (2001)
Amyloid β-Peptide Inhibits Neuronal Glucose Uptake by Preventing ExocytosisExperimental Neurology, 170
A. Rasola, P. Bernardi (2007)
The mitochondrial permeability transition pore and its involvement in cell death and in disease pathogenesisApoptosis, 12
A. Abramov, C. Fraley, C. Diao, R. Winkfein, M. Colicos, M. Duchen, R. French, E. Pavlov (2007)
Targeted polyphosphatase expression alters mitochondrial metabolism and inhibits calcium-dependent cell deathProceedings of the National Academy of Sciences, 104
(1998)
p40 Is Phosphorylated on Threonine 154 and Serine 315 during Activation of the Phagocyte NADPH Oxidase IMPLICATION OF A PROTEIN KINASE C-TYPE KINASE IN THE PHOSPHORYLATION PROCESS*
A. Abramov, J. Jacobson, F. Wientjes, J. Hothersall, L. Canevari, M. Duchen (2005)
Expression and Modulation of an NADPH Oxidase in Mammalian AstrocytesThe Journal of Neuroscience, 25
J. Sheehan, R. Swerdlow, Scott Miller, Davis Re, J. Parks, Parker Wd, J. Tuttle (1997)
Calcium Homeostasis and Reactive Oxygen Species Production in Cells Transformed by Mitochondria from Individuals with Sporadic Alzheimer’s DiseaseThe Journal of Neuroscience, 17
A. Bürkle (2005)
Poly(ADP‐ribose)The FEBS Journal, 272
A. Parpura-Gill, D. Beitz, E. Uemura (1997)
The inhibitory effects of β-amyloid on glutamate and glucose uptakes by cultured astrocytesBrain Research, 754
B. Chance (1976)
Pyridine Nucleotide as an Indicator of the Oxygen Requirements for Energy‐Linked Functions of MitochondriaCirculation Research, 38
A. Abramov, M. Duchen (2008)
Mechanisms underlying the loss of mitochondrial membrane potential in glutamate excitotoxicity.Biochimica et biophysica acta, 1777 7-8
M. Crompton, E. Barksby, N. Johnson, M. Capano (2002)
Mitochondrial intermembrane junctional complexes and their involvement in cell death.Biochimie, 84 2-3
S. Love, R. Barber, G. Wilcock (1999)
Increased poly(ADP-ribosyl)ation of nuclear proteins in Alzheimer's disease.Brain : a journal of neurology, 122 ( Pt 2)
Lina Du, Xiaopeng Zhang, Y. Han, N. Burke, P. Kochanek, Simon Watkins, S. Graham, J. Carcillo, C. Szabó, R. Clark (2003)
Intra-mitochondrial Poly(ADP-ribosylation) Contributes to NAD+ Depletion and Cell Death Induced by Oxidative Stress*The Journal of Biological Chemistry, 278
A. Abramov, L. Canevari, M. Duchen (2004)
Calcium signals induced by amyloid beta peptide and their consequences in neurons and astrocytes in culture.Biochimica et biophysica acta, 1742 1-3
Burkle (2005)
Poly(ADP-ribose)The most elaborate metabolite of NAD+. FEBS J, 272
C. Casley, L. Canevari, John Land, John Clark, M. Sharpe (2001)
β‐Amyloid inhibits integrated mitochondrial respiration and key enzyme activitiesJournal of Neurochemistry, 80
A. Abramov, L. Canevari, M. Duchen (2003)
Changes in Intracellular Calcium and Glutathione in Astrocytes as the Primary Mechanism of Amyloid NeurotoxicityThe Journal of Neuroscience, 23
C. Baines, R. Kaiser, N. Purcell, N. Blair, H. Osińska, Michael Hambleton, E. Brunskill, M. Sayen, R. Gottlieb, G. Dorn, J. Robbins, J. Molkentin (2005)
Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell deathNature, 434
C. Masters, G. Multhaup, G. Simms, J. Pottgiesser, R. Martins, K. Beyreuther (1985)
Neuronal origin of a cerebral amyloid: neurofibrillary tangles of Alzheimer's disease contain the same protein as the amyloid of plaque cores and blood vessels.The EMBO Journal, 4
J. Heeres, P. Hergenrother (2007)
Poly(ADP-ribose) makes a date with death.Current opinion in chemical biology, 11 6
J. Parks, Trisha Smith, P. Trimmer, J. Bennett, W. Parker (2001)
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 vitroJournal of Neurochemistry, 76
G. Wilcock, M. Esiri (1982)
Plaques, tangles and dementia A quantitative studyJournal of the Neurological Sciences, 56
J. Hardy, D. Selkoe (2009)
The Amyloid Hypothesis of Alzheimer ’ s Disease : Progress and Problems on the Road to Therapeutics
(2005)
ADP-ribose). The most elaborate metabolite of NAD +
George Perry, K. Hirai, G. Aliev, A. Nunomura, S. Siedlak, Mark Smith (2000)
Mitochondrial abnormalities in Alzheimer diseaseNeurobiology of Aging, 21
E. Shevtzova, E. Kireeva, Sergey Bachurin (2001)
Effect of beta-Amyloid Peptide Fragment 25-35 on Nonselective Permeability of MitochondriaBulletin of Experimental Biology and Medicine, 132
J. Keller, Zheng Pang, J. Geddes, J. Begley, A. Germeyer, G. Waeg, M. Mattson (1997)
Impairment of Glucose and Glutamate Transport and Induction of Mitochondrial Oxidative Stress and Dysfunction in Synaptosomes by Amyloid β‐Peptide: Role of the Lipid Peroxidation Product 4‐HydroxynonenalJournal of Neurochemistry, 69
Alzheimers disease is characterized by -amyloid accumulation in the central nervous system. As -amyloid is neurotoxic in culture, we have explored the mechanisms of toxicity in the search for therapeutic targets for Alzheimers disease and now identify a key role for poly(ADP-ribose) polymerase in -amyloid-induced neuronal death. Exposure of hippocampal neuronal/glial co-cultures to -amyloid peptides activates the glial nicotinamide adenine dinucleotide phosphate oxidase, followed by predominantly neuronal cell death. -amyloid exposure caused the progressive loss of mitochondrial membrane potential in astrocytes, accompanied by transient mitochondrial depolarizations caused by reversible openings of the mitochondrial permeability transition pore. The transients were absent in cultures from cyclophilin D knockout mice, leaving the slow depolarization available for study in isolation. -amyloid exposure decreased both nicotinamide adenine dinucleotide fluorescence and oxygen consumption, while provision of mitochondrial substrates reversed the depolarization, suggesting that substrate supply was limiting. Poly(ADP-ribose) polymerase is activated by oxidative stress and consumes nicotinamide adenine dinucleotide, decreasing substrate availability. -amyloid exposure caused accumulation of the poly(ADP-ribose) polymerase product, poly-ADP-ribose polymers, in astrocytes. Inhibition of either poly(ADP-ribose) polymerase or of the nicotinamide adenine dinucleotide phosphate oxidase prevented the appearance of poly-ADP-ribose polymers and the mitochondrial depolarization. Exposure of co-cultures to -amyloid for >8 h decreased nicotinamide adenine dinucleotide and mitochondrial membrane potential and increased cell death in neurons, all of which were prevented by poly(ADP-ribose) polymerase inhibitors. Poly-ADP-ribose polymers increased with age in the brains of the TASTPM Alzheimer mouse model. We conclude that -amyloid-induced neuronal death is mediated by poly(ADP-ribose) polymerase in response to oxidative stress generated by the astrocytic nicotinamide adenine dinucleotide phosphate oxidase.
Brain – Oxford University Press
Published: Jun 24, 2011
Keywords: amyloid PARP mitochondria reactive oxygen production NADPH oxidise
Read and print from thousands of top scholarly journals.
Already have an account? Log in
Bookmark this article. You can see your Bookmarks on your DeepDyve Library.
To save an article, log in first, or sign up for a DeepDyve account if you don’t already have one.
Copy and paste the desired citation format or use the link below to download a file formatted for EndNote
Access the full text.
Sign up today, get DeepDyve free for 14 days.
All DeepDyve websites use cookies to improve your online experience. They were placed on your computer when you launched this website. You can change your cookie settings through your browser.