ParkinsonFranceV1, PubMed, Corpus, bibRecord, 000913

Neuroinflammation in Parkinson's disease.

Identifieur interne : 000913 ( PubMed/Corpus ); précédent : 000912; suivant : 000914

Neuroinflammation in Parkinson's disease.

Auteurs : Etienne C. Hirsch ; Sheela Vyas ; Stéphane Hunot

Source :

Parkinsonism & related disorders [ 1873-5126 ] ; 2012.

RBID : pubmed:22166438

English descriptors

KwdEn :
- Animals, Anti-Inflammatory Agents, Non-Steroidal (therapeutic use), Humans, Inflammation (drug therapy), Inflammation (metabolism), Inflammation (pathology), Nerve Degeneration (drug therapy), Nerve Degeneration (metabolism), Nerve Degeneration (pathology), Parkinson Disease (drug therapy), Parkinson Disease (metabolism), Parkinson Disease (pathology).
MESH :
- chemical , therapeutic use : Anti-Inflammatory Agents, Non-Steroidal.
- drug therapy : Inflammation, Nerve Degeneration, Parkinson Disease.
- metabolism : Inflammation, Nerve Degeneration, Parkinson Disease.
- pathology : Inflammation, Nerve Degeneration, Parkinson Disease.
- Animals, Humans.

Abstract

Both epidemiological and genetic studies support a role of neuroinflammation in the pathophysiology of Parkinson's disease (PD). Furthermore, post mortem studies confirm the involvement of innate as well as adaptive immunity in the affected brain regions in patients with PD. Indeed, activated microglial cells and T lymphocytes have been detected in the substantia nigra of patients concomitantly with an increased expression of pro-inflammatory mediators. Preclinical investigations conducted in various animal models of PD indicate that inflammatory processes are instrumental in neuronal cell death even though they are unlikely to be a primary cause for neuronal loss. Neuroinflammatory processes in PD are rather involved in self-perpetuating deleterious events that lead to protracted neuronal degeneration. In line with this, recent data indicate that glucocorticoid receptors are important in curtailing microglial reactivity, and deregulation in their activity in PD could lead to sustained inflammation-mediated degeneration. Altogether, neuroinflammatory processes might represent a target for neuroprotection in PD.

DOI: 10.1016/S1353-8020(11)70065-7
PubMed: 22166438

Links to Exploration step

pubmed:22166438

Le document en format XML

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<author><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C" last="Hirsch">Etienne C. Hirsch</name>
<affiliation><nlm:affiliation>INSERM, UMR_S975, CRicm, Experimental Therapeutics of neurodegeneration, F-75013, Paris, France. etienne.hirsch@upmc.fr</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Vyas, Sheela" sort="Vyas, Sheela" uniqKey="Vyas S" first="Sheela" last="Vyas">Sheela Vyas</name>
</author>
<author><name sortKey="Hunot, Stephane" sort="Hunot, Stephane" uniqKey="Hunot S" first="Stéphane" last="Hunot">Stéphane Hunot</name>
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<term>Nerve Degeneration (drug therapy)</term>
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<front><div type="abstract" xml:lang="en">Both epidemiological and genetic studies support a role of neuroinflammation in the pathophysiology of Parkinson's disease (PD). Furthermore, post mortem studies confirm the involvement of innate as well as adaptive immunity in the affected brain regions in patients with PD. Indeed, activated microglial cells and T lymphocytes have been detected in the substantia nigra of patients concomitantly with an increased expression of pro-inflammatory mediators. Preclinical investigations conducted in various animal models of PD indicate that inflammatory processes are instrumental in neuronal cell death even though they are unlikely to be a primary cause for neuronal loss. Neuroinflammatory processes in PD are rather involved in self-perpetuating deleterious events that lead to protracted neuronal degeneration. In line with this, recent data indicate that glucocorticoid receptors are important in curtailing microglial reactivity, and deregulation in their activity in PD could lead to sustained inflammation-mediated degeneration. Altogether, neuroinflammatory processes might represent a target for neuroprotection in PD.</div>
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<Abstract><AbstractText>Both epidemiological and genetic studies support a role of neuroinflammation in the pathophysiology of Parkinson's disease (PD). Furthermore, post mortem studies confirm the involvement of innate as well as adaptive immunity in the affected brain regions in patients with PD. Indeed, activated microglial cells and T lymphocytes have been detected in the substantia nigra of patients concomitantly with an increased expression of pro-inflammatory mediators. Preclinical investigations conducted in various animal models of PD indicate that inflammatory processes are instrumental in neuronal cell death even though they are unlikely to be a primary cause for neuronal loss. Neuroinflammatory processes in PD are rather involved in self-perpetuating deleterious events that lead to protracted neuronal degeneration. In line with this, recent data indicate that glucocorticoid receptors are important in curtailing microglial reactivity, and deregulation in their activity in PD could lead to sustained inflammation-mediated degeneration. Altogether, neuroinflammatory processes might represent a target for neuroprotection in PD.</AbstractText>
<CopyrightInformation>Copyright © 2011 Elsevier Ltd. All rights reserved.</CopyrightInformation>
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Neuroinflammation in Parkinson's disease.

Neuroinflammation in Parkinson's disease.

Source :

English descriptors

Abstract

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki