Table of Contents Author Guidelines Submit a Manuscript
Table of Contents Alerts

To receive news and publication updates for Mediators of Inflammation, enter your email address in the box below.

Mediators of Inflammation
Volume 2012, Article ID 946813, 13 pages
http://dx.doi.org/10.1155/2012/946813
Review Article

Role of Prostaglandins in Neuroinflammatory and Neurodegenerative Diseases

Isabel Vieira de Assis Lima,1 Leandro Francisco Silva Bastos,2,3 Marcelo Limborço-Filho,2 Bernd L. Fiebich,4,5 and Antonio Carlos Pinheiro de Oliveira1,4

1Department of Pharmacology, Federal University of Minas Gerais, Avenida Antonio Carlos, 6627, 31270-901 Belo Horizonte, MG, Brazil
2Department of Physiology and Biophysics, Federal University of Minas Gerais, Avenida Antonio Carlos, 6627, 31270-901 Belo Horizonte, Brazil
3Department of Psychology and Neuroscience, Muenzinger Building, Colorado University of Colorado Boulder, Avenida, Boulder, CO 80309-0354, USA
4Department of Psychiatry and Psychotherapy, University of Freiburg Medical School, Hauptstraße 5, 79104 Freiburg, Germany
5VivaCell Biotechnology GmbH, Ferdinand-Porsche-Straße 5, 79211 Denzlingen, Germany

Received 15 December 2011; Accepted 5 April 2012

Academic Editor: Lúcia Helena Faccioli

Copyright © 2012 Isabel Vieira de Assis Lima et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Linked References

  1. J. K. Andersen, “Oxidative stress in neurodegeneration: cause or consequence?” Nature Medicine, vol. 10, pp. S18–S25, 2004. View at Google Scholar · View at Scopus
  2. J. M. Craft, D. M. Watterson, and L. J. Van Eldik, “Neuroinflammation: a potential therapeutic target,” Expert Opinion on Therapeutic Targets, vol. 9, no. 5, pp. 887–900, 2005. View at Publisher · View at Google Scholar · View at Scopus
  3. D. W. Dickson, S. C. Lee, L. A. Mattiace, S. H. Yen, and C. Brosnan, “Microglia and cytokines in neurological disease, with special reference to AIDS and Alzheimer's disease,” Glia, vol. 7, no. 1, pp. 75–83, 1993. View at Google Scholar · View at Scopus
  4. J. J. Hoozemans, S. M. Chafekar, F. Baas, P. Eikelenboom, and W. Scheper, “Always around, never the same: pathways of amyloid beta induced neurodegeneration throughout the pathogenic cascade of Alzheimer's disease,” Current Medicinal Chemistry, vol. 13, no. 22, pp. 2599–2605, 2006. View at Publisher · View at Google Scholar · View at Scopus
  5. P. L. McGeer, S. Itagaki, B. E. Boyes, and E. G. McGeer, “Reactive microglia are positive for HLA-DR in the substantia nigra of Parkinson's and Alzheimer's disease brains,” Neurology, vol. 38, no. 8, pp. 1285–1291, 1988. View at Google Scholar · View at Scopus
  6. L. Minghetti, M. A. Ajmone-Cat, M. A. De Berardinis, and R. De Simone, “Microglial activation in chronic neurodegenerative diseases: roles of apoptotic neurons and chronic stimulation,” Brain Research Reviews, vol. 48, no. 2, pp. 251–256, 2005. View at Publisher · View at Google Scholar · View at Scopus
  7. M. P. Sherman, J. M. Griscavage, and L. J. Ignarro, “Nitric oxide-mediated neuronal injury in multiple sclerosis,” Medical Hypotheses, vol. 39, no. 2, pp. 143–146, 1992. View at Publisher · View at Google Scholar · View at Scopus
  8. H. M. Gao and J. S. Hong, “Why neurodegenerative diseases are progressive: uncontrolled inflammation drives disease progression,” Trends in Immunology, vol. 29, no. 8, pp. 357–365, 2008. View at Publisher · View at Google Scholar · View at Scopus
  9. S. M. Lucas, N. J. Rothwell, and R. M. Gibson, “The role of inflammation in CNS injury and disease,” British Journal of Pharmacology, vol. 147, supplement 1, pp. S232–S240, 2006. View at Publisher · View at Google Scholar · View at Scopus
  10. M. L. Block and J. S. Hong, “Microglia and inflammation-mediated neurodegeneration: multiple triggers with a common mechanism,” Progress in Neurobiology, vol. 76, no. 2, pp. 77–98, 2005. View at Publisher · View at Google Scholar · View at Scopus
  11. P. J. Jakobsson, S. Thoren, R. Morgenstern, and B. Samuelsson, “Identification of human prostaglandin E synthase: a microsomal, glutathione-dependent, inducible enzyme, constituting a potential novel drug target,” Proceedings of the National Academy of Sciences of the United States of America, vol. 96, no. 13, pp. 7220–7225, 1999. View at Publisher · View at Google Scholar · View at Scopus
  12. N. Tanikawa, Y. Ohmiya, H. Ohkubo et al., “Identification and characterization of a novel type of membrane-associated prostaglandin E synthase,” Biochemical and Biophysical Research Communications, vol. 291, no. 4, pp. 884–889, 2002. View at Publisher · View at Google Scholar · View at Scopus
  13. T. Tanioka, Y. Nakatani, N. Semmyo, M. Murakami, and I. Kudo, “Molecular identification of cytosolic prostaglandin E2 synthase that is functionally coupled with cyclooxygenase-1 in immediate prostaglandin E2 biosynthesis,” Journal of Biological Chemistry, vol. 275, no. 42, pp. 32775–32782, 2000. View at Google Scholar · View at Scopus
  14. K. Watanabe, K. Kurihara, and T. Suzuki, “Purification and characterization of membrane-bound prostaglandin E synthase from bovine heart,” Biochimica et Biophysica Acta, vol. 1439, no. 3, pp. 406–414, 1999. View at Publisher · View at Google Scholar · View at Scopus
  15. A. C. P. de Oliveira, E. Cadelario-Jalil, H. S. Bhatia, K. Lieb, M. Hull, and B. L. Fiebich, “Regulation of prostaglandin E2 synthase expression in activated primary rat microglia: evidence for uncoupled regulation of mPGES-1 and COX-2,” Glia, vol. 56, no. 8, pp. 844–855, 2008. View at Publisher · View at Google Scholar · View at Scopus
  16. A. C. de Oliveira, E. Candelario-Jalil, J. Langbein et al., “Pharmacological inhibition of Akt and downstream pathways modulates the expression of COX-2 and mPGES-1 in activated microglia,” Journal of Neuroinflammation, vol. 9, article 2, 2012. View at Publisher · View at Google Scholar
  17. L. Minghetti, “Prostaglandin E2 downregulates inducible nitric oxide synthase expression in microglia by increasing cAMP levels,” Advances in Experimental Medicine and Biology, vol. 433, pp. 181–184, 1997. View at Google Scholar · View at Scopus
  18. L. Minghetti, A. Nicolini, E. Polazzi, C. Creminon, J. Maclouf, and G. Levi, “Inducible nitric oxide synthase expression in activated rat microglial cultures is downregulated by exogenous prostaglandin E2 and by cyclooxygenase inhibitors,” Glia, vol. 19, no. 2, pp. 152–160, 1997. View at Publisher · View at Google Scholar
  19. A. O. Caggiano and R. P. Kraig, “Prostaglandin E receptor subtypes in cultured rat microglia and their role in reducing lipopolysaccharide-induced interleukin-1β production,” Journal of Neurochemistry, vol. 72, no. 2, pp. 565–575, 1999. View at Publisher · View at Google Scholar · View at Scopus
  20. J. Shi, J. Johansson, N. S. Woodling, Q. Wang, T. J. Montine, and K. Andreasson, “The prostaglandin E2 E-prostanoid 4 receptor exerts anti-inflammatory effects in brain innate immunity,” Journal of Immunology, vol. 184, no. 12, pp. 7207–7218, 2010. View at Publisher · View at Google Scholar · View at Scopus
  21. T. A. Rosenberger, N. E. Villacreses, J. T. Hovda et al., “Rat brain arachidonic acid metabolism is increased by a 6-day intracerebral ventricular infusion of bacterial lipopolysaccharide,” Journal of Neurochemistry, vol. 88, no. 5, pp. 1168–1178, 2004. View at Publisher · View at Google Scholar
  22. I. Mohri, M. Taniike, I. Okazaki et al., “Lipocalin-type prostaglandin D synthase is up-regulated in oligodendrocytes in lysosomal storage diseases and binds gangliosides,” Journal of Neurochemistry, vol. 97, no. 3, pp. 641–651, 2006. View at Publisher · View at Google Scholar · View at Scopus
  23. I. Mohri, K. Kadoyama, T. Kanekiyo et al., “Hematopoietic prostaglandin D synthase and DP1 receptor are selectively upregulated in microglia and astrocytes within senile plaques from human patients and in a mouse model of Alzheimer disease,” Journal of Neuropathology & Experimental Neurology, vol. 66, no. 6, pp. 469–480, 2007. View at Publisher · View at Google Scholar · View at Scopus
  24. Z. Xiang, T. Lin, and S. A. Reeves, “15d-PGJ2 induces apoptosis of mouse oligodendrocyte precursor cells,” Journal of Neuroinflammation, vol. 4, article 18, 2007. View at Publisher · View at Google Scholar · View at Scopus
  25. M. Taniike, I. Mohri, N. Eguchi, C. T. Beuckmann, K. Suzuki, and Y. Urade, “Perineuronal oligodendrocytes protect against neuronal apoptosis through the production of lipocalin-type prostaglandin D synthase in a genetic demyelinating model,” Journal of Neuroscience, vol. 22, no. 12, pp. 4885–4896, 2002. View at Google Scholar · View at Scopus
  26. A. Bernardo, G. Levi, and L. Minghetti, “Role of the peroxisome proliferator-activated receptor-γ (PPAR-γ) and its natural ligand 15-deoxy-Δ12,14-prostaglandin J2 in the regulation of microglial functions,” European Journal of Neuroscience, vol. 12, no. 7, pp. 2215–2223, 2000. View at Publisher · View at Google Scholar · View at Scopus
  27. N. K. Phulwani, D. L. Feinstein, V. Gavrilyuk, C. Akar, and T. Kielian, “15-Deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) and ciglitazone modulate Staphylococcus aureus-dependent astrocyte activation primarily through a PPAR-γ-independent pathway,” Journal of Neurochemistry, vol. 99, no. 5, pp. 1389–1402, 2006. View at Publisher · View at Google Scholar · View at Scopus
  28. M. J. Tsai, S. K. Shyue, C. F. Weng et al., “Effect of enhanced prostacyclin synthesis by adenovirus-mediated transfer on lipopolysaccharide stimulation in neuron-glia cultures,” Annals of the New York Academy of Sciences, vol. 1042, pp. 338–348, 2005. View at Publisher · View at Google Scholar · View at Scopus
  29. T. Satoh, Y. Ishikawa, Y. Kataoka et al., “CNS-specific prostacyclin ligands as neuronal survival-promoting factors in the brain,” European Journal of Neuroscience, vol. 11, no. 9, pp. 3115–3124, 1999. View at Publisher · View at Google Scholar · View at Scopus
  30. H. Takamatsu, H. Tsukada, Y. Watanabe et al., “Specific ligand for a central type prostacyclin receptor attenuates neuronal damage in a rat model of focal cerebral ischemia,” Brain Research, vol. 925, no. 2, pp. 176–182, 2002. View at Publisher · View at Google Scholar · View at Scopus
  31. W. Li, S. Wu, R. W. Hickey, M. E. Rose, J. Chen, and S. H. Graham, “Neuronal cyclooxygenase-2 activity and prostaglandins PGE2, PGD2, and PGF2α exacerbate hypoxic neuronal injury in neuron-enriched primary culture,” Neurochemical Research, vol. 33, no. 3, pp. 490–499, 2008. View at Publisher · View at Google Scholar · View at Scopus
  32. C. Brenneis, O. Coste, K. Altenrath et al., “Anti-inflammatory role of microsomal prostaglandin E synthase-1 in a model of neuroinflammation,” The Journal of Biological Chemistry, vol. 286, pp. 2331–2342, 2011. View at Google Scholar
  33. S. Saleem, A. S. Ahmad, T. Maruyama, S. Narumiya, and S. Dore, “PGF2α FP receptor contributes to brain damage following transient focal brain ischemia,” Neurotoxicity Research, vol. 15, no. 1, pp. 62–70, 2009. View at Publisher · View at Google Scholar · View at Scopus
  34. A. Compston and A. Coles, “Multiple sclerosis,” The Lancet, vol. 359, no. 9313, pp. 1221–1231, 2002. View at Publisher · View at Google Scholar · View at Scopus
  35. A. R. Pachner, “Experimental models of multiple sclerosis,” Current Opinion in Neurology, vol. 24, no. 3, pp. 291–299, 2011. View at Publisher · View at Google Scholar · View at Scopus
  36. A. Kalyvas and S. David, “Cytosolic phospholipase A2 plays a key role in the pathogenesis of multiple sclerosis-like disease,” Neuron, vol. 41, no. 3, pp. 323–335, 2004. View at Publisher · View at Google Scholar · View at Scopus
  37. S. Marusic, M. W. Leach, J. W. Pelker et al., “Cytosolic phospholipase A2α-deficient mice are resistant to experimental autoimmune encephalomyelitis,” Journal of Experimental Medicine, vol. 202, no. 6, pp. 841–851, 2005. View at Publisher · View at Google Scholar · View at Scopus
  38. S. Marusic, P. Thakker, J. W. Pelker et al., “Blockade of cytosolic phospholipase A2α prevents experimental autoimmune encephalomyelitis and diminishes development of Th1 and Th17 responses,” Journal of Neuroimmunology, vol. 204, no. 1-2, pp. 29–37, 2008. View at Publisher · View at Google Scholar · View at Scopus
  39. P. Thakker, S. Marusic, N.L. Stedman et al., “Cytosolic phospholipase A2α blockade abrogates disease during the tissue-damage effector phase of experimental autoimmune encephalomyelitis by its action on APCs,” Journal of Immunology, vol. 187, no. 4, pp. 1986–1997, 2011. View at Publisher · View at Google Scholar
  40. A. Kalyvas, C. Baskakis, V. Magrioti et al., “Differing roles for members of the phospholipase A2 superfamily in experimental autoimmune encephalomyelitis,” Brain, vol. 132, no. 5, pp. 1221–1235, 2009. View at Publisher · View at Google Scholar · View at Scopus
  41. S. S. Ayoub, E. G. Wood, S. U. Hassan, and C. Bolton, “Cyclooxygenase expression and prostaglandin levels in central nervous system tissues during the course of chronic relapsing experimental autoimmune encephalomyelitis (EAE),” Inflammation Research, vol. 60, no. 10, pp. 919–928, 2011. View at Publisher · View at Google Scholar · View at Scopus
  42. P. G. Weston and P. V. Johnston, “Incidence and severity of experimental allergic encephalomyelitis and cerebral prostaglandin synthesis in essential fatty acid deficient and aspirin-treated rats,” Lipids, vol. 13, no. 12, pp. 867–872, 1978. View at Google Scholar · View at Scopus
  43. A. T. Reder, M. Thapar, A. M. Sapugay, and M. A. Jensen, “Prostaglandins and inhibitors of arachidonate metabolism suppress experimental allergic encephalomyelitis,” Journal of Neuroimmunology, vol. 54, no. 1-2, pp. 117–127, 1994. View at Publisher · View at Google Scholar · View at Scopus
  44. C. Bolton, D. Gordon, and J. L. Turk, “A longitudinal study of the prostaglandin content of central nervous system tissues from guinea pigs with acute experimental allergic encephalomyelitis (EAE),” International Journal of Immunopharmacology, vol. 6, no. 2, pp. 155–161, 1984. View at Publisher · View at Google Scholar · View at Scopus
  45. Y. Pollak, H. Ovadia, E. Orion, J. Weidenfeld, and R. Yirmiya, “The EAE-associated behavioral syndrome: I. Temporal correlation with inflammatory mediators,” Journal of Neuroimmunology, vol. 137, no. 1-2, pp. 94–99, 2003. View at Publisher · View at Google Scholar · View at Scopus
  46. Y. Kihara, T. Matsushita, Y. Kita et al., “Targeted lipidomics reveals mPGES-1-PGE2 as a therapeutic target for multiple sclerosis,” Proceedings of the National Academy of Sciences of the United States of America, vol. 106, no. 51, pp. 21807–21812, 2009. View at Publisher · View at Google Scholar · View at Scopus
  47. Y. Esaki, Y. Li, D. Sakata et al., “Dual roles of PGE2-EP4 signaling in mouse experimental autoimmune encephalomyelitis,” Proceedings of the National Academy of Sciences of the United States of America, vol. 107, no. 27, pp. 12233–12238, 2010. View at Publisher · View at Google Scholar · View at Scopus
  48. G. A. Fitzgerald, “Coxibs and cardiovascular disease,” The New England Journal of Medicine, vol. 351, no. 17, pp. 1709–1711, 2004. View at Publisher · View at Google Scholar · View at Scopus
  49. L. F. S. Bastos, A. C. P. de Oliveira, J. C. M. Schlachetzki, and B. L. Fiebich, “Minocycline reduces prostaglandin E synthase expression and 8-isoprostane formation in LPS-activated primary rat microglia,” Immunopharmacology and Immunotoxicology, vol. 33, no. 3, pp. 576–580, 2011. View at Publisher · View at Google Scholar · View at Scopus
  50. E. Candelario-Jalil, A. C. P. de Oliveira, S. Graf et al., “Resveratrol potently reduces prostaglandin E2 production and free radical formation in lipopolysaccharide-activated primary rat microglia,” Journal of Neuroinflammation, vol. 4, article 25, 2007. View at Publisher · View at Google Scholar · View at Scopus
  51. M. D. Guerrero, M. Aquino, I. Bruno, R. Riccio, M. C. Terencio, and M. Payá, “Anti-inflammatory and analgesic activity of a novel inhibitor of microsomal prostaglandin E synthase-1 expression,” European Journal of Pharmacology, vol. 620, no. 1–3, pp. 112–119, 2009. View at Publisher · View at Google Scholar · View at Scopus
  52. C. Natarajan and J. J. Bright, “Peroxisome proliferator-activated receptor-gamma agonist inhibit experimental allergic encephalomyelitis by blocking IL-12 production, IL-12 signaling and Th1 differentiation,” Genes and Immunity, vol. 3, no. 2, pp. 59–70, 2002. View at Publisher · View at Google Scholar · View at Scopus
  53. A. Diab, C. Deng, J. D. Smith et al., “Peroxisome proliferator-activated receptor-γ agonist 15-deoxy-Δ12,14-prostaglandin J2 ameliorates experimental autoimmune encephalomyelitis,” Journal of Immunology, vol. 168, no. 5, pp. 2508–2515, 2002. View at Google Scholar · View at Scopus
  54. P. D. Storer, J. Xu, J. Chavis, and P. D. Drew, “Peroxisome proliferator-activated receptor-gamma agonists inhibit the activation of microglia and astrocytes: implications for multiple sclerosis,” Journal of Neuroimmunology, vol. 161, no. 1-2, pp. 113–122, 2005. View at Publisher · View at Google Scholar · View at Scopus
  55. J. Xu and P. D. Drew, “Peroxisome proliferator-activated receptor-γ agonists suppress the production of IL-12 family cytokines by activated glia,” Journal of Immunology, vol. 178, no. 3, pp. 1904–1913, 2007. View at Google Scholar · View at Scopus
  56. H. P. Raikwar, G. Muthian, J. Rajasingh, C. N. Johnson, and J. J. Bright, “PPARγ antagonists reverse the inhibition of neural antigen-specific Th1 response and experimental allergic encephalomyelitis by Ciglitazone and 15-Deoxy-Δ12,14-Prostaglandin J2,” Journal of Neuroimmunology, vol. 178, no. 1-2, pp. 76–86, 2006. View at Publisher · View at Google Scholar · View at Scopus
  57. R. Pedotti, J. J. DeVoss, S. Youssef et al., “Multiple elements of the allergic arm of the immune response modulate autoimmune demyelination,” Proceedings of the National Academy of Sciences of the United States of America, vol. 100, no. 4, pp. 1867–1872, 2003. View at Publisher · View at Google Scholar · View at Scopus
  58. Y. Fujitani, Y. Kanaoka, K. Aritake, N. Uodome, K. Okazaki-Hatake, and Y. Urade, “Pronounced eosinophilic lung inflammation and Th2 cytokine release in human lipocalin-type prostaglandin D synthase transgenic mice,” Journal of Immunology, vol. 168, no. 1, pp. 443–449, 2002. View at Google Scholar · View at Scopus
  59. T. Matsuoka, M. Hirata, H. Tanaka et al., “Prostaglandin D2 as a mediator of allergic asthma,” Science, vol. 287, no. 5460, pp. 2013–2017, 2000. View at Publisher · View at Google Scholar · View at Scopus
  60. P. L. McGeer, H. Akiyama, S. Itagaki, and E. G. McGeer, “Activation of the classical complement pathway in brain tissue of Alzheimer patients,” Neuroscience Letters, vol. 107, no. 1–3, pp. 341–346, 1989. View at Publisher · View at Google Scholar · View at Scopus
  61. P. L. McGeer, H. Akiyama, S. Itagaki, and E. G. McGeer, “Immune system response in Alzheimer's disease,” Canadian Journal of Neurological Sciences, vol. 16, no. 4, pp. 516–527, 1989. View at Google Scholar · View at Scopus
  62. P. L. McGeer, S. Itagaki, H. Tago, and E. G. McGeer, “Reactive microglia in patients with senile dementia of the Alzheimer type are positive for the histocompatibility glycoprotein HLA-DR,” Neuroscience Letters, vol. 79, no. 1-2, pp. 195–200, 1987. View at Google Scholar · View at Scopus
  63. J. Rogers, J. Luber-Narod, S. D. Styren, and W. H. Civin, “Expression of immune system-associated antigens by cells of the human central nervous system: relationship to the pathology of Alzheimer's disease,” Neurobiology of Aging, vol. 9, no. 4, pp. 339–349, 1988. View at Google Scholar · View at Scopus
  64. J. M. Rozemuller, P. Eikelenboom, S. T. Pals, and F. C. Stam, “Microglial cells around amyloid plaques in Alzheimer's disease express leucocyte adhesion molecules of the LFA-1 family,” Neuroscience Letters, vol. 101, no. 3, pp. 288–292, 1989. View at Google Scholar · View at Scopus
  65. P. L. McGeer, E. McGeer, J. Rogers, and J. Sibley, “Anti-inflammatory drugs and Alzheimer disease,” The Lancet, vol. 335, no. 8696, p. 1037, 1990. View at Google Scholar · View at Scopus
  66. J. Rogers, L. C. Kirby, S. R. Hempelman et al., “Clinical trial of indomethacin in Alzheimer's disease,” Neurology, vol. 43, no. 8, pp. 1609–1611, 1993. View at Google Scholar · View at Scopus
  67. K. P. Townsend and D. Pratico, “Novel therapeutic opportunities for Alzheimer's disease: focus on nonsteroidal anti-inflammatory drugs,” The FASEB Journal, vol. 19, no. 12, pp. 1592–1601, 2005. View at Publisher · View at Google Scholar · View at Scopus
  68. D. T. Stephenson, C. A. Lemere, D. J. Selkoe, and J. A. Clemens, “Cytosolic phospholipase A2 (cPLA2) immunoreactivity is elevated in Alzheimer's disease brain,” Neurobiology of Disease, vol. 3, no. 1, pp. 51–63, 1996. View at Publisher · View at Google Scholar · View at Scopus
  69. C. Chen, J. C. Magee, and N. G. Bazan, “Cyclooxygenase-2 regulates prostaglandin E2 signaling in hippocampal long-term synaptic plasticity,” Journal of Neurophysiology, vol. 87, no. 6, pp. 2851–2857, 2002. View at Google Scholar · View at Scopus
  70. C. Chen and N. G. Bazan, “Endogenous PGE2 regulates membrane excitability and synaptic transmission in hippocampal CA1 pyramidal neurons,” Journal of Neurophysiology, vol. 93, no. 2, pp. 929–941, 2005. View at Publisher · View at Google Scholar · View at Scopus
  71. J. J. Hoozemans, A. J. Rozemuller, I. Janssen, C. J. De Groot, R. Veerhuis, and P. Eikelenboom, “Cyclooxygenase expression in microglia and neurons in Alzheimer's disease and control brain,” Acta Neuropathologica, vol. 101, no. 1, pp. 2–8, 2001. View at Google Scholar · View at Scopus
  72. K. Yasojima, C. Schwab, E. G. McGeer, and P. L. McGeer, “Distribution of cyclooxygenase-1 and cyclooxygenase-2 mRNAs and proteins in human brain and peripheral organs,” Brain Research, vol. 830, no. 2, pp. 226–236, 1999. View at Publisher · View at Google Scholar · View at Scopus
  73. U. Chaudhry, H. Zhuang, and S. Dore, “Microsomal prostaglandin E synthase-2: cellular distribution and expression in Alzheimer's disease,” Experimental Neurology, vol. 223, no. 2, pp. 359–365, 2010. View at Publisher · View at Google Scholar · View at Scopus
  74. U. A. Chaudhry, H. Zhuang, B. J. Crain, and S. Dore, “Elevated microsomal prostaglandin-E synthase-1 in Alzheimer's disease,” Alzheimer's and Dementia, vol. 4, no. 1, pp. 6–13, 2008. View at Publisher · View at Google Scholar · View at Scopus
  75. T. J. Montine, K. R. Sidell, B. C. Crews et al., “Elevated CSF prostaglandin E2 levels in patients with probable AD,” Neurology, vol. 53, no. 7, pp. 1495–1498, 1999. View at Google Scholar · View at Scopus
  76. T. Hoshino, T. Namba, M. Takehara et al., “Prostaglandin E2 stimulates the production of amyloid-β peptides through internalization of the EP4 receptor,” Journal of Biological Chemistry, vol. 284, no. 27, pp. 18493–18502, 2009. View at Publisher · View at Google Scholar · View at Scopus
  77. R. K. Lee, S. Knapp, and R. J. Wurtman, “Prostaglandin E2 stimulates amyloid precursor protein gene expression: inhibition by immunosuppressants,” Journal of Neuroscience, vol. 19, no. 3, pp. 940–947, 1999. View at Google Scholar · View at Scopus
  78. A. M. Pooler, A. A. Arjona, R. K. Lee, and R. J. Wurtman, “Prostaglandin E2 regulates amyloid precursor protein expression via the EP2 receptor in cultured rat microglia,” Neuroscience Letters, vol. 362, no. 2, pp. 127–130, 2004. View at Publisher · View at Google Scholar · View at Scopus
  79. T. Hoshino, T. Nakaya, T. Homan et al., “Involvement of prostaglandin E2 in production of amyloid-β peptides both in vitro and in vivo,” Journal of Biological Chemistry, vol. 282, no. 45, pp. 32676–32688, 2007. View at Publisher · View at Google Scholar · View at Scopus
  80. L. A. Kotilinek, M. A. Westerman, Q. Wang et al., “Cyclooxygenase-2 inhibition improves amyloid-β-mediated suppression of memory and synaptic plasticity,” Brain, vol. 131, no. 3, pp. 651–664, 2008. View at Publisher · View at Google Scholar · View at Scopus
  81. A. Savonenko, P. Munoz, T. Melnikova et al., “Impaired cognition, sensorimotor gating, and hippocampal long-term depression in mice lacking the prostaglandin E2 EP2 receptor,” Experimental Neurology, vol. 217, no. 1, pp. 63–73, 2009. View at Publisher · View at Google Scholar · View at Scopus
  82. N. Iwamoto, K. Kobayashi, and K. Kosaka, “The formation of prostaglandins in the postmortem cerebral cortex of Alzheimer-type dementia patients,” Journal of Neurology, vol. 236, no. 2, pp. 80–84, 1989. View at Google Scholar · View at Scopus
  83. T. T. Rohn, S. M. Wong, C. W. Cotman, and D. H. Cribbs, “15-Deoxy-Δ12,14-prostaglandin J2, a specific ligand for peroxisome proliferator-activated receptor-γ, induces neuronal apoptosis,” NeuroReport, vol. 12, no. 4, pp. 839–843, 2001. View at Google Scholar · View at Scopus
  84. K. Takata, Y. Kitamura, M. Umeki et al., “Possible involvement of small oligomers of amyloid-β peptides in 15-deoxy-Δ12,14 prostaglandin J2-sensitive microglial activation,” Journal Pharmacological Sciences, vol. 91, no. 4, pp. 330–333, 2003. View at Google Scholar · View at Scopus
  85. H. Chen, S. M. Zhang, M. A. Hernan et al., “Nonsteroidal anti-inflammatory drugs and the risk of Parkinson disease,” Archives of Neurology, vol. 60, no. 8, pp. 1059–1064, 2003. View at Publisher · View at Google Scholar · View at Scopus
  86. Y. C. Chung, H. W. Ko, E. Bok et al., “The role of neuroinflammation on the pathogenesis of Parkinson's disease,” BMB Reports, vol. 43, no. 4, pp. 225–232, 2010. View at Google Scholar · View at Scopus
  87. A. MacHado, A. J. Herrera, J. L. Venero et al., “Peripheral inflammation increases the damage in animal models of nigrostriatal dopaminergic neurodegeneration: possible implication in parkinson's disease incidence,” Parkinson's Disease, vol. 2011, Article ID 393769, 10 pages, 2011. View at Publisher · View at Google Scholar · View at Scopus
  88. E. C. Hirsch, “Glial cells and Parkinson's disease,” Journal of Neurology, vol. 247, supplement 2, pp. II58–II62, 2000. View at Google Scholar · View at Scopus
  89. G. W. Kreutzberg, “Principles of neuronal regeneration,” Acta Neurochirurgica, vol. 66, pp. 103–106, 1996. View at Google Scholar · View at Scopus
  90. P. Klivenyi, M. F. Beal, R. J. Ferrante et al., “Mice deficient in group IV cytosolic phospholipase A2 are resistant to MPTP neurotoxicity,” Journal of Neurochemistry, vol. 71, no. 6, pp. 2634–2637, 1998. View at Google Scholar · View at Scopus
  91. T. Hayakawa, M. C. Chang, S. I. Rapoport, and N. M. Appel, “Selective dopamine receptor stimulation differentially affects [3H]arachidonic acid incorporation, a surrogate marker for phospholipase A2-mediated neurotransmitter signal transduction, in a rodent model of Parkinson's disease,” Journal of Pharmacology and Experimental Therapeutics, vol. 296, no. 3, pp. 1074–1084, 2001. View at Google Scholar · View at Scopus
  92. A. Przybylkowski, I. Kurkowska-Jastrzebska, I. Joniec, A. Ciesielska, A. Czlonkowska, and A. Czlonkowski, “Cyclooxygenases mRNA and protein expression in striata in the experimental mouse model of Parkinson's disease induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine administration to mouse,” Brain Research, vol. 1019, no. 1-2, pp. 144–151, 2004. View at Publisher · View at Google Scholar · View at Scopus
  93. P. Teismann, K. Tieu, D. K. Choi et al., “Cyclooxygenase-2 is instrumental in Parkinson's disease neurodegeneration,” Proceedings of the National Academy of Sciences of the United States of America, vol. 100, no. 9, pp. 5473–5478, 2003. View at Publisher · View at Google Scholar · View at Scopus
  94. T. Wang, Z. Pei, W. Zhang et al., “MPP+-induced COX-2 activation and subsequent dopaminergic neurodegeneration,” The FASEB Journal, vol. 19, no. 9, pp. 1134–1136, 2005. View at Publisher · View at Google Scholar · View at Scopus
  95. C. Knott, G. Stern, and G. P. Wilkin, “Inflammatory regulators in Parkinson's disease: iNOS, lipocortin-1, and cyclooxygenases-1 and -2,” Molecular and Cellular Neuroscience, vol. 16, no. 6, pp. 724–739, 2000. View at Publisher · View at Google Scholar · View at Scopus
  96. P. Teismann, M. Vila, D. K. Choi et al., “COX-2 and neurodegeneration in Parkinson's disease,” Annals of the New York Academy of Sciences, vol. 991, pp. 272–277, 2003. View at Google Scholar · View at Scopus
  97. R. Sanchez-Pernaute, A. Ferree, O. Cooper, M. Yu, A. L. Brownell, and O. Isacson, “Selective COX-2 inhibition prevents progressive dopamine neuron degeneration in a rat model of Parkinson's disease,” Journal of Neuroinflammation, vol. 1, article 6, 2004. View at Publisher · View at Google Scholar · View at Scopus
  98. P. Teismann and B. Ferger, “Inhibition of the cyclooxygenase isoenzymes COX-1 and COX-2 provide neuroprotection in the MPTP-mouse model of Parkinson's disease,” Synapse, vol. 39, no. 2, pp. 167–174, 2001. View at Google Scholar
  99. R. Vijitruth, M. Liu, D. Y. Choi, X. V. Nguyen, R. L. Hunter, and G. Bing, “Cyclooxygenase-2 mediates microglial activation and secondary dopaminergic cell death in the mouse MPTP model of Parkinson's disease,” Journal of Neuroinflammation, vol. 3, article 6, 2006. View at Publisher · View at Google Scholar · View at Scopus
  100. Z. Feng, D. Li, P. C. Fung, Z. Pei, D. B. Ramsden, and S. L. Ho, “COX-2-deficient mice are less prone to MPTP-neurotoxicity than wild-type mice,” NeuroReport, vol. 14, no. 15, pp. 1927–1929, 2003. View at Publisher · View at Google Scholar · View at Scopus
  101. Z. H. Feng, T. G. Wang, D. D. Li et al., “Cyclooxygenase-2-deficient mice are resistant to 1-methyl-4-phenyl1, 2, 3, 6-tetrahydropyridine-induced damage of dopaminergic neurons in the substantia nigra,” Neuroscience Letters, vol. 329, no. 3, pp. 354–358, 2002. View at Publisher · View at Google Scholar · View at Scopus
  102. H. Chen, E. Jacobs, M. A. Schwarzschild et al., “Nonsteroidal antiinflammatory drug use and the risk for Parkinson's disease,” Annals of Neurology, vol. 58, no. 6, pp. 963–967, 2005. View at Publisher · View at Google Scholar · View at Scopus
  103. J. A. Driver, G. Logroscino, L. Lu, J. M. Gaziano, and T. Kurth, “Use of non-steroidal anti-inflammatory drugs and risk of Parkinson's disease: nested case-control study,” British Medical Journal, vol. 342, p. d198, 2011. View at Publisher · View at Google Scholar · View at Scopus
  104. A. Samii, M. Etminan, M. O. Wiens, and S. Jafari, “NSAID use and the risk of parkinsons disease: systematic review and meta-analysis of observational studies,” Drugs and Aging, vol. 26, no. 9, pp. 769–779, 2009. View at Publisher · View at Google Scholar · View at Scopus
  105. E. Esposito, V. Di Matteo, A. Benigno, M. Pierucci, G. Crescimanno, and G. Di Giovanni, “Non-steroidal anti-inflammatory drugs in Parkinson's disease,” Experimental Neurology, vol. 205, no. 2, pp. 295–312, 2007. View at Publisher · View at Google Scholar · View at Scopus
  106. M. B. Mattammal, R. Strong, V. M. Lakshmi, H. D. Chung, and A. H. Stephenson, “Prostaglandin H synthetase-mediated metabolism of dopamine: implication for Parkinson's disease,” Journal of Neurochemistry, vol. 64, no. 4, pp. 1645–1654, 1995. View at Google Scholar · View at Scopus
  107. W. Zhang, T. Wang, Z. Pei et al., “Aggregated α-synuclein activates microglia: a process leading to disease progression in Parkinson's disease,” The FASEB Journal, vol. 19, no. 6, pp. 533–542, 2005. View at Publisher · View at Google Scholar · View at Scopus
  108. I. Branchi, I. D'Andrea, M. Armida et al., “Striatal 6-OHDA lesion in mice: investigating early neurochemical changes underlying Parkinson's disease,” Behavioural Brain Research, vol. 208, no. 1, pp. 137–143, 2010. View at Google Scholar · View at Scopus
  109. E. Carrasco, D. Casper, and P. Werner, “PGE2 receptor EP1 renders dopaminergic neurons selectively vulnerable to low-level oxidative stress and direct PGE2 neurotoxicity,” Journal of Neuroscience Research, vol. 85, no. 14, pp. 3109–3117, 2007. View at Publisher · View at Google Scholar · View at Scopus
  110. E. Carrasco, P. Werner, and D. Casper, “Prostaglandin receptor EP2 protects dopaminergic neurons against 6-OHDA-mediated low oxidative stress,” Neuroscience Letters, vol. 441, no. 1, pp. 44–49, 2008. View at Publisher · View at Google Scholar · View at Scopus
  111. J. Jin, F. S. Shie, J. Liu et al., “Prostaglandin E2 receptor subtype 2 (EP2) regulates microglial activation and associated neurotoxicity induced by aggregated α-synuclein,” Journal of Neuroinflammation, vol. 4, article 2, 2007. View at Publisher · View at Google Scholar · View at Scopus
  112. G. Aldini, M. Carini, G. Vistoli et al., “Identification of actin as a 15-deoxy-Δ12,14-prostaglandin J2 target in neuroblastoma cells: mass spectrometric, computational, and functional approaches to investigate the effect on cytoskeletal derangement,” Biochemistry, vol. 46, no. 10, pp. 2707–2718, 2007. View at Publisher · View at Google Scholar · View at Scopus
  113. K. D. Ogburn and M. E. Figueiredo-Pereira, “Cytoskeleton/endoplasmic reticulum collapse induced by prostaglandin J2 parallels centrosomal deposition of ubiquitinated protein aggregates,” Journal of Biological Chemistry, vol. 281, no. 32, pp. 23274–23284, 2006. View at Publisher · View at Google Scholar · View at Scopus
  114. Z. Li, F. Melandri, I. Berdo et al., “Δ12-Prostaglandin J2 inhibits the ubiquitin hydrolase UCH-L1 and elicits ubiquitin-protein aggregation without proteasome inhibition,” Biochemical and Biophysical Research Communications, vol. 319, no. 4, pp. 1171–1180, 2004. View at Publisher · View at Google Scholar · View at Scopus
  115. L. M. Koharudin, H. Liu, R. Di Maio, R. B. Kodali, S. H. Graham, and A. M. Gronenborn, “Cyclopentenone prostaglandin-induced unfolding and aggregation of the Parkinson disease-associated UCH-L1,” Proceedings of the National Academy of Sciences of the United States of America, vol. 107, no. 15, pp. 6835–6840, 2010. View at Publisher · View at Google Scholar · View at Scopus
  116. X. Wang, Z. H. Qin, Y. Leng et al., “Prostaglandin A1 inhibits rotenone-induced apoptosis in SH-SY5Y cells,” Journal of Neurochemistry, vol. 83, no. 5, pp. 1094–1102, 2002. View at Publisher · View at Google Scholar · View at Scopus
  117. L. Lacomblez, G. Bensimon, P. N. Leigh, P. Guillet, and V. Meininger, “Dose-ranging study of riluzole in amyotrophic lateral sclerosis,” The Lancet, vol. 347, no. 9013, pp. 1425–1431, 1996. View at Google Scholar · View at Scopus
  118. J. P. Julien, “Amyotrophic lateral sclerosis: unfolding the toxicity of the misfolded,” Cell, vol. 104, no. 4, pp. 581–591, 2001. View at Publisher · View at Google Scholar · View at Scopus
  119. K. Moisse and M. J. Strong, “Innate immunity in amyotrophic lateral sclerosis,” Biochimica et Biophysica Acta, vol. 1762, no. 11-12, pp. 1083–1093, 2006. View at Publisher · View at Google Scholar · View at Scopus
  120. M. Kiaei, K. Kipiani, S. Petri et al., “Integrative role of cPLA2 with COX-2 and the effect of non-steriodal anti-inflammatory drugs in a transgenic mouse model of amyotrophic lateral sclerosis,” Journal of Neurochemistry, vol. 93, no. 2, pp. 403–411, 2005. View at Publisher · View at Google Scholar · View at Scopus
  121. D. Stephenson, K. Rash, B. Smalstig et al., “Cytosolic phospholipase A2 is induced in reactive glia following different forms of neurodegeneration,” Glia, vol. 27, pp. 110–128, 1999. View at Google Scholar
  122. N. Shibata, A. Kakita, H. Takahashi et al., “Increased expression and activation of cytosolic phospholipase A2 in the spinal cord of patients with sporadic amyotrophic lateral sclerosis,” Acta Neuropathologica, vol. 119, no. 3, pp. 345–354, 2010. View at Publisher · View at Google Scholar · View at Scopus
  123. G. Almer, C. Guegan, P. Teismann et al., “Increased expression of the pro-inflammatory enzyme cyclooxygenase-2 in amyotrophic lateral sclerosis,” Annals of Neurology, vol. 49, no. 2, pp. 176–185, 2001. View at Google Scholar
  124. X. Liang, Q. Wang, J. Shi et al., “The prostaglandin E2 EP2 receptor accelerates disease progression and inflammation in a model of amyotrophic lateral sclerosis,” Annals of Neurology, vol. 64, no. 3, pp. 304–314, 2008. View at Publisher · View at Google Scholar · View at Scopus
  125. G. Almer, P. Teismann, Z. Stevic et al., “Increased levels of the pro-inflammatory prostaglandin PGE2 in CSF from ALS patients,” Neurology, vol. 58, no. 8, pp. 1277–1279, 2002. View at Google Scholar · View at Scopus
  126. K. Yasojima, W. W. Tourtellotte, E. G. McGeer, and P. L. McGeer, “Marked increase in cyclooxygenase-2 in ALS spinal cord: Implications for therapy,” Neurology, vol. 57, no. 6, pp. 952–956, 2001. View at Google Scholar · View at Scopus
  127. C. Maihofner, S. Probst-Cousin, M. Bergmann, W. Neuhuber, B. Neundorfer, and D. Heuss, “Expression and localization of cyclooxygenase-1 and -2 in human sporadic amyotrophic lateral sclerosis,” European Journal of Neuroscience, vol. 18, no. 6, pp. 1527–1534, 2003. View at Publisher · View at Google Scholar · View at Scopus
  128. D.B. Drachman and J.D. Rothstein, “Inhibition of cyclooxygenase-2 protects motor neurons in an organotypic model of amyotrophic lateral sclerosis,” Annals of Neurology, vol. 48, no. 5, pp. 792–795, 2000. View at Google Scholar
  129. M. F. Azari, C. Profyris, M. R. Le Grande et al., “Effects of intraperitoneal injection of Rofecoxib in a mouse model of ALS,” European Journal of Neurology, vol. 12, no. 5, pp. 357–364, 2005. View at Publisher · View at Google Scholar · View at Scopus
  130. D. B. Drachman, K. Frank, M. Dykes-Hoberg et al., “Cyclooxygenase 2 inhibition protects motor neurons and prolongs survival in a transgenic mouse model of ALS,” Annals of Neurology, vol. 52, no. 6, pp. 771–778, 2002. View at Publisher · View at Google Scholar · View at Scopus
  131. P. N. Pompl, L. Ho, M. Bianchi, T. McManus, W. Qin, and G. M. Pasinetti, “A therapeutic role for cyclooxygenase-2 inhibitors in a transgenic mouse model of amyotrophic lateral sclerosis,” The FASEB Journal, vol. 17, no. 6, pp. 725–727, 2003. View at Google Scholar · View at Scopus
  132. L. Minghetti, “Cyclooxygenase-2 (COX-2) in inflammatory and degenerative brain diseases,” Journal of Neuropathology & Experimental Neurology, vol. 63, no. 9, pp. 901–910, 2004. View at Google Scholar · View at Scopus
  133. P. Bezzi, G. Carmignoto, L. Pasti et al., “Prostaglandins stimulate calcium-dependent glutamate release in astrocytes,” Nature, vol. 391, no. 6664, pp. 281–285, 1998. View at Publisher · View at Google Scholar · View at Scopus
  134. G. Almer, H. Kikuchi, P. Teismann, and S. Przedborski, “Is prostaglandin E2 a pathogenic factor in amyotrophic lateral sclerosis?” Annals of Neurology, vol. 59, no. 6, pp. 980–983, 2006. View at Publisher · View at Google Scholar · View at Scopus
  135. J. Iłzecka, “Prostaglandin E2 is increased in amyotrophic lateral sclerosis patients,” Acta Neurologica Scandinavica, vol. 108, no. 2, pp. 125–129, 2003. View at Publisher · View at Google Scholar · View at Scopus
  136. M. Bilak, L. Wu, Q. Wang et al., “PGE2 receptors rescue motor neurons in a model of amyotrophic lateral sclerosis,” Annals of Neurology, vol. 56, no. 2, pp. 240–248, 2004. View at Publisher · View at Google Scholar · View at Scopus
  137. J. H. Shin, Y. A. Lee, J. K. Lee et al., “Concurrent blockade of free radical and microsomal prostaglandin E synthase-1-mediated PGE(2) production improves safety and efficacy in a mouse model of amyotrophic lateral sclerosis,” Journal of Neurochemistry. In press.
  138. M. Kondo, T. Shibata, T. Kumagai et al., “15-Deoxy-Δ12,14-prostaglandin J2: the endogenous electrophile that induces neuronal apoptosis,” Proceedings of the National Academy of Sciences of the United States of America, vol. 99, no. 11, pp. 7367–7372, 2002. View at Publisher · View at Google Scholar · View at Scopus
  139. H. Y. Hsiao and Y. Chern, “Targeting glial cells to elucidate the pathogenesis of huntington's disease,” Molecular Neurobiology, vol. 41, no. 2-3, pp. 248–255, 2010. View at Publisher · View at Google Scholar · View at Scopus
  140. F. O. Walker, “Huntington's disease,” Seminars in Neurology, vol. 27, no. 2, pp. 143–150, 2007. View at Publisher · View at Google Scholar
  141. T. Moller, “Neuroinflammation in Huntington's disease,” Journal of Neural Transmission, vol. 117, no. 8, pp. 1001–1008, 2010. View at Publisher · View at Google Scholar · View at Scopus
  142. L. Ma, A. J. Morton, and L. F. Nicholson, “Microglia density decreases with age in a mouse model of Huntington's disease,” Glia, vol. 43, no. 3, pp. 274–280, 2003. View at Publisher · View at Google Scholar · View at Scopus
  143. E. Sapp, K. B. Kegel, N. Aronin et al., “Early and progressive accumulation of reactive microglia in the Huntington disease brain,” Journal of Neuropathology & Experimental Neurology, vol. 60, no. 2, pp. 161–172, 2001. View at Google Scholar · View at Scopus
  144. P. Guidetti and R. Schwarcz, “3-Hydroxykynurenine and quinolinate: pathogenic synergism in early grade huntington's disease?” Advances in Experimental Medicine and Biology, vol. 527, pp. 137–145, 2003. View at Google Scholar · View at Scopus
  145. A. C. Ludolph, F. He, P. S. Spencer, J. Hammerstad, and M. Sabri, “3-Nitropropionic acid-exogenous animal neurotoxin and possible human striatal toxin,” Canadian Journal of Neurological Sciences, vol. 18, no. 4, pp. 492–498, 1991. View at Google Scholar · View at Scopus
  146. M. E. Olds, D. B. Jacques, and O. Kopyov, “Behavioral and anatomical effects of quinolinic acid in the striatum of the hemiparkinsonian rat,” Synapse, vol. 55, no. 1, pp. 26–36, 2005. View at Publisher · View at Google Scholar · View at Scopus
  147. J. K. Ryu, H. B. Choi, and J. G. McLarnon, “Combined minocycline plus pyruvate treatment enhances effects of each agent to inhibit inflammation, oxidative damage, and neuronal loss in an excitotoxic animal model of Huntington's disease,” Neuroscience, vol. 141, no. 4, pp. 1835–1848, 2006. View at Publisher · View at Google Scholar · View at Scopus
  148. H. Kalonia and A. Kumar, “Suppressing inflammatory cascade by cyclo-oxygenase inhibitors attenuates quinolinic acid induced Huntington's disease-like alterations in rats,” Life Sciences, vol. 88, no. 17-18, pp. 784–791, 2011. View at Publisher · View at Google Scholar · View at Scopus
  149. H. Kalonia, P. Kumar, A. Kumar, and B. Nehru, “Effects of caffeic acid, rofecoxib, and their combination against quinolinic acid-induced behavioral alterations and disruption in glutathione redox status,” Neuroscience Bulletin, vol. 25, no. 6, pp. 343–352, 2009. View at Publisher · View at Google Scholar · View at Scopus
  150. H. Kalonia, P. Kumar, A. Kumar, and B. Nehru, “Protective effect of rofecoxib and nimesulide against intra-striatal quinolinic acid-induced behavioral, oxidative stress and mitochondrial dysfunctions in rats,” NeuroToxicology, vol. 31, no. 2, pp. 195–203, 2010. View at Publisher · View at Google Scholar · View at Scopus
  151. P. Kumar, S. S. Padi, P. S. Naidu, and A. Kumar, “Cyclooxygenase inhibition attenuates 3-nitropropionic acid-induced neurotoxicity in rats: possible antioxidant mechanisms,” Fundamental and Clinical Pharmacology, vol. 21, no. 3, pp. 297–306, 2007. View at Publisher · View at Google Scholar · View at Scopus
  152. F. Norflus, A. Nanje, C. A. Gutekunst et al., “Anti-inflammatory treatment with acetylsalicylate or rofecoxib is not neuroprotective in Huntington's disease transgenic mice,” Neurobiology of Disease, vol. 17, no. 2, pp. 319–325, 2004. View at Publisher · View at Google Scholar · View at Scopus
  153. G. Schilling, A. V. Savonenko, M. L. Coonfield et al., “Environmental, pharmacological, and genetic modulation of the HD phenotype in transgenic mice,” Experimental Neurology, vol. 187, no. 1, pp. 137–149, 2004. View at Publisher · View at Google Scholar · View at Scopus
  154. K. Bantubungi, C. Jacquard, A. Greco et al., “Minocycline in phenotypic models of Huntington's disease,” Neurobiology of Disease, vol. 18, no. 1, pp. 206–217, 2005. View at Publisher · View at Google Scholar · View at Scopus
  155. P. Kumar, H. Kalonia, and A. Kumar, “Role of LOX/COX pathways in 3-nitropropionic acid-induced Huntington's disease-like symptoms in rats: protective effect of licofelone,” British Journal of Pharmacology, vol. 164, pp. 644–654, 2011. View at Google Scholar
  156. L. Minghetti, A. Greco, R. L. Potenza et al., “Effects of the adenosine A2A receptor antagonist SCH 58621 on cyclooxygenase-2 expression, glial activation, and brain-derived neurotrophic factor availability in a rat model of striatal neurodegeneration,” Journal of Neuropathology & Experimental Neurology, vol. 66, no. 5, pp. 363–371, 2007. View at Publisher · View at Google Scholar · View at Scopus
  157. H. Slawik, B. Volk, B. Fiebich, and M. Hull, “Microglial expression of prostaglandin EP3 receptor in excitotoxic lesions in the rat striatum,” Neurochemistry International, vol. 45, no. 5, pp. 653–660, 2004. View at Google Scholar · View at Scopus
  158. Z. H. Qin, Y. Wang, R. W. Chen et al., “Prostaglandin A1 protects striatal neurons against excitotoxic injury in rat striatum,” Journal of Pharmacology and Experimental Therapeutics, vol. 297, no. 1, pp. 78–87, 2001. View at Google Scholar · View at Scopus
  159. D. L. Krause and N. Muller, “Neuroinflammation, microglia and implications for anti-inflammatory treatment in Alzheimer's disease,” International Journal of Alzheimer's Disease, vol. 2010, Article ID 732806, 9 pages, 2010. View at Publisher · View at Google Scholar · View at Scopus
  160. T. C. Frank-Cannon, L. T. Alto, F. E. McAlpine, and M. G. Tansey, “Does neuroinflammation fan the flame in neurodegenerative diseases?” Molecular Neurodegeneration, vol. 4, no. 1, article 47, 2009. View at Publisher · View at Google Scholar · View at Scopus
  161. W. J. Streit, “Microglial senescence: does the brain's immune system have an expiration date?” Trends in Neurosciences, vol. 29, no. 9, pp. 506–510, 2006. View at Publisher · View at Google Scholar · View at Scopus
  162. M. L. Block, L. Zecca, and J. S. Hong, “Microglia-mediated neurotoxicity: uncovering the molecular mechanisms,” Nature Reviews Neuroscience, vol. 8, no. 1, pp. 57–69, 2007. View at Publisher · View at Google Scholar · View at Scopus
  163. B. Hauss-Wegrzyniak, P. Dobrzanski, J. D. Stoehr, and G. L. Wenk, “Chronic neuroinflammation in rats reproduces components of the neurobiology of Alzheimer's disease,” Brain Research, vol. 780, no. 2, pp. 294–303, 1998. View at Publisher · View at Google Scholar · View at Scopus
  164. T. Farooqui and A. A. Farooqui, “Lipid-mediated oxidative stress and inflammation in the pathogenesis of Parkinson's disease,” Parkinson's Disease, vol. 2011, Article ID 247467, 9 pages, 2011. View at Publisher · View at Google Scholar · View at Scopus
  165. S. E. Hickman, E. K. Allison, and J. El Khoury, “Microglial dysfunction and defective β-amyloid clearance pathways in aging Alzheimer's disease mice,” Journal of Neuroscience, vol. 28, no. 33, pp. 8354–8360, 2008. View at Publisher · View at Google Scholar · View at Scopus
  166. X. G. Luo, J. Q. Ding, and S. D. Chen, “Microglia in the aging brain: relevance to neurodegeneration,” Molecular Neurodegeneration, vol. 5, no. 1, article 12, 2010. View at Publisher · View at Google Scholar · View at Scopus
  167. L. Qian, P. M. Flood, and J. S. Hong, “Neuroinflammation is a key player in Parkinson's disease and a prime target for therapy,” Journal of Neural Transmission, vol. 117, no. 8, pp. 971–979, 2010. View at Publisher · View at Google Scholar · View at Scopus