Wed, 20 Aug 2008 22:18:56 BST CiteULike: psique ros http://www.citeulike.org/user/psique/tag/ros CiteULike.org en-gb Copyright © 2004-2008 citeulike.org http://www.citeulike.org/user/psique/article/2889801 <i>Brain and nerve = Shinkei kenkyū no shinpo, Vol. 60, No. 2. (February 2008), pp. 157-170.</i><br /><br />A growing body of evidence suggests oxidative stress involvement in neurodegenerative diseases; however, it remains to be determined whether oxidative stress is a cause, result, or epiphenomenon of the pathological processes. This review concerns the current issue, focusing on Alzheimer disease (AD), Parkinson disease (PD), and amyotrophic lateral sclerosis (ALS). Several studies have indicated that oxidative stress initially occurs in the disease-specific, site-restricted sources such as amyloid-beta in the cerebral cortex of AD brain, alpha-synuclein in the brain stem of PD brain, and glutamate receptor-coupled Ca2+ channel in the motor system of ALS spinal cord. Subsequent events in the neurons common to these diseases are glutamate-induced neurotoxicity and increased cytosolic Ca2+ levels, resulting in activation of Ca2+ -dependent enzymes including NADPH oxidase, cytosolic phospholipase A2, xanthine oxidase, and neuronal nitric oxide synthase (NOS). These enzymes produce reactive oxygen and nitrogen species (ROS/RNS), which oxidatively modify nucleic acid, lipid, sugar, and protein, leading to nuclear damage, mitochondrial damage, proteasome inhibition, and endoplasmic reticulum (ER) stress. Mitochondrial damage results in both ROS leakage from the electron transport system and Ca2+ release. Nuclear damage induces p53 activation, and proteasome inhibition reduces p53 degradation. The resultant increased p53 levels in the nucleus induce Bax activation and Bcl-2 inhibition, followed by a release of cytochrome c into the cytosol that truncates procaspase-9. ER stress triggers activation of caspase-12 as well as caspase-9 via the tumor necrosis factor (TNF) receptor-associated factor-2 / apoptosis-signaling kinase-1 / c-Jun N-terminal kinase pathway. Oxidative stress also stimulates astrocytes and microglia to yield and secrete cytokines such as TNFa and FasL that cause not only neuronal caspase-8 activation but also glial inflammatory response through induction of nuclear factor-kappaB-mediated, proinflammatory gene products including cytokines, chemokines, growth factors, cell adhesion molecules, and ROS/RNS-producing enzymes. The activated caspases truncate procaspase-3 to exert classical apoptosis. Moreover, oxidative DNA damage leads to the release and nuclear truncation of mitochondrial apoptosis-inducing kinase, which triggers apoptosis-like programmed cell death via cyclophilin A. These observations could indicate crucial implications for oxidative stress in several steps of the pathomechanisms of neurodegenerative diseases. [The role for oxidative stress in neurodegenerative diseases] N Shibata M Kobayashi Brain and nerve = Shinkei kenkyū no shinpo, Vol. 60, No. 2. (February 2008), pp. 157-170. 2008-06-12T17:39:29-00:00 2008 Brain and nerve = Shinkei kenkyū no shinpo 1881-6096 60 2 157 170 neurodegeneration oxidative_stress ros http://www.citeulike.org/user/psique/article/2800043 <i>Mechanisms of Ageing and Development, Vol. In Press, Corrected Proof</i><br /><br />DNA damage and mutations have been implicated as key causal events in the biological process of aging. In this context, it has been hypothesized that the complex of genome maintenance systems acts as a longevity assurance system by signaling and repairing damage or removing cells that are beyond repair. In the past, various approaches have been taken to clarify the importance of preserving genome integrity for healthy aging. Here I will briefly review these approaches in the context of the progress made in improving our understanding of the interrelationship between DNA damage, genome maintenance and mutations. The role of DNA damage and repair in aging: New approaches to an old problem Jan Vijg doi:10.1016/j.mad.2008.02.009 Mechanisms of Ageing and Development, Vol. In Press, Corrected Proof 2008-05-14T21:20:18-00:00 Mechanisms of Ageing and Development In Press, Corrected Proof aging dna ros http://www.citeulike.org/user/psique/article/2600472 <i>Nature Neuroscience, Vol. 11, No. 4. (23 March 2008), pp. 476-487.</i> Synaptic NMDA receptor activity boosts intrinsic antioxidant defenses Sofia Papadia Francesc Soriano Frédéric Léveillé Marc-Andre Martel Kelly Dakin Henrik Hansen Angela Kaindl Marco Sifringer Jill Fowler Vanya Stefovska Grahame Mckenzie Marie Craigon Roderick Corriveau Peter Ghazal Karen Horsburgh Bruce Yankner David Wyllie Chrysanthy Ikonomidou Giles Hardingham doi:10.1038/nn2071 Nature Neuroscience, Vol. 11, No. 4. (23 March 2008), pp. 476-487. 2008-03-27T04:34:10-00:00 2008 Nature Neuroscience 1097-6256 11 4 476 487 Nature Publishing Group 2008 antioxidant glutamate ros http://www.citeulike.org/user/psique/article/2158223 <i>Journal of Neurochemistry, Vol. 104, No. 2. (January 2008), pp. 298-305.</i> Mitochondrial dysfunction, oxidative stress, regulation of exocytosis and their relevance to neurodegenerative diseases Keating J Damien doi:10.1111/j.1471-4159.2007.04997.x Journal of Neurochemistry, Vol. 104, No. 2. (January 2008), pp. 298-305. 2007-12-22T03:07:17-00:00 2008 Journal of Neurochemistry 0022-3042 104 2 298 305 Blackwell Publishing 2008 mitochondria neurodegeneration ros