Neuroinflammatory processes in Parkinson's disease
Identifieur interne : 001220 ( Istex/Corpus ); précédent : 001219; suivant : 001221Neuroinflammatory processes in Parkinson's disease
Auteurs : Stephane Hunot ; E. C. HirschSource :
- Annals of Neurology [ 0364-5134 ] ; 2003.
Abstract
Parkinson's disease (PD) is a movement disorder characterized by the progressive degeneration of dopaminergic neurons in the midbrain. To date, its cause remains unknown and the mechanism of nerve cell death uncertain. Apart from the massive loss of dopaminergic neurons, PD brains also show a conspicuous glial reaction together with signs of a neuroinflammatory reaction manifested by elevated cytokine levels and upregulation of inflammatory‐associated factors such as cyclooxygenase‐2 and inducible nitric oxide synthase. Mounting evidence also suggests a possible deleterious effect of these neuroinflammatory processes in experimental models of the disease. We propose that, in PD, neuroinflammation plays a role in the cascade of events leading to nerve cell death, thus propagating the neurodegenerative process. In this review, we summarize and discuss the latest findings regarding neuroinflammatory aspects in PD. Ann Neurol 2003;53 (suppl 3):S49–S60
Url:
DOI: 10.1002/ana.10481
Links to Exploration step
ISTEX:BF5A7E3CCACFF44C9861F7B07E7911FF2BF80A88Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Neuroinflammatory processes in Parkinson's disease</title>
<author><name sortKey="Hunot, Stephane" sort="Hunot, Stephane" uniqKey="Hunot S" first="Stephane" last="Hunot">Stephane Hunot</name>
<affiliation><mods:affiliation>INSERM U289, Hôpital de la Salpêtrière, Paris, France</mods:affiliation>
</affiliation>
<affiliation><mods:affiliation>INSERM U289, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière, 47 Boulevard de l'Hôpital, 75013 Paris, France</mods:affiliation>
</affiliation>
</author>
<author><name sortKey="Hirsch, E C" sort="Hirsch, E C" uniqKey="Hirsch E" first="E. C." last="Hirsch">E. C. Hirsch</name>
<affiliation><mods:affiliation>INSERM U289, Hôpital de la Salpêtrière, Paris, France</mods:affiliation>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">ISTEX</idno>
<idno type="RBID">ISTEX:BF5A7E3CCACFF44C9861F7B07E7911FF2BF80A88</idno>
<date when="2003" year="2003">2003</date>
<idno type="doi">10.1002/ana.10481</idno>
<idno type="url">https://api.istex.fr/document/BF5A7E3CCACFF44C9861F7B07E7911FF2BF80A88/fulltext/pdf</idno>
<idno type="wicri:Area/Istex/Corpus">001220</idno>
<idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001220</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Neuroinflammatory processes in Parkinson's disease</title>
<author><name sortKey="Hunot, Stephane" sort="Hunot, Stephane" uniqKey="Hunot S" first="Stephane" last="Hunot">Stephane Hunot</name>
<affiliation><mods:affiliation>INSERM U289, Hôpital de la Salpêtrière, Paris, France</mods:affiliation>
</affiliation>
<affiliation><mods:affiliation>INSERM U289, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière, 47 Boulevard de l'Hôpital, 75013 Paris, France</mods:affiliation>
</affiliation>
</author>
<author><name sortKey="Hirsch, E C" sort="Hirsch, E C" uniqKey="Hirsch E" first="E. C." last="Hirsch">E. C. Hirsch</name>
<affiliation><mods:affiliation>INSERM U289, Hôpital de la Salpêtrière, Paris, France</mods:affiliation>
</affiliation>
</author>
</analytic>
<monogr></monogr>
<series><title level="j">Annals of Neurology</title>
<title level="j" type="sub">Official Journal of the American Neurological Association and the Child Neurology Society</title>
<title level="j" type="abbrev">Ann Neurol.</title>
<idno type="ISSN">0364-5134</idno>
<idno type="eISSN">1531-8249</idno>
<imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher>
<pubPlace>New York</pubPlace>
<date type="published" when="2003">2003</date>
<biblScope unit="volume">53</biblScope>
<biblScope unit="issue">S3</biblScope>
<biblScope unit="supplement">3</biblScope>
<biblScope unit="page" from="S49">S49</biblScope>
<biblScope unit="page" to="S60">S60</biblScope>
</imprint>
<idno type="ISSN">0364-5134</idno>
</series>
<idno type="istex">BF5A7E3CCACFF44C9861F7B07E7911FF2BF80A88</idno>
<idno type="DOI">10.1002/ana.10481</idno>
<idno type="ArticleID">ANA10481</idno>
</biblStruct>
</sourceDesc>
<seriesStmt><idno type="ISSN">0364-5134</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass></textClass>
<langUsage><language ident="en">en</language>
</langUsage>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is a movement disorder characterized by the progressive degeneration of dopaminergic neurons in the midbrain. To date, its cause remains unknown and the mechanism of nerve cell death uncertain. Apart from the massive loss of dopaminergic neurons, PD brains also show a conspicuous glial reaction together with signs of a neuroinflammatory reaction manifested by elevated cytokine levels and upregulation of inflammatory‐associated factors such as cyclooxygenase‐2 and inducible nitric oxide synthase. Mounting evidence also suggests a possible deleterious effect of these neuroinflammatory processes in experimental models of the disease. We propose that, in PD, neuroinflammation plays a role in the cascade of events leading to nerve cell death, thus propagating the neurodegenerative process. In this review, we summarize and discuss the latest findings regarding neuroinflammatory aspects in PD. Ann Neurol 2003;53 (suppl 3):S49–S60</div>
</front>
</TEI>
<istex><corpusName>wiley</corpusName>
<author><json:item><name>Stephane Hunot PhD</name>
<affiliations><json:string>INSERM U289, Hôpital de la Salpêtrière, Paris, France</json:string>
<json:string>INSERM U289, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière, 47 Boulevard de l'Hôpital, 75013 Paris, France</json:string>
</affiliations>
</json:item>
<json:item><name>E. C. Hirsch PhD</name>
<affiliations><json:string>INSERM U289, Hôpital de la Salpêtrière, Paris, France</json:string>
</affiliations>
</json:item>
</author>
<articleId><json:string>ANA10481</json:string>
</articleId>
<language><json:string>eng</json:string>
</language>
<originalGenre><json:string>article</json:string>
</originalGenre>
<abstract>Parkinson's disease (PD) is a movement disorder characterized by the progressive degeneration of dopaminergic neurons in the midbrain. To date, its cause remains unknown and the mechanism of nerve cell death uncertain. Apart from the massive loss of dopaminergic neurons, PD brains also show a conspicuous glial reaction together with signs of a neuroinflammatory reaction manifested by elevated cytokine levels and upregulation of inflammatory‐associated factors such as cyclooxygenase‐2 and inducible nitric oxide synthase. Mounting evidence also suggests a possible deleterious effect of these neuroinflammatory processes in experimental models of the disease. We propose that, in PD, neuroinflammation plays a role in the cascade of events leading to nerve cell death, thus propagating the neurodegenerative process. In this review, we summarize and discuss the latest findings regarding neuroinflammatory aspects in PD. Ann Neurol 2003;53 (suppl 3):S49–S60</abstract>
<qualityIndicators><score>6.62</score>
<pdfVersion>1.3</pdfVersion>
<pdfPageSize>612 x 801 pts</pdfPageSize>
<refBibsNative>true</refBibsNative>
<abstractCharCount>961</abstractCharCount>
<pdfWordCount>7815</pdfWordCount>
<pdfCharCount>49690</pdfCharCount>
<pdfPageCount>12</pdfPageCount>
<abstractWordCount>135</abstractWordCount>
</qualityIndicators>
<title>Neuroinflammatory processes in Parkinson's disease</title>
<refBibs><json:item><author><json:item><name>S Fahn</name>
</json:item>
<json:item><name>S Przedborski</name>
</json:item>
</author>
<host><pages><last>693</last>
<first>679</first>
</pages>
<author></author>
<title>Meritt's neurology</title>
</host>
<title>Parkinsonism</title>
</json:item>
<json:item><author><json:item><name>MH Polymeropoulos</name>
</json:item>
<json:item><name>C Lavedan</name>
</json:item>
<json:item><name>E Leroy</name>
</json:item>
</author>
<host><volume>276</volume>
<pages><last>2047</last>
<first>2045</first>
</pages>
<author></author>
<title>Science</title>
</host>
<title>Mutation in the alpha‐synuclein gene identified in families with Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>T Kitada</name>
</json:item>
<json:item><name>S Asakawa</name>
</json:item>
<json:item><name>N Hattori</name>
</json:item>
</author>
<host><volume>392</volume>
<pages><last>608</last>
<first>605</first>
</pages>
<author></author>
<title>Nature</title>
</host>
<title>Mutations in the parkin gene causes autosomal recessive juvenile parkinsonism</title>
</json:item>
<json:item><author><json:item><name>CW Olanow</name>
</json:item>
<json:item><name>WG Tatton</name>
</json:item>
</author>
<host><volume>22</volume>
<pages><last>144</last>
<first>123</first>
</pages>
<author></author>
<title>Annu Rev Neurosci</title>
</host>
<title>Etiology and pathogenesis of Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>KSP McNaught</name>
</json:item>
<json:item><name>CW Olanow</name>
</json:item>
<json:item><name>B Halliwell</name>
</json:item>
</author>
<host><volume>2</volume>
<pages><last>594</last>
<first>589</first>
</pages>
<author></author>
<title>Nat Rev Neurosci</title>
</host>
<title>Failure of the ubiquitin‐proteasome system in Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>JW Langston</name>
</json:item>
<json:item><name>LS Forno</name>
</json:item>
<json:item><name>J Tetrud</name>
</json:item>
</author>
<host><volume>46</volume>
<pages><last>605</last>
<first>598</first>
</pages>
<author></author>
<title>Ann Neurol</title>
</host>
<title>Evidence of active nerve cell degeneration in the substantia nigra of humans years after 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine exposure</title>
</json:item>
<json:item><host><author></author>
<title>Janeway CA Jr,Travers P.Immunobiology: the immune system in health and disease.London/New York:Current Biology Ltd/Garland Publishing,1994.</title>
</host>
</json:item>
<json:item><author><json:item><name>PL McGeer</name>
</json:item>
<json:item><name>S Itagaki</name>
</json:item>
<json:item><name>BE Boyes</name>
</json:item>
<json:item><name>EG McGeer</name>
</json:item>
</author>
<host><volume>38</volume>
<pages><last>1291</last>
<first>1285</first>
</pages>
<author></author>
<title>Neurology</title>
</host>
<title>Reactive microglia are positive for HLA‐DR in the substantia nigra of Parkinson's and Alzheimer's disease brains</title>
</json:item>
<json:item><author><json:item><name>M Mogi</name>
</json:item>
<json:item><name>M Harada</name>
</json:item>
<json:item><name>T Kondo</name>
</json:item>
</author>
<host><volume>9</volume>
<pages><last>92</last>
<first>87</first>
</pages>
<author></author>
<title>J Neural Transm Park Dis Dement Sect</title>
</host>
<title>Brain beta 2‐microglobulin levels are elevated in the striatum in Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>I Kurkowska‐Jastrzebska</name>
</json:item>
<json:item><name>A Wronska</name>
</json:item>
<json:item><name>M Kohutnicka</name>
</json:item>
</author>
<host><volume>156</volume>
<pages><last>61</last>
<first>50</first>
</pages>
<author></author>
<title>Exp Neurol</title>
</host>
<title>The inflammatory reaction following 1‐methyl‐4‐phenyl‐1,2,3, 6‐tetrahydropyridine intoxication in mouse</title>
</json:item>
<json:item><author><json:item><name>PL McGeer</name>
</json:item>
<json:item><name>EG McGeer</name>
</json:item>
<json:item><name>S Itagaki</name>
</json:item>
<json:item><name>K Mizukawa</name>
</json:item>
</author>
<host><volume>14</volume>
<pages><last>372</last>
<first>363</first>
</pages>
<author></author>
<title>Can J Neurol Sci</title>
</host>
<title>Anatomy and pathology of the basal ganglia</title>
</json:item>
<json:item><author><json:item><name>T Nagatsu</name>
</json:item>
<json:item><name>M Mogi</name>
</json:item>
<json:item><name>H Ichinose</name>
</json:item>
<json:item><name>A Togari</name>
</json:item>
</author>
<host><volume>60</volume>
<pages><last>290</last>
<first>277</first>
</pages>
<issue>Suppl</issue>
<author></author>
<title>J Neural Transm</title>
</host>
<title>Changes in cytokines and neurotrophins in Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>G Boka</name>
</json:item>
<json:item><name>P Anglade</name>
</json:item>
<json:item><name>D Wallach</name>
</json:item>
</author>
<host><volume>172</volume>
<pages><last>154</last>
<first>151</first>
</pages>
<author></author>
<title>Neurosci Lett</title>
</host>
<title>Immunohistochemical analysis of tumor necrosis factor and its receptors in Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>S Hunot</name>
</json:item>
<json:item><name>N Dugas</name>
</json:item>
<json:item><name>B Faucheux</name>
</json:item>
</author>
<host><volume>19</volume>
<pages><last>3447</last>
<first>3440</first>
</pages>
<author></author>
<title>J Neurosci</title>
</host>
<title>FcεRII/CD23 is expressed in Parkinson's disease and induces, in vitro, production of nitric oxide and tumor necrosis factor‐α in glial cells</title>
</json:item>
<json:item><author><json:item><name>R Kiefer</name>
</json:item>
<json:item><name>CA Haas</name>
</json:item>
<json:item><name>GW Kreutzberg</name>
</json:item>
</author>
<host><volume>45</volume>
<pages><last>560</last>
<first>551</first>
</pages>
<author></author>
<title>Neuroscience</title>
</host>
<title>Gamma interferon‐like immunoreactive material in rat neurons: evidence against a close relationship to gamma interferon</title>
</json:item>
<json:item><author><json:item><name>T Olsson</name>
</json:item>
<json:item><name>S Kelic</name>
</json:item>
<json:item><name>C Edlund</name>
</json:item>
</author>
<host><volume>24</volume>
<pages><last>314</last>
<first>308</first>
</pages>
<author></author>
<title>Eur J Immunol</title>
</host>
<title>Neuronal interferon‐gamma immunoreactive molecule: bioactivities and purification</title>
</json:item>
<json:item><author><json:item><name>R De Simone</name>
</json:item>
<json:item><name>G Levi</name>
</json:item>
<json:item><name>F Aloisi</name>
</json:item>
</author>
<host><volume>10</volume>
<pages><last>422</last>
<first>418</first>
</pages>
<author></author>
<title>Cytokine</title>
</host>
<title>Interferon gamma gene expression in rat central nervous system glial cells</title>
</json:item>
<json:item><author><json:item><name>JN Ijzermans</name>
</json:item>
<json:item><name>RL Marquet</name>
</json:item>
</author>
<host><volume>179</volume>
<pages><last>473</last>
<first>456</first>
</pages>
<author></author>
<title>Immunobiology</title>
</host>
<title>Interferon‐gamma: a review</title>
</json:item>
<json:item><author><json:item><name>E Farkas</name>
</json:item>
<json:item><name>GI De Jong</name>
</json:item>
<json:item><name>RA de Vos</name>
</json:item>
</author>
<host><volume>100</volume>
<pages><last>402</last>
<first>395</first>
</pages>
<author></author>
<title>Acta Neuropathol</title>
</host>
<title>Pathological features of cerebral cortical capillaries are doubled in Alzheimer's disease and Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>B Faucheux</name>
</json:item>
<json:item><name>A‐M Bonnet</name>
</json:item>
<json:item><name>Y Agid</name>
</json:item>
<json:item><name>EC Hirsch</name>
</json:item>
</author>
<host><volume>353</volume>
<pages><last>982</last>
<first>981</first>
</pages>
<author></author>
<title>Lancet</title>
</host>
<title>Blood vessels change in the mesencephalon of patients with Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>J Casals</name>
</json:item>
<json:item><name>TS Elizan</name>
</json:item>
<json:item><name>MD Yahr</name>
</json:item>
</author>
<host><volume>105</volume>
<pages><last>676</last>
<first>645</first>
</pages>
<author></author>
<title>J Neural Transm</title>
</host>
<title>Postencephalitic parkinsonism—a review</title>
</json:item>
<json:item><author><json:item><name>M Takahashi</name>
</json:item>
<json:item><name>T Yamada</name>
</json:item>
</author>
<host><volume>86</volume>
<pages><last>104</last>
<first>91</first>
</pages>
<author></author>
<title>Adv Neurol</title>
</host>
<title>A possible role of influenza A virus infection for Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>A Ogata</name>
</json:item>
<json:item><name>K Tashiro</name>
</json:item>
<json:item><name>S Nakuzuma</name>
</json:item>
</author>
<host><volume>3</volume>
<pages><last>147</last>
<first>141</first>
</pages>
<author></author>
<title>J Neurovirol</title>
</host>
<title>A rat model of Parkinson's disease induced by Japanese encephalitis virus</title>
</json:item>
<json:item><author><json:item><name>K Hisanaga</name>
</json:item>
<json:item><name>M Asagi</name>
</json:item>
<json:item><name>Y Itoyama</name>
</json:item>
<json:item><name>T Iwasaki</name>
</json:item>
</author>
<host><volume>58</volume>
<pages><last>1583</last>
<first>1580</first>
</pages>
<author></author>
<title>Arch Neurol</title>
</host>
<title>Increase in peripheral CD4 bright+ CD8 dull+ T cells in Parkinson disease</title>
</json:item>
<json:item><author><json:item><name>A McRae Degueurce</name>
</json:item>
<json:item><name>CG Gottfries</name>
</json:item>
<json:item><name>I Karlsson</name>
</json:item>
</author>
<host><volume>126</volume>
<pages><last>315</last>
<first>313</first>
</pages>
<author></author>
<title>Acta Physiol Scand</title>
</host>
<title>Antibodies in the CSF of a Parkinson patient recognizes neurons in rat mesencephalic regions</title>
</json:item>
<json:item><author><json:item><name>PM Carvey</name>
</json:item>
<json:item><name>A McRae</name>
</json:item>
<json:item><name>TF Lint</name>
</json:item>
</author>
<host><volume>41</volume>
<pages><last>58</last>
<first>53</first>
</pages>
<author></author>
<title>Neurology</title>
</host>
<title>The potential use of a dopamine neuron antibody and a striatal‐derived neurotrophic factor as diagnostic markers in Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>G Defazio</name>
</json:item>
<json:item><name>R Dal Toso</name>
</json:item>
<json:item><name>D Benvegnu</name>
</json:item>
</author>
<host><volume>633</volume>
<pages><last>212</last>
<first>206</first>
</pages>
<author></author>
<title>Brain Res</title>
</host>
<title>Parkinsonian serum carries complement‐dependent toxicity for rat mesencephalic dopaminergic neurons in culture</title>
</json:item>
<json:item><author><json:item><name>DB Rowe</name>
</json:item>
<json:item><name>W Le</name>
</json:item>
<json:item><name>RG Smith</name>
</json:item>
<json:item><name>SH Appel</name>
</json:item>
</author>
<host><volume>53</volume>
<pages><last>558</last>
<first>551</first>
</pages>
<author></author>
<title>J Neurosci Res</title>
</host>
<title>Antibodies from patients with Parkinson's disease react with protein modified by dopamine oxidation</title>
</json:item>
<json:item><author><json:item><name>M Bokor</name>
</json:item>
<json:item><name>A Farago</name>
</json:item>
<json:item><name>T Garam</name>
</json:item>
</author>
<host><volume>115</volume>
<pages><last>50</last>
<first>47</first>
</pages>
<author></author>
<title>J Neurol Sci</title>
</host>
<title>Antibody‐dependent cell‐mediated cytotoxicity (ADCC) in Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>SH Appel</name>
</json:item>
<json:item><name>WD Le</name>
</json:item>
<json:item><name>J Tajti</name>
</json:item>
</author>
<host><volume>32</volume>
<pages><last>501</last>
<first>494</first>
</pages>
<author></author>
<title>Ann Neurol</title>
</host>
<title>Nigral damage and dopaminergic hypofunction in mesencephalon‐immunized guinea pigs</title>
</json:item>
<json:item><author><json:item><name>WD Le</name>
</json:item>
<json:item><name>J Engelhardt</name>
</json:item>
<json:item><name>WJ Xie</name>
</json:item>
</author>
<host><volume>57</volume>
<pages><last>53</last>
<first>45</first>
</pages>
<author></author>
<title>J Neuroimmunol</title>
</host>
<title>Experimental autoimmune nigral damage in guinea pigs</title>
</json:item>
<json:item><author><json:item><name>S Chen</name>
</json:item>
<json:item><name>WD Le</name>
</json:item>
<json:item><name>WJ Xie</name>
</json:item>
</author>
<host><volume>55</volume>
<pages><last>1080</last>
<first>1075</first>
</pages>
<author></author>
<title>Arch Neurol</title>
</host>
<title>Experimental destruction of substantia nigra initiated by Parkinson disease immunoglobulins</title>
</json:item>
<json:item><author><json:item><name>AC Hayday</name>
</json:item>
</author>
<host><volume>18</volume>
<pages><last>1026</last>
<first>975</first>
</pages>
<author></author>
<title>Annu Rev Immunol</title>
</host>
<title>γδ cells: a right time and a right place for a conserved third way of protection</title>
</json:item>
<json:item><author><json:item><name>U Fiszer</name>
</json:item>
<json:item><name>E Mix</name>
</json:item>
<json:item><name>S Fredrikson</name>
</json:item>
</author>
<host><volume>121</volume>
<pages><last>45</last>
<first>39</first>
</pages>
<author></author>
<title>J Neurol Sci</title>
</host>
<title>gamma delta+ T cells are increased in patients with Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>U Fiszer</name>
</json:item>
<json:item><name>S Fredrikson</name>
</json:item>
<json:item><name>A Czlonkowska</name>
</json:item>
</author>
<host><volume>139</volume>
<pages><last>70</last>
<first>66</first>
</pages>
<author></author>
<title>J Neurol Sci</title>
</host>
<title>Humoral response to hsp 65 and hsp 70 in cerebrospinal fluid in Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>M Mogi</name>
</json:item>
<json:item><name>A Togari</name>
</json:item>
<json:item><name>M Ogawa</name>
</json:item>
</author>
<host><volume>250</volume>
<pages><last>28</last>
<first>25</first>
</pages>
<author></author>
<title>Neurosci Lett</title>
</host>
<title>Effects of repeated systemic administration of 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) to mice on interleukin‐1beta and nerve growth factor in the striatum</title>
</json:item>
<json:item><author><json:item><name>E Grünblatt</name>
</json:item>
<json:item><name>S Mandel</name>
</json:item>
<json:item><name>G Maor</name>
</json:item>
<json:item><name>MB Youdim</name>
</json:item>
</author>
<host><volume>78</volume>
<pages><last>12</last>
<first>1</first>
</pages>
<author></author>
<title>J Neurochem</title>
</host>
<title>Gene expression analysis in N‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine mice model of Parkinson's disease using cDNA microarray: effect of R‐apomorphine</title>
</json:item>
<json:item><author><json:item><name>M Mogi</name>
</json:item>
<json:item><name>A Togari</name>
</json:item>
<json:item><name>K Tanaka</name>
</json:item>
</author>
<host><volume>268</volume>
<pages><last>104</last>
<first>101</first>
</pages>
<author></author>
<title>Neurosci Lett</title>
</host>
<title>Increase in level of tumor necrosis factor (TNF)‐alpha in 6‐hydroxydopamine‐lesioned striatum in rats without influence of systemic L‐DOPA on the TNF‐alpha induction</title>
</json:item>
<json:item><author><json:item><name>N Aubin</name>
</json:item>
<json:item><name>O Curet</name>
</json:item>
<json:item><name>A Deffois</name>
</json:item>
<json:item><name>C Carter</name>
</json:item>
</author>
<host><volume>71</volume>
<pages><last>1642</last>
<first>1635</first>
</pages>
<author></author>
<title>J Neurochem</title>
</host>
<title>Aspirin and salicylate protect against MPTP‐induced dopamine depletion in mice</title>
</json:item>
<json:item><author><json:item><name>A Boireau</name>
</json:item>
<json:item><name>F Bordier</name>
</json:item>
<json:item><name>P Dubedat</name>
</json:item>
</author>
<host><volume>234</volume>
<pages><last>126</last>
<first>123</first>
</pages>
<author></author>
<title>Neurosci Lett</title>
</host>
<title>Thalidomide reduces MPTP‐induced decrease in striatal dopamine levels in mice</title>
</json:item>
<json:item><author><json:item><name>Y Kitamura</name>
</json:item>
<json:item><name>Y Itano</name>
</json:item>
<json:item><name>T Kubo</name>
</json:item>
<json:item><name>Y Nomura</name>
</json:item>
</author>
<host><volume>50</volume>
<pages><last>224</last>
<first>221</first>
</pages>
<author></author>
<title>J Neuroimmunol</title>
</host>
<title>Suppressive effect of FK‐506, a novel immunosuppressant, against MPTP‐induced dopamine depletion in the striatum of young C57BL/6 mice</title>
</json:item>
<json:item><author><json:item><name>K Matsuura</name>
</json:item>
<json:item><name>H Makino</name>
</json:item>
<json:item><name>N Ogawa</name>
</json:item>
</author>
<host><volume>146</volume>
<pages><last>535</last>
<first>526</first>
</pages>
<author></author>
<title>Exp Neurol</title>
</host>
<title>Cyclosporin A attenuates the decrease in tyrosine hydroxylase immunoreactivity in nigrostriatal dopaminergic neurons and in striatal dopamine content in rats with intrastriatal injection of 6‐hydroxydopamine</title>
</json:item>
<json:item><author><json:item><name>P Teismann</name>
</json:item>
<json:item><name>B Ferger</name>
</json:item>
</author>
<host><volume>39</volume>
<pages><last>174</last>
<first>167</first>
</pages>
<author></author>
<title>Synapse</title>
</host>
<title>Inhibition of the cyclooxygenase isoenzymes COX‐1 and COX‐2 provide neuroprotection in the MPTP‐mouse model of Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>JR Vane</name>
</json:item>
<json:item><name>YS Bakhle</name>
</json:item>
<json:item><name>RM Botting</name>
</json:item>
</author>
<host><volume>38</volume>
<pages><last>120</last>
<first>97</first>
</pages>
<author></author>
<title>Annu Rev Pharmacol Toxicol</title>
</host>
<title>Cyclooxygenases 1 and 2</title>
</json:item>
<json:item><author><json:item><name>LL Dugan</name>
</json:item>
<json:item><name>DW Choi</name>
</json:item>
</author>
<host><pages><last>729</last>
<first>711</first>
</pages>
<author></author>
<title>Basic neurochemistry</title>
</host>
<title>Hypoxic‐ischemia brain injury and oxidative stress</title>
</json:item>
<json:item><author><json:item><name>HP Rang</name>
</json:item>
<json:item><name>MM Dale</name>
</json:item>
<json:item><name>JM Ritter</name>
</json:item>
</author>
<host><pages><last>514</last>
<first>500</first>
</pages>
<author></author>
<title>Pharmacology</title>
</host>
<title>Neurodegenerative disorders</title>
</json:item>
<json:item><author><json:item><name>C Knott</name>
</json:item>
<json:item><name>G Stern</name>
</json:item>
<json:item><name>GP Wilkin</name>
</json:item>
</author>
<host><volume>16</volume>
<pages><last>739</last>
<first>724</first>
</pages>
<author></author>
<title>Mol Cell Neurosci</title>
</host>
<title>Inflammatory regulators in Parkinson's disease: iNOS, lipocortin‐1, and cyclooxygenase‐1 and –2</title>
</json:item>
<json:item><author><json:item><name>P Teismann</name>
</json:item>
<json:item><name>V Jackson‐Lewis</name>
</json:item>
<json:item><name>M Vila</name>
</json:item>
<json:item><name>S Przedborski</name>
</json:item>
</author>
<host><pages><last>2</last>
<first>688</first>
</pages>
<author></author>
<title>Soc Neurosci Abstr</title>
</host>
<title>Cyclooxygenase‐2 deficient mice are resistant to MPTP</title>
</json:item>
<json:item><author><json:item><name>PG Sullivan</name>
</json:item>
<json:item><name>MB Thompson</name>
</json:item>
<json:item><name>S Scheff</name>
</json:item>
</author>
<host><volume>160</volume>
<pages><last>234</last>
<first>226</first>
</pages>
<author></author>
<title>Exp Neurol</title>
</host>
<title>Cyclosporin A attenuates acute mitochondrial dysfunction following traumatic brain injury</title>
</json:item>
<json:item><author><json:item><name>DR Green</name>
</json:item>
<json:item><name>JC Reed</name>
</json:item>
</author>
<host><volume>281</volume>
<pages><last>1312</last>
<first>1309</first>
</pages>
<author></author>
<title>Science</title>
</host>
<title>Mitochondria and apoptosis</title>
</json:item>
<json:item><author><json:item><name>HJ Chae</name>
</json:item>
<json:item><name>SW Chae</name>
</json:item>
<json:item><name>JS Kang</name>
</json:item>
</author>
<host><volume>141</volume>
<pages><last>2913</last>
<first>2904</first>
</pages>
<author></author>
<title>Endocrinology</title>
</host>
<title>Dexamethasone suppresses tumor necrosis factor‐alpha‐induced apoptosis in osteoblasts: possible role for ceramide</title>
</json:item>
<json:item><author><json:item><name>MV Gonzalez</name>
</json:item>
<json:item><name>B Jimenez</name>
</json:item>
<json:item><name>MT Berciano</name>
</json:item>
</author>
<host><volume>150</volume>
<pages><last>1208</last>
<first>1199</first>
</pages>
<author></author>
<title>J Cell Biol</title>
</host>
<title>Glucocorticoids antagonize AP‐1 by inhibiting the activation/phosphorylation of JNK without affecting its subcellular distribution</title>
</json:item>
<json:item><author><json:item><name>AM Gorman</name>
</json:item>
<json:item><name>UA Hirt</name>
</json:item>
<json:item><name>S Orrenius</name>
</json:item>
<json:item><name>S Ceccatelli</name>
</json:item>
</author>
<host><volume>96</volume>
<pages><last>425</last>
<first>417</first>
</pages>
<author></author>
<title>Neuroscience</title>
</host>
<title>Dexamethasone pre‐treatment interferes with apoptotic death in glioma cells</title>
</json:item>
<json:item><author><json:item><name>VL Dawson</name>
</json:item>
<json:item><name>TM Dawson</name>
</json:item>
<json:item><name>DA Bartley</name>
</json:item>
</author>
<host><volume>13</volume>
<pages><last>2661</last>
<first>2651</first>
</pages>
<author></author>
<title>J Neurosci</title>
</host>
<title>Mechanisms of nitric oxide‐mediated neurotoxicity in primary brain cultures</title>
</json:item>
<json:item><author><json:item><name>S Hunot</name>
</json:item>
<json:item><name>F Boissiere</name>
</json:item>
<json:item><name>B Faucheux</name>
</json:item>
</author>
<host><volume>72</volume>
<pages><last>363</last>
<first>355</first>
</pages>
<author></author>
<title>Neuroscience</title>
</host>
<title>Nitric oxide synthase and neuronal vulnerability in Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>GA Qureshi</name>
</json:item>
<json:item><name>S Baig</name>
</json:item>
<json:item><name>I Bednar</name>
</json:item>
</author>
<host><volume>6</volume>
<pages><last>1644</last>
<first>1642</first>
</pages>
<author></author>
<title>Neuroreport</title>
</host>
<title>Increased cerebrospinal fluid concentration of nitrite in Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>GT Liberatore</name>
</json:item>
<json:item><name>V Jackson‐Lewis</name>
</json:item>
<json:item><name>S Vukosavic</name>
</json:item>
</author>
<host><volume>5</volume>
<pages><last>1409</last>
<first>1403</first>
</pages>
<author></author>
<title>Nat Med</title>
</host>
<title>Inducible nitric oxide synthase stimulates dopaminergic neurodegeneration in the MPTP model of Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>T Dehmer</name>
</json:item>
<json:item><name>J Lindenau</name>
</json:item>
<json:item><name>S Haid</name>
</json:item>
</author>
<host><volume>74</volume>
<pages><last>2216</last>
<first>2213</first>
</pages>
<author></author>
<title>J Neurochem</title>
</host>
<title>Deficiency of inducible nitric oxide synthase protects against MPTP toxicity in vivo</title>
</json:item>
<json:item><author><json:item><name>MM Iravani</name>
</json:item>
<json:item><name>K Kashefi</name>
</json:item>
<json:item><name>P Mander</name>
</json:item>
</author>
<host><volume>110</volume>
<pages><last>58</last>
<first>49</first>
</pages>
<author></author>
<title>Neuroscience</title>
</host>
<title>Involvement of inducible nitric oxide synthase in inflammation‐induced dopaminergic neurodegeneration</title>
</json:item>
<json:item><author><json:item><name>H Ischiropoulos</name>
</json:item>
<json:item><name>L Zhu</name>
</json:item>
<json:item><name>J Chen</name>
</json:item>
</author>
<host><volume>298</volume>
<pages><last>437</last>
<first>431</first>
</pages>
<author></author>
<title>Arch Biochem Biophys</title>
</host>
<title>Peroxynitrite‐mediated tyrosine nitration catalyzed by superoxide dismutase</title>
</json:item>
<json:item><author><json:item><name>PF Good</name>
</json:item>
<json:item><name>A Hsu</name>
</json:item>
<json:item><name>P Werner</name>
</json:item>
</author>
<host><volume>57</volume>
<pages><last>342</last>
<first>338</first>
</pages>
<author></author>
<title>J Neuropathol Exp Neurol</title>
</host>
<title>Protein nitration in Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>JB Schulz</name>
</json:item>
<json:item><name>RT Matthews</name>
</json:item>
<json:item><name>MM Muqit</name>
</json:item>
</author>
<host><volume>64</volume>
<pages><last>939</last>
<first>936</first>
</pages>
<author></author>
<title>J Neurochem</title>
</host>
<title>Inhibition of neuronal nitric oxide synthase by 7‐nitroindazole protects against MPTP‐induced neurotoxicity in mice</title>
</json:item>
<json:item><author><json:item><name>S Pennathur</name>
</json:item>
<json:item><name>V Jackson‐Lewis</name>
</json:item>
<json:item><name>S Przedborski</name>
</json:item>
</author>
<host><volume>274</volume>
<pages><last>34628</last>
<first>34621</first>
</pages>
<author></author>
<title>J Biol Chem</title>
</host>
<title>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</title>
</json:item>
<json:item><author><json:item><name>JC Drapier</name>
</json:item>
<json:item><name>H Hirling</name>
</json:item>
<json:item><name>J Wietzerbin</name>
</json:item>
</author>
<host><volume>12</volume>
<pages><last>3649</last>
<first>3643</first>
</pages>
<author></author>
<title>EMBO J</title>
</host>
<title>Biosynthesis of nitric oxide activates iron regulatory factor in macrophages</title>
</json:item>
<json:item><author><json:item><name>SR Jaffrey</name>
</json:item>
<json:item><name>NA Cohen</name>
</json:item>
<json:item><name>TA Rouault</name>
</json:item>
</author>
<host><volume>91</volume>
<pages><last>12998</last>
<first>12994</first>
</pages>
<author></author>
<title>Proc Natl Acad Sci USA</title>
</host>
<title>The iron‐responsive element binding protein: a target for synaptic actions of nitric oxide</title>
</json:item>
<json:item><author><json:item><name>K Pantopoulos</name>
</json:item>
<json:item><name>MW Hentze</name>
</json:item>
</author>
<host><volume>92</volume>
<pages><last>1271</last>
<first>1267</first>
</pages>
<author></author>
<title>Proc Natl Acad Sci USA</title>
</host>
<title>Nitric oxide signaling to iron‐regulatory protein: direct control of ferritin mRNA translation and transferrin receptor mRNA stability in transfected fibroblasts</title>
</json:item>
<json:item><author><json:item><name>EC Hirsch</name>
</json:item>
<json:item><name>B Faucheux</name>
</json:item>
</author>
<host><volume>13</volume>
<pages><last>45</last>
<first>39</first>
</pages>
<issue>suppl 1</issue>
<author></author>
<title>Mov Disord</title>
</host>
<title>Iron metabolism and Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>N Janabi</name>
</json:item>
<json:item><name>S Chabrier</name>
</json:item>
<json:item><name>M Tardieu</name>
</json:item>
</author>
<host><volume>157</volume>
<pages><last>2135</last>
<first>2129</first>
</pages>
<author></author>
<title>J Immunol</title>
</host>
<title>Endogenous nitric oxide activates prostaglandin F2 alpha production in human microglial cells but not in astrocytes: a study of interactions between eicosanoids, nitric oxide, and superoxide anion (O2‐) regulatory pathways</title>
</json:item>
<json:item><author><json:item><name>M Ding</name>
</json:item>
<json:item><name>BA St. Pierre</name>
</json:item>
<json:item><name>JF Parkinson</name>
</json:item>
</author>
<host><volume>17</volume>
<pages><last>11335</last>
<first>11327</first>
</pages>
<author></author>
<title>J Biol Chem</title>
</host>
<title>Inducible nitric‐oxide synthase and nitric oxide production in human fetal astrocytes and microglia</title>
</json:item>
<json:item><author><json:item><name>J Liu</name>
</json:item>
<json:item><name>M‐L Zhao</name>
</json:item>
<json:item><name>CF Brosnan</name>
</json:item>
<json:item><name>SC Lee</name>
</json:item>
</author>
<host><volume>57</volume>
<pages><last>3576</last>
<first>3569</first>
</pages>
<author></author>
<title>J Immunol</title>
</host>
<title>Expression of type II nitric oxide synthase in primary human astrocytes and microglia. Role of IL‐1β and IL‐1 receptor antagonist</title>
</json:item>
<json:item><author><json:item><name>PK Peterson</name>
</json:item>
<json:item><name>S Hu</name>
</json:item>
<json:item><name>WR Anderson</name>
</json:item>
<json:item><name>CC Chao</name>
</json:item>
</author>
<host><volume>170</volume>
<pages><last>460</last>
<first>457</first>
</pages>
<author></author>
<title>J Infect Dis</title>
</host>
<title>Nitric oxide production and neurotoxicity mediated by activated microglia from human versus mouse brain</title>
</json:item>
<json:item><author><json:item><name>N Dugas</name>
</json:item>
<json:item><name>C Lacroix</name>
</json:item>
<json:item><name>E Kilchherr</name>
</json:item>
</author>
<host><volume>15</volume>
<pages><last>107</last>
<first>96</first>
</pages>
<author></author>
<title>Cytokine</title>
</host>
<title>Role of CD23 in astrocytes inflammatory reaction during HIV‐1 related encephalitis</title>
</json:item>
<json:item><author><json:item><name>JY Bonnefoy</name>
</json:item>
<json:item><name>S Lecoanet‐Henchoz</name>
</json:item>
<json:item><name>JF Gauchat</name>
</json:item>
</author>
<host><volume>16</volume>
<pages><last>128</last>
<first>113</first>
</pages>
<author></author>
<title>Int Rev Immunol</title>
</host>
<title>Structure and functions of CD23</title>
</json:item>
<json:item><author><json:item><name>T Kawamata</name>
</json:item>
<json:item><name>H Akiyama</name>
</json:item>
<json:item><name>T Yamada</name>
</json:item>
<json:item><name>PL McGeer</name>
</json:item>
</author>
<host><volume>40</volume>
<pages><last>707</last>
<first>691</first>
</pages>
<author></author>
<title>Am J Pathol</title>
</host>
<title>Immunological reactions in amyotrophic lateral sclerosis brain and spinal cord tissue</title>
</json:item>
<json:item><author><json:item><name>H Akiyama</name>
</json:item>
<json:item><name>PL McGeer</name>
</json:item>
</author>
<host><volume>30</volume>
<pages><last>93</last>
<first>81</first>
</pages>
<author></author>
<title>J Neuroimmunol</title>
</host>
<title>Brain microglia constitutively express beta‐2 integrins</title>
</json:item>
<json:item><author><json:item><name>M Mogi</name>
</json:item>
<json:item><name>A Togari</name>
</json:item>
<json:item><name>T Kondo</name>
</json:item>
</author>
<host><volume>107</volume>
<pages><last>341</last>
<first>335</first>
</pages>
<author></author>
<title>J Neural Transm</title>
</host>
<title>Caspase activities and tumor necrosis factor receptor R1 (p55) level are elevated in the substantia nigra from parkinsonian brain</title>
</json:item>
<json:item><author><json:item><name>MO Hengartner</name>
</json:item>
</author>
<host><volume>407</volume>
<pages><last>776</last>
<first>770</first>
</pages>
<author></author>
<title>Nature</title>
</host>
<title>The biochemistry of apoptosis</title>
</json:item>
<json:item><author><json:item><name>R Testi</name>
</json:item>
</author>
<host><volume>21</volume>
<pages><last>471</last>
<first>468</first>
</pages>
<author></author>
<title>Trends Biochem Sci</title>
</host>
<title>Sphingomyelin breakdown and cell fate</title>
</json:item>
<json:item><author><json:item><name>S Hunot</name>
</json:item>
<json:item><name>B Brugg</name>
</json:item>
<json:item><name>D Ricard</name>
</json:item>
</author>
<host><volume>94</volume>
<pages><last>7536</last>
<first>7531</first>
</pages>
<author></author>
<title>Proc Natl Acad Sci USA</title>
</host>
<title>Nuclear translocation of NF‐kappaB is increased in dopaminergic neurons of patients with parkinson disease</title>
</json:item>
<json:item><author><json:item><name>A Hartmann</name>
</json:item>
<json:item><name>JD Troadec</name>
</json:item>
<json:item><name>S Hunot</name>
</json:item>
</author>
<host><volume>21</volume>
<pages><last>2255</last>
<first>2247</first>
</pages>
<author></author>
<title>J Neurosci</title>
</host>
<title>Caspase‐8 is an effector in apoptotic death of dopaminergic neurons in Parkinson's disease, but pathway inhibition results in neuronal necrosis</title>
</json:item>
<json:item><author><json:item><name>A Hartmann</name>
</json:item>
<json:item><name>S Hunot</name>
</json:item>
<json:item><name>PP Michel</name>
</json:item>
</author>
<host><volume>97</volume>
<pages><last>2880</last>
<first>2875</first>
</pages>
<author></author>
<title>Proc Natl Acad Sci USA</title>
</host>
<title>Caspase‐3: a vulnerability factor and final effector in apoptotic death of dopaminergic neurons in Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>EC Hirsch</name>
</json:item>
<json:item><name>S Hunot</name>
</json:item>
<json:item><name>B Faucheux</name>
</json:item>
</author>
<host><volume>14</volume>
<pages><last>385</last>
<first>383</first>
</pages>
<author></author>
<title>Mov Disord</title>
</host>
<title>Dopaminergic neurons degenerate by apoptosis in Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>P Rockwell</name>
</json:item>
<json:item><name>H Yuan</name>
</json:item>
<json:item><name>R Magnusson</name>
</json:item>
<json:item><name>ME Figueiredo‐Pereira</name>
</json:item>
</author>
<host><volume>374</volume>
<pages><last>333</last>
<first>325</first>
</pages>
<author></author>
<title>Arch Biochem Biophys</title>
</host>
<title>Proteasome inhibition in neuronal cells induces a proinflammatory response manifested by upregulation of cyclooxygenase‐2, its accumulation as ubiquitin conjugates, and production of the prostaglandin PGE(2)</title>
</json:item>
</refBibs>
<genre><json:string>article</json:string>
</genre>
<host><volume>53</volume>
<publisherId><json:string>ANA</json:string>
</publisherId>
<pages><total>12</total>
<last>S60</last>
<first>S49</first>
</pages>
<issn><json:string>0364-5134</json:string>
</issn>
<issue>S3</issue>
<subject><json:item><value>Research Articles</value>
</json:item>
</subject>
<genre><json:string>journal</json:string>
</genre>
<language><json:string>unknown</json:string>
</language>
<eissn><json:string>1531-8249</json:string>
</eissn>
<title>Annals of Neurology</title>
<doi><json:string>10.1002/(ISSN)1531-8249</json:string>
</doi>
</host>
<categories><wos><json:string>science</json:string>
<json:string>neurosciences</json:string>
<json:string>clinical neurology</json:string>
</wos>
<scienceMetrix><json:string>health sciences</json:string>
<json:string>clinical medicine</json:string>
<json:string>neurology & neurosurgery</json:string>
</scienceMetrix>
</categories>
<publicationDate>2003</publicationDate>
<copyrightDate>2003</copyrightDate>
<doi><json:string>10.1002/ana.10481</json:string>
</doi>
<id>BF5A7E3CCACFF44C9861F7B07E7911FF2BF80A88</id>
<score>0.22074789</score>
<fulltext><json:item><extension>pdf</extension>
<original>true</original>
<mimetype>application/pdf</mimetype>
<uri>https://api.istex.fr/document/BF5A7E3CCACFF44C9861F7B07E7911FF2BF80A88/fulltext/pdf</uri>
</json:item>
<json:item><extension>zip</extension>
<original>false</original>
<mimetype>application/zip</mimetype>
<uri>https://api.istex.fr/document/BF5A7E3CCACFF44C9861F7B07E7911FF2BF80A88/fulltext/zip</uri>
</json:item>
<istex:fulltextTEI uri="https://api.istex.fr/document/BF5A7E3CCACFF44C9861F7B07E7911FF2BF80A88/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Neuroinflammatory processes in Parkinson's disease</title>
</titleStmt>
<publicationStmt><authority>ISTEX</authority>
<publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher>
<pubPlace>New York</pubPlace>
<availability><p>Copyright © 2003 Wiley‐Liss, Inc.</p>
</availability>
<date>2003</date>
</publicationStmt>
<notesStmt><note>INSERM</note>
<note>CNRS</note>
<note>National Parkinson Foundation (Miami, FL)</note>
</notesStmt>
<sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Neuroinflammatory processes in Parkinson's disease</title>
<author xml:id="author-1"><persName><forename type="first">Stephane</forename>
<surname>Hunot</surname>
</persName>
<roleName type="degree">PhD</roleName>
<affiliation>INSERM U289, Hôpital de la Salpêtrière, Paris, France</affiliation>
<affiliation>INSERM U289, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière, 47 Boulevard de l'Hôpital, 75013 Paris, France</affiliation>
</author>
<author xml:id="author-2"><persName><forename type="first">E. C.</forename>
<surname>Hirsch</surname>
</persName>
<roleName type="degree">PhD</roleName>
<affiliation>INSERM U289, Hôpital de la Salpêtrière, Paris, France</affiliation>
</author>
</analytic>
<monogr><title level="j">Annals of Neurology</title>
<title level="j" type="sub">Official Journal of the American Neurological Association and the Child Neurology Society</title>
<title level="j" type="abbrev">Ann Neurol.</title>
<idno type="pISSN">0364-5134</idno>
<idno type="eISSN">1531-8249</idno>
<idno type="DOI">10.1002/(ISSN)1531-8249</idno>
<imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher>
<pubPlace>New York</pubPlace>
<date type="published" when="2003"></date>
<biblScope unit="volume">53</biblScope>
<biblScope unit="issue">S3</biblScope>
<biblScope unit="supplement">3</biblScope>
<biblScope unit="page" from="S49">S49</biblScope>
<biblScope unit="page" to="S60">S60</biblScope>
</imprint>
</monogr>
<idno type="istex">BF5A7E3CCACFF44C9861F7B07E7911FF2BF80A88</idno>
<idno type="DOI">10.1002/ana.10481</idno>
<idno type="ArticleID">ANA10481</idno>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><creation><date>2003</date>
</creation>
<langUsage><language ident="en">en</language>
</langUsage>
<abstract xml:lang="en"><p>Parkinson's disease (PD) is a movement disorder characterized by the progressive degeneration of dopaminergic neurons in the midbrain. To date, its cause remains unknown and the mechanism of nerve cell death uncertain. Apart from the massive loss of dopaminergic neurons, PD brains also show a conspicuous glial reaction together with signs of a neuroinflammatory reaction manifested by elevated cytokine levels and upregulation of inflammatory‐associated factors such as cyclooxygenase‐2 and inducible nitric oxide synthase. Mounting evidence also suggests a possible deleterious effect of these neuroinflammatory processes in experimental models of the disease. We propose that, in PD, neuroinflammation plays a role in the cascade of events leading to nerve cell death, thus propagating the neurodegenerative process. In this review, we summarize and discuss the latest findings regarding neuroinflammatory aspects in PD. Ann Neurol 2003;53 (suppl 3):S49–S60</p>
</abstract>
<textClass><keywords scheme="Journal Subject"><list><head>article-category</head>
<item><term>Research Articles</term>
</item>
</list>
</keywords>
</textClass>
</profileDesc>
<revisionDesc><change when="2003">Published</change>
</revisionDesc>
</teiHeader>
</istex:fulltextTEI>
<json:item><extension>txt</extension>
<original>false</original>
<mimetype>text/plain</mimetype>
<uri>https://api.istex.fr/document/BF5A7E3CCACFF44C9861F7B07E7911FF2BF80A88/fulltext/txt</uri>
</json:item>
</fulltext>
<metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration>
<istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName>
<publisherLoc>New York</publisherLoc>
</publisherInfo>
<doi registered="yes">10.1002/(ISSN)1531-8249</doi>
<issn type="print">0364-5134</issn>
<issn type="electronic">1531-8249</issn>
<idGroup><id type="product" value="ANA"></id>
</idGroup>
<titleGroup><title type="main" xml:lang="en" sort="ANNALS OF NEUROLOGY">Annals of Neurology</title>
<title type="subtitle">Official Journal of the American Neurological Association and the Child Neurology Society</title>
<title type="short">Ann Neurol.</title>
</titleGroup>
</publicationMeta>
<publicationMeta level="part" position="45"><doi origin="wiley" registered="yes">10.1002/ana.v53:3+</doi>
<titleGroup><title type="supplementTitle">Neurogeneration and Prospects for Neuroprotection and Rescue in Parkinson's Disease</title>
</titleGroup>
<numberingGroup><numbering type="journalVolume" number="53">53</numbering>
<numbering type="journalIssue">S3</numbering>
<numbering type="supplement" number="3">3</numbering>
</numberingGroup>
<coverDate startDate="2003">2003</coverDate>
</publicationMeta>
<publicationMeta level="unit" type="article" position="6" status="forIssue"><doi origin="wiley" registered="yes">10.1002/ana.10481</doi>
<idGroup><id type="unit" value="ANA10481"></id>
</idGroup>
<countGroup><count type="pageTotal" number="12"></count>
</countGroup>
<titleGroup><title type="articleCategory">Research Articles</title>
<title type="tocHeading1">Research Articles</title>
</titleGroup>
<copyright ownership="publisher">Copyright © 2003 Wiley‐Liss, Inc.</copyright>
<eventGroup><event type="firstOnline" date="2003-03-24"></event>
<event type="publishedOnlineFinalForm" date="2003-03-24"></event>
<event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.1 mode:FullText source:FullText result:FullText" date="2010-02-23"></event>
<event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-03"></event>
<event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-14"></event>
</eventGroup>
<numberingGroup><numbering type="pageFirst">S49</numbering>
<numbering type="pageLast">S60</numbering>
</numberingGroup>
<correspondenceTo>INSERM U289, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière, 47 Boulevard de l'Hôpital, 75013 Paris, France</correspondenceTo>
<linkGroup><link type="toTypesetVersion" href="file:ANA.ANA10481.pdf"></link>
</linkGroup>
</publicationMeta>
<contentMeta><countGroup><count type="figureTotal" number="3"></count>
<count type="tableTotal" number="0"></count>
<count type="referenceTotal" number="83"></count>
<count type="wordTotal" number="8552"></count>
</countGroup>
<titleGroup><title type="main" xml:lang="en">Neuroinflammatory processes in Parkinson's disease</title>
<title type="short" xml:lang="en">Neuroinflammatory Process in PD</title>
</titleGroup>
<creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Stephane</givenNames>
<familyName>Hunot</familyName>
<degrees>PhD</degrees>
</personName>
<contactDetails><email>hunot@ccr.jussieu.fr</email>
</contactDetails>
</creator>
<creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>E. C.</givenNames>
<familyName>Hirsch</familyName>
<degrees>PhD</degrees>
</personName>
</creator>
</creators>
<affiliationGroup><affiliation xml:id="af1" countryCode="FR" type="organization"><unparsedAffiliation>INSERM U289, Hôpital de la Salpêtrière, Paris, France</unparsedAffiliation>
</affiliation>
</affiliationGroup>
<fundingInfo><fundingAgency>INSERM</fundingAgency>
</fundingInfo>
<fundingInfo><fundingAgency>CNRS</fundingAgency>
</fundingInfo>
<fundingInfo><fundingAgency>National Parkinson Foundation (Miami, FL)</fundingAgency>
</fundingInfo>
<abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title>
<p>Parkinson's disease (PD) is a movement disorder characterized by the progressive degeneration of dopaminergic neurons in the midbrain. To date, its cause remains unknown and the mechanism of nerve cell death uncertain. Apart from the massive loss of dopaminergic neurons, PD brains also show a conspicuous glial reaction together with signs of a neuroinflammatory reaction manifested by elevated cytokine levels and upregulation of inflammatory‐associated factors such as cyclooxygenase‐2 and inducible nitric oxide synthase. Mounting evidence also suggests a possible deleterious effect of these neuroinflammatory processes in experimental models of the disease. We propose that, in PD, neuroinflammation plays a role in the cascade of events leading to nerve cell death, thus propagating the neurodegenerative process. In this review, we summarize and discuss the latest findings regarding neuroinflammatory aspects in PD. Ann Neurol 2003;53 (suppl 3):S49–S60</p>
</abstract>
</abstractGroup>
</contentMeta>
</header>
</component>
</istex:document>
</istex:metadataXml>
<mods version="3.6"><titleInfo lang="en"><title>Neuroinflammatory processes in Parkinson's disease</title>
</titleInfo>
<titleInfo type="abbreviated" lang="en"><title>Neuroinflammatory Process in PD</title>
</titleInfo>
<titleInfo type="alternative" contentType="CDATA" lang="en"><title>Neuroinflammatory processes in Parkinson's disease</title>
</titleInfo>
<name type="personal"><namePart type="given">Stephane</namePart>
<namePart type="family">Hunot</namePart>
<namePart type="termsOfAddress">PhD</namePart>
<affiliation>INSERM U289, Hôpital de la Salpêtrière, Paris, France</affiliation>
<affiliation>INSERM U289, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière, 47 Boulevard de l'Hôpital, 75013 Paris, France</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">E. C.</namePart>
<namePart type="family">Hirsch</namePart>
<namePart type="termsOfAddress">PhD</namePart>
<affiliation>INSERM U289, Hôpital de la Salpêtrière, Paris, France</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<typeOfResource>text</typeOfResource>
<genre type="article" displayLabel="article"></genre>
<originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher>
<place><placeTerm type="text">New York</placeTerm>
</place>
<dateIssued encoding="w3cdtf">2003</dateIssued>
<copyrightDate encoding="w3cdtf">2003</copyrightDate>
</originInfo>
<language><languageTerm type="code" authority="rfc3066">en</languageTerm>
<languageTerm type="code" authority="iso639-2b">eng</languageTerm>
</language>
<physicalDescription><internetMediaType>text/html</internetMediaType>
<extent unit="figures">3</extent>
<extent unit="references">83</extent>
<extent unit="words">8552</extent>
</physicalDescription>
<abstract lang="en">Parkinson's disease (PD) is a movement disorder characterized by the progressive degeneration of dopaminergic neurons in the midbrain. To date, its cause remains unknown and the mechanism of nerve cell death uncertain. Apart from the massive loss of dopaminergic neurons, PD brains also show a conspicuous glial reaction together with signs of a neuroinflammatory reaction manifested by elevated cytokine levels and upregulation of inflammatory‐associated factors such as cyclooxygenase‐2 and inducible nitric oxide synthase. Mounting evidence also suggests a possible deleterious effect of these neuroinflammatory processes in experimental models of the disease. We propose that, in PD, neuroinflammation plays a role in the cascade of events leading to nerve cell death, thus propagating the neurodegenerative process. In this review, we summarize and discuss the latest findings regarding neuroinflammatory aspects in PD. Ann Neurol 2003;53 (suppl 3):S49–S60</abstract>
<note type="funding">INSERM</note>
<note type="funding">CNRS</note>
<note type="funding">National Parkinson Foundation (Miami, FL)</note>
<relatedItem type="host"><titleInfo><title>Annals of Neurology</title>
<subTitle>Official Journal of the American Neurological Association and the Child Neurology Society</subTitle>
</titleInfo>
<titleInfo type="abbreviated"><title>Ann Neurol.</title>
</titleInfo>
<genre type="journal">journal</genre>
<subject><genre>article-category</genre>
<topic>Research Articles</topic>
</subject>
<identifier type="ISSN">0364-5134</identifier>
<identifier type="eISSN">1531-8249</identifier>
<identifier type="DOI">10.1002/(ISSN)1531-8249</identifier>
<identifier type="PublisherID">ANA</identifier>
<part><date>2003</date>
<detail type="volume"><caption>vol.</caption>
<number>53</number>
</detail>
<detail type="issue"><caption>no.</caption>
<number>S3</number>
</detail>
<detail type="supplement"><caption>Suppl. no.</caption>
<number>3</number>
</detail>
<extent unit="pages"><start>S49</start>
<end>S60</end>
<total>12</total>
</extent>
</part>
</relatedItem>
<identifier type="istex">BF5A7E3CCACFF44C9861F7B07E7911FF2BF80A88</identifier>
<identifier type="DOI">10.1002/ana.10481</identifier>
<identifier type="ArticleID">ANA10481</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 2003 Wiley‐Liss, Inc.</accessCondition>
<recordInfo><recordContentSource>WILEY</recordContentSource>
<recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin>
</recordInfo>
</mods>
</metadata>
<serie></serie>
</istex>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonFranceV1/Data/Istex/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001220 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Istex/Corpus/biblio.hfd -nk 001220 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Wicri/Sante |area= ParkinsonFranceV1 |flux= Istex |étape= Corpus |type= RBID |clé= ISTEX:BF5A7E3CCACFF44C9861F7B07E7911FF2BF80A88 |texte= Neuroinflammatory processes in Parkinson's disease }}
![]() | This area was generated with Dilib version V0.6.29. | ![]() |