The role of glial cells in Parkinson's disease

Parkinson's disease is a common neurodegenerative disorder characterized by the progressive loss of the dopaminergic neurons in the substantia nigra pars compacta. The loss of these neurons is associated with a glial response composed mainly of activated microglial cells and, to a lesser extent, of reactive astrocytes. This glial response may be the source of trophic factors and can protect against reactive oxygen species and glutamate. Aside from these beneficial effects, the glial response can mediate a variety of deleterious events related to the production of reactive species, and pro-inflammatory prostaglandin and cytokines. This article reviews the potential protective and deleterious effects of glial cells in the substantia nigra pars compacta of Parkinson's disease.

[1]  S. Korsmeyer,et al.  Bax ablation prevents dopaminergic neurodegeneration in the 1-methyl- 4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson's disease , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[2]  B. Ferger,et al.  Inhibition of the cyclooxygenase isoenzymes COX‐1 and COX‐2 provide neuroprotection in the MPTP‐mouse model of Parkinson's disease , 2001, Synapse.

[3]  Virginia M. Y. Lee,et al.  Oxidative post‐translational modifications of α‐synuclein in the 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) mouse model of Parkinson's disease , 2001, Journal of neurochemistry.

[4]  J. Dichgans,et al.  Protection by Synergistic Effects of Adenovirus-Mediated X-Chromosome-Linked Inhibitor of Apoptosis and Glial Cell Line-Derived Neurotrophic Factor Gene Transfer in the 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine Model of Parkinson's Disease , 2000, The Journal of Neuroscience.

[5]  G. Wilkin,et al.  Inflammatory Regulators in Parkinson's Disease: iNOS, Lipocortin-1, and Cyclooxygenases-1 and -2 , 2000, Molecular and Cellular Neuroscience.

[6]  J. Trojanowski,et al.  Oxidative damage linked to neurodegeneration by selective alpha-synuclein nitration in synucleinopathy lesions. , 2000, Science.

[7]  J. Bloch,et al.  Neurodegeneration prevented by lentiviral vector delivery of GDNF in primate models of Parkinson's disease. , 2000, Science.

[8]  C. Sortwell,et al.  Oligodendrocyte‐type 2 astrocyte‐derived trophic factors increase survival of developing dopamine neurons through the inhibition of apoptotic cell death , 2000, The Journal of comparative neurology.

[9]  S. Yang,et al.  Systemic infusion of naloxone reduces degeneration of rat substantia nigral dopaminergic neurons induced by intranigral injection of lipopolysaccharide. , 2000, The Journal of pharmacology and experimental therapeutics.

[10]  G. Donnan,et al.  Inhibition of brain‐derived neurotrophic factor and glial cell line‐derived neurotrophic factor expression reduces dopaminergic sprouting in the injured striatum , 2000, The European journal of neuroscience.

[11]  R. Mohney,et al.  Regional Difference in Susceptibility to Lipopolysaccharide-Induced Neurotoxicity in the Rat Brain: Role of Microglia , 2000, The Journal of Neuroscience.

[12]  Vila,et al.  Reply: a new look at the pathogenesis of Parkinson's disease , 2000, TIPS - Trends in Pharmacological Sciences.

[13]  J. Dichgans,et al.  Deficiency of Inducible Nitric Oxide Synthase Protects Against MPTP Toxicity In Vivo , 2000, Journal of neurochemistry.

[14]  E. Hirsch,et al.  Caspase-3: A vulnerability factor and final effector in apoptotic death of dopaminergic neurons in Parkinson's disease. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[15]  A L Benabid,et al.  Implication of the Subthalamic Nucleus in the Pathophysiology and Pathogenesis of Parkinson's Disease , 2000, Cell transplantation.

[16]  S. Hayashi,et al.  NACP/α-synuclein-positive filamentous inclusions in astrocytes and oligodendrocytes of Parkinson’s disease brains , 2000, Acta Neuropathologica.

[17]  S. Pennathur,et al.  Mass Spectrometric Quantification of 3-Nitrotyrosine, ortho-Tyrosine, and o,o′-Dityrosine in Brain Tissue of 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated Mice, a Model of Oxidative Stress in Parkinson's Disease* , 1999, The Journal of Biological Chemistry.

[18]  Ted M. Dawson,et al.  Inducible nitric oxide synthase stimulates dopaminergic neurodegeneration in the MPTP model of Parkinson disease , 1999, Nature Medicine.

[19]  T. Moos,et al.  The absence of reactive astrocytosis is indicative of a unique inflammatory process in Parkinson's disease , 1999, Neuroscience.

[20]  J. Langston,et al.  Evidence of active nerve cell degeneration in the substantia nigra of humans years after 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine exposure , 1999, Annals of neurology.

[21]  Timothy Sendera,et al.  Clinicopathological findings following intraventricular glial‐derived neurotrophic factor treatment in a patient with Parkinson's disease , 1999, Annals of neurology.

[22]  E. Hirsch,et al.  FcεRII/CD23 Is Expressed in Parkinson’s Disease and Induces, In Vitro, Production of Nitric Oxide and Tumor Necrosis Factor-α in Glial Cells , 1999, The Journal of Neuroscience.

[23]  R. Djaldetti,et al.  IL-1β, IL-2, IL-6 and TNF-α production by peripheral blood mononuclear cells from patients with Parkinson's disease , 1999 .

[24]  Geoffrey A. Donnan,et al.  Activated Macrophages and Microglia Induce Dopaminergic Sprouting in the Injured Striatum and Express Brain-Derived Neurotrophic Factor and Glial Cell Line-Derived Neurotrophic Factor , 1999, The Journal of Neuroscience.

[25]  R. Burke,et al.  Glial Cell Line‐Derived Neurotrophic Growth Factor Inhibits Apoptotic Death of Postnatal Substantia Nigra Dopamine Neurons in Primary Culture , 1998, Journal of neurochemistry.

[26]  S. Przedborski,et al.  Inactivation of tyrosine hydroxylase by nitration following exposure to peroxynitrite and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[27]  A. Członkowska,et al.  Microglial and astrocytic involvement in a murine model of Parkinson's disease induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). , 1998, Immunopharmacology.

[28]  S. Daniel,et al.  Glial pathology but absence of apoptotic nigral neurons in long‐standing Parkinson's disease , 1998, Movement disorders : official journal of the Movement Disorder Society.

[29]  Y Agid,et al.  Nuclear translocation of NF-kappaB is increased in dopaminergic neurons of patients with parkinson disease. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[30]  J. Zweier,et al.  Superoxide and peroxynitrite generation from inducible nitric oxide synthase in macrophages. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[31]  T. Nagatsu,et al.  Interleukin (IL)-1β, IL-2, IL-4, IL-6 and transforming growth factor-α levels are elevated in ventricular cerebrospinal fluid in juvenile parkinsonism and Parkinson's disease , 1996, Neuroscience Letters.

[32]  A. Członkowska,et al.  Microglial reaction in MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) induced Parkinson's disease mice model. , 1996, Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration.

[33]  T. Dawson,et al.  Role of neuronal nitric oxide in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced dopaminergic neurotoxicity. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[34]  Y. Agid,et al.  Nitric oxide synthase and neuronal vulnerability in parkinson's disease , 1996, Neuroscience.

[35]  B. Hoffer,et al.  Functional recovery in parkinsonian monkeys treated with GDNF , 1996, Nature.

[36]  P. Worley,et al.  COX-2, a synaptically induced enzyme, is expressed by excitatory neurons at postsynaptic sites in rat cerebral cortex. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[37]  R. Strong,et al.  Prostaglandin H Synthetase‐Mediated Metabolism of Dopamine: Implication for Parkinson's Disease , 1995, Journal of neurochemistry.

[38]  G. Kreutzberg,et al.  Microglia: Intrinsic immuneffector cell of the brain , 1995, Brain Research Reviews.

[39]  C. Nathan,et al.  Regulation of biosynthesis of nitric oxide. , 1994, The Journal of biological chemistry.

[40]  Minoru Harada,et al.  Tumor necrosis factor-α (TNF-α) increases both in the brain and in the cerebrospinal fluid from parkinsonian patients , 1994, Neuroscience Letters.

[41]  M. Eddleston,et al.  Molecular profile of reactive astrocytes—Implications for their role in neurologic disease , 1993, Neuroscience.

[42]  E. Hirsch,et al.  Glutathione peroxidase, glial cells and Parkinson's disease , 1993, Neuroscience.

[43]  G. Kreutzberg,et al.  Cytotoxicity of microglia , 1992, Journal of Neuroimmunology.

[44]  V. Perry,et al.  Heterogeneity in the distribution and morphology of microglia in the normal adult mouse brain , 1990, Neuroscience.

[45]  J. O'Callaghan,et al.  Characterization of the origins of astrocyte response to injury using the dopaminergic neurotoxicant, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine , 1990, Brain Research.

[46]  P. Mcgeer,et al.  Reactive microglia are positive for HLA‐DR in the substantia nigra of Parkinson's and Alzheimer's disease brains , 1988, Neurology.

[47]  H. Ichinose,et al.  Caspase activities and tumor necrosis factor receptor R1 (p55) level are elevated in the substantia nigra from Parkinsonian brain , 2000, Journal of Neural Transmission.

[48]  M. Vila,et al.  The parkinsonian toxin MPTP: action and mechanism. , 2000, Restorative neurology and neuroscience.

[49]  S. Hayashi,et al.  NACP/alpha-synuclein-positive filamentous inclusions in astrocytes and oligodendrocytes of Parkinson's disease brains. , 2000, Acta neuropathologica.

[50]  E. Hirsch,et al.  FcepsilonRII/CD23 is expressed in Parkinson's disease and induces, in vitro, production of nitric oxide and tumor necrosis factor-alpha in glial cells. , 1999, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[51]  R. Djaldetti,et al.  IL-1 beta, IL-2, IL-6 and TNF-alpha production by peripheral blood mononuclear cells from patients with Parkinson's disease. , 1999, Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie.

[52]  E. Hirsch,et al.  Glial cell participation in the degeneration of dopaminergic neurons in Parkinson's disease. , 1999, Advances in neurology.

[53]  G. Wilkin,et al.  Glia: a curtain raiser. , 1999, Advances in neurology.

[54]  M. O’Banion,et al.  Cyclooxygenase-2: molecular biology, pharmacology, and neurobiology. , 1999, Critical reviews in neurobiology.

[55]  T. Nagatsu,et al.  Interleukin (IL)-1 beta, IL-2, IL-4, IL-6 and transforming growth factor-alpha levels are elevated in ventricular cerebrospinal fluid in juvenile parkinsonism and Parkinson's disease. , 1996, Neuroscience letters.

[56]  K. Seibert,et al.  Mediation of inflammation by cyclooxygenase-2. , 1995, Agents and actions. Supplements.

[57]  P. Riederer,et al.  Tumor necrosis factor-alpha (TNF-alpha) increases both in the brain and in the cerebrospinal fluid from parkinsonian patients. , 1994, Neuroscience letters.

[58]  J. Langston,et al.  Astrocytes and Parkinson's disease. , 1992, Progress in brain research.

[59]  J. Langston,et al.  Chapter 36: Astrocytes and Parkinson's disease , 1992 .

[60]  S J Kish,et al.  Biochemical pathophysiology of Parkinson's disease. , 1987, Advances in neurology.