Neuroinflammation in Parkinson's disease: a target for neuroprotection?
Identifieur interne : 000C02 ( PubMed/Corpus ); précédent : 000C01; suivant : 000C03Neuroinflammation in Parkinson's disease: a target for neuroprotection?
Auteurs : Etienne C. Hirsch ; 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
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pubmed:19296921Le document en format XML
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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><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19296921</PMID><DateCreated><Year>2009</Year><Month>03</Month><Day>19</Day></DateCreated><DateCompleted><Year>2009</Year><Month>04</Month><Day>23</Day></DateCompleted><DateRevised><Year>2014</Year><Month>08</Month><Day>15</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1474-4422</ISSN><JournalIssue CitedMedium="Print"><Volume>8</Volume><Issue>4</Issue><PubDate><Year>2009</Year><Month>Apr</Month></PubDate></JournalIssue><Title>The Lancet. 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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. 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