ParkinsonCanadaV1, Main, Exploration, bibRecord, 002317

Glial reactions in Parkinson's disease

Identifieur interne : 002317 ( Main/Exploration ); précédent : 002316; suivant : 002318

Glial reactions in Parkinson's disease

Auteurs : Patrick L. Mcgeer [Canada] ; Edith G. Mcgeer [Canada]

Source :

Movement Disorders [ 0885-3185 ] ; 2008-03-15.

RBID : ISTEX:98A18F4EFC1048970EF17CEA369726841EBA1582

Descripteurs français

Pascal (Inist)
- Astrocyte, Inflammation, Maladie de Parkinson, Microglie, Oligodendroglie, Pathologie du système nerveux, Stress oxydatif.

English descriptors

KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (adverse effects), Animals, Anti-Inflammatory Agents, Non-Steroidal (pharmacology), Astrocyte, Astrocytes (immunology), Astrocytes (metabolism), Astrocytes (pathology), Brain (drug effects), Dopamine (metabolism), Female, HLA-DR Antigens (immunology), Haplorhini, Humans, Immunohistochemistry, Inflammation, Inflammation (chemically induced), Inflammation (pathology), Intercellular Adhesion Molecule-1 (immunology), MPTP, Male, Microglia, Microglia (immunology), Microglia (metabolism), Microglia (pathology), Nervous system diseases, Neurons (immunology), Neurons (metabolism), Neurons (pathology), Neurotoxins (adverse effects), Oligodendroglia, Oxidative Stress (physiology), Oxidative stress, Parkinson Disease (immunology), Parkinson Disease (metabolism), Parkinson Disease (pathology), Parkinson disease, Substantia Nigra (immunology), Substantia Nigra (metabolism), Substantia Nigra (pathology), alpha-Synuclein (metabolism), astrocytes, inflammation, microglia, oligodendroglia, oxidative stress, α‐synuclein.
MESH :
- chemical , adverse effects : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Neurotoxins.
- chemical , immunology : HLA-DR Antigens, Intercellular Adhesion Molecule-1.
- chemical , metabolism : Dopamine, alpha-Synuclein.
- chemical , pharmacology : Anti-Inflammatory Agents, Non-Steroidal.
- chemically induced : Inflammation.
- drug effects : Brain.
- immunology : Astrocytes, Microglia, Neurons, Parkinson Disease, Substantia Nigra.
- metabolism : Astrocytes, Microglia, Neurons, Parkinson Disease, Substantia Nigra.
- pathology : Astrocytes, Inflammation, Microglia, Neurons, Parkinson Disease, Substantia Nigra.
- physiology : Oxidative Stress.
- Animals, Female, Haplorhini, Humans, Immunohistochemistry, Male.

Abstract

Dopaminergic neurons of the substantia nigra are particularly vulnerable to oxidative and inflammatory attack. Such processes may play a crucial role in the etiology of Parkinson disease (PD). Since glia are the main generators of these processes, the possibility that PD may be caused by glial dysfunction needs to be considered. This review concentrates on glial reactions in PD. Reactive astrocytes and reactive microglia are abundant in the substantia nigra (SN) of PD cases indicating a robust inflammatory state. Glia normally serve neuroprotective roles but, given adverse stimulation, they may contribute to damaging chronic inflammation. Microglia, the phagocytes of brain, may be the main contributors since they can produce large numbers of superoxide anions and other neurotoxins. Their toxicity towards dopaminergic neurons has been demonstrated in tissue culture and various animal models of PD. The MPTP and α‐synuclein models are of particular interest. Years after exposure to MPTP, inflammation has been observed in the SN. This has established that an acute insult to the SN can result in a sustained local inflammation. The α‐synuclein model indicates that an endogenous protein can induce inflammation, and, when overexpressed, can lead to autosomal dominant PD. Less is known about the role of astrocytes than microglia, but they are known to secrete both inflammatory and anti‐inflammatory molecules and may play a role in modulating microglial activity. Oligodendrocytes do not seem to play a role in promoting inflammation although, like neurons, they may be damaged by inflammatory processes. Further research concerning glial reactions in PD may lead to disease‐modifying therapeutic approaches. © 2007 Movement Disorder Society

Url:

https://api-v5.istex.fr/document/98A18F4EFC1048970EF17CEA369726841EBA1582/fulltext/pdf

DOI: 10.1002/mds.21751

Affiliations:

Canada

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<front><div type="abstract" xml:lang="en">Dopaminergic neurons of the substantia nigra are particularly vulnerable to oxidative and inflammatory attack. Such processes may play a crucial role in the etiology of Parkinson disease (PD). Since glia are the main generators of these processes, the possibility that PD may be caused by glial dysfunction needs to be considered. This review concentrates on glial reactions in PD. Reactive astrocytes and reactive microglia are abundant in the substantia nigra (SN) of PD cases indicating a robust inflammatory state. Glia normally serve neuroprotective roles but, given adverse stimulation, they may contribute to damaging chronic inflammation. Microglia, the phagocytes of brain, may be the main contributors since they can produce large numbers of superoxide anions and other neurotoxins. Their toxicity towards dopaminergic neurons has been demonstrated in tissue culture and various animal models of PD. The MPTP and α‐synuclein models are of particular interest. Years after exposure to MPTP, inflammation has been observed in the SN. This has established that an acute insult to the SN can result in a sustained local inflammation. The α‐synuclein model indicates that an endogenous protein can induce inflammation, and, when overexpressed, can lead to autosomal dominant PD. Less is known about the role of astrocytes than microglia, but they are known to secrete both inflammatory and anti‐inflammatory molecules and may play a role in modulating microglial activity. Oligodendrocytes do not seem to play a role in promoting inflammation although, like neurons, they may be damaged by inflammatory processes. Further research concerning glial reactions in PD may lead to disease‐modifying therapeutic approaches. © 2007 Movement Disorder Society</div>
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La maladie de Parkinson au Canada (serveur d'exploration)

Glial reactions in Parkinson's disease

Glial reactions in Parkinson's disease

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

	La maladie de Parkinson au Canada (serveur d'exploration)
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.