Neuroinflammation in Parkinson's disease: a target for neuroprotection?
Identifieur interne : 000982 ( Ncbi/Curation ); précédent : 000981; suivant : 000983Neuroinflammation in Parkinson's disease: a target for neuroprotection?
Auteurs : Etienne C. Hirsch [France] ; Stéphane HunotSource :
- The Lancet. Neurology [ 1474-4422 ] ; 2009.
English descriptors
- KwdEn :
- Animals, Anti-Inflammatory Agents (therapeutic use), Cell Death (physiology), Dopamine (metabolism), Humans, Immunization, Immunologic Factors (therapeutic use), Inflammation (pathology), Inflammation (physiopathology), Nerve Degeneration (physiopathology), Nerve Degeneration (therapy), Neuroimmunomodulation, Neurons (physiology), Neuroprotective Agents (therapeutic use), Parkinson Disease (pathology), Parkinson Disease (physiopathology), Parkinson Disease (therapy).
- MESH :
- chemical , metabolism : Dopamine.
- chemical , therapeutic use : Anti-Inflammatory Agents, Immunologic Factors, Neuroprotective Agents.
- pathology : Inflammation, Parkinson Disease.
- physiology : Cell Death, Neurons.
- physiopathology : Inflammation, Nerve Degeneration, Parkinson Disease.
- therapy : Nerve Degeneration, Parkinson Disease.
- Animals, Humans, Immunization, Neuroimmunomodulation.
Abstract
Parkinson's disease is characterised by a slow and progressive degeneration of dopaminergic neurons in the substantia nigra. Despite intensive research, the cause of the neuronal loss in Parkinson's disease is poorly understood. Neuroinflammatory mechanisms might contribute to the cascade of events leading to neuronal degeneration. In this Review, we describe the evidence for neuroinflammatory processes from post-mortem and in vivo studies in Parkinson's disease. We further identify the cellular and molecular events associated with neuroinflammation that are involved in the degeneration of dopaminergic neurons in animal models of the disease. Overall, available data support the importance of non-cell-autonomous pathological mechanisms in Parkinson's disease, which are mostly mediated by activated glial and peripheral immune cells. This cellular response to neurodegeneration triggers deleterious events (eg, oxidative stress and cytokine-receptor-mediated apoptosis), which might eventually lead to dopaminergic cell death and hence disease progression. Finally, we highlight possible therapeutic strategies (including immunomodulatory drugs and therapeutic immunisation) aimed at downregulating these inflammatory processes that might be important to slow the progression of Parkinson's disease.
DOI: 10.1016/S1474-4422(09)70062-6
PubMed: 19296921
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: Pour aller vers cette notice dans l'étape Curation :000C02
- to stream PubMed, to step Curation: Pour aller vers cette notice dans l'étape Curation :000B62
- to stream PubMed, to step Checkpoint: Pour aller vers cette notice dans l'étape Curation :000B62
- to stream Ncbi, to step Merge: Pour aller vers cette notice dans l'étape Curation :000982
Links to Exploration step
pubmed:19296921Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Neuroinflammation in Parkinson's disease: a target for neuroprotection?</title><author><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C" last="Hirsch">Etienne C. Hirsch</name><affiliation wicri:level="3"><nlm:affiliation>INSERM, UMRS 975, Centre de Recherche de l'Institut du Cerveau et de la Moelle épinière, Experimental Therapeutics of Neurodegeneration, Paris, France. etienne.hirsch@upmc.fr</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>INSERM, UMRS 975, Centre de Recherche de l'Institut du Cerveau et de la Moelle épinière, Experimental Therapeutics of Neurodegeneration, Paris</wicri:regionArea><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Hunot, Stephane" sort="Hunot, Stephane" uniqKey="Hunot S" first="Stéphane" last="Hunot">Stéphane Hunot</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2009">2009</date><idno type="RBID">pubmed:19296921</idno><idno type="pmid">19296921</idno><idno type="doi">10.1016/S1474-4422(09)70062-6</idno><idno type="wicri:Area/PubMed/Corpus">000C02</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000C02</idno><idno type="wicri:Area/PubMed/Curation">000B62</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000B62</idno><idno type="wicri:Area/PubMed/Checkpoint">000B62</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000B62</idno><idno type="wicri:Area/Ncbi/Merge">000982</idno><idno type="wicri:Area/Ncbi/Curation">000982</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Neuroinflammation in Parkinson's disease: a target for neuroprotection?</title><author><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C" last="Hirsch">Etienne C. Hirsch</name><affiliation wicri:level="3"><nlm:affiliation>INSERM, UMRS 975, Centre de Recherche de l'Institut du Cerveau et de la Moelle épinière, Experimental Therapeutics of Neurodegeneration, Paris, France. etienne.hirsch@upmc.fr</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>INSERM, UMRS 975, Centre de Recherche de l'Institut du Cerveau et de la Moelle épinière, Experimental Therapeutics of Neurodegeneration, Paris</wicri:regionArea><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Hunot, Stephane" sort="Hunot, Stephane" uniqKey="Hunot S" first="Stéphane" last="Hunot">Stéphane Hunot</name></author></analytic><series><title level="j">The Lancet. Neurology</title><idno type="ISSN">1474-4422</idno><imprint><date when="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Anti-Inflammatory Agents (therapeutic use)</term><term>Cell Death (physiology)</term><term>Dopamine (metabolism)</term><term>Humans</term><term>Immunization</term><term>Immunologic Factors (therapeutic use)</term><term>Inflammation (pathology)</term><term>Inflammation (physiopathology)</term><term>Nerve Degeneration (physiopathology)</term><term>Nerve Degeneration (therapy)</term><term>Neuroimmunomodulation</term><term>Neurons (physiology)</term><term>Neuroprotective Agents (therapeutic use)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson Disease (therapy)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Anti-Inflammatory Agents</term><term>Immunologic Factors</term><term>Neuroprotective Agents</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Inflammation</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Cell Death</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Inflammation</term><term>Nerve Degeneration</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Nerve Degeneration</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term><term>Immunization</term><term>Neuroimmunomodulation</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease is characterised by a slow and progressive degeneration of dopaminergic neurons in the substantia nigra. Despite intensive research, the cause of the neuronal loss in Parkinson's disease is poorly understood. Neuroinflammatory mechanisms might contribute to the cascade of events leading to neuronal degeneration. In this Review, we describe the evidence for neuroinflammatory processes from post-mortem and in vivo studies in Parkinson's disease. We further identify the cellular and molecular events associated with neuroinflammation that are involved in the degeneration of dopaminergic neurons in animal models of the disease. Overall, available data support the importance of non-cell-autonomous pathological mechanisms in Parkinson's disease, which are mostly mediated by activated glial and peripheral immune cells. This cellular response to neurodegeneration triggers deleterious events (eg, oxidative stress and cytokine-receptor-mediated apoptosis), which might eventually lead to dopaminergic cell death and hence disease progression. Finally, we highlight possible therapeutic strategies (including immunomodulatory drugs and therapeutic immunisation) aimed at downregulating these inflammatory processes that might be important to slow the progression of Parkinson's disease.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonFranceV1/Data/Ncbi/Curation
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000982 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Ncbi/Curation/biblio.hfd -nk 000982 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= ParkinsonFranceV1
|flux= Ncbi
|étape= Curation
|type= RBID
|clé= pubmed:19296921
|texte= Neuroinflammation in Parkinson's disease: a target for neuroprotection?
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Ncbi/Curation/RBID.i -Sk "pubmed:19296921" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Ncbi/Curation/biblio.hfd \
| NlmPubMed2Wicri -a ParkinsonFranceV1
| This area was generated with Dilib version V0.6.29. |  |