La maladie de Parkinson au Canada (serveur d'exploration)

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Glial Reactions in Parkinson's Disease

Identifieur interne : 000651 ( PascalFrancis/Curation ); précédent : 000650; suivant : 000652

Glial Reactions in Parkinson's Disease

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

Source :

RBID : Pascal:08-0199299

Descripteurs français

English descriptors

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.
pA  
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A08 01  1  ENG  @1 Glial Reactions in Parkinson's Disease
A11 01  1    @1 MCGEER (Patrick L.)
A11 02  1    @1 MCGEER (Edith G.)
A14 01      @1 Kinsmen Laboratory of Neurological Research, University of British Columbia @2 Vancouver, British Columbia @3 CAN @Z 1 aut. @Z 2 aut.
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C01 01    ENG  @0 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.
C02 01  X    @0 002B17
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C03 01  X  SPA  @0 Parkinson enfermedad @2 NM @5 01
C03 02  X  FRE  @0 Pathologie du système nerveux @5 02
C03 02  X  ENG  @0 Nervous system diseases @5 02
C03 02  X  SPA  @0 Sistema nervioso patología @5 02
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C03 04  X  FRE  @0 Inflammation @5 10
C03 04  X  ENG  @0 Inflammation @5 10
C03 04  X  SPA  @0 Inflamación @5 10
C03 05  X  FRE  @0 Astrocyte @5 11
C03 05  X  ENG  @0 Astrocyte @5 11
C03 05  X  SPA  @0 Astrocito @5 11
C03 06  X  FRE  @0 Oligodendroglie @5 12
C03 06  X  ENG  @0 Oligodendroglia @5 12
C03 06  X  SPA  @0 Oligodendroglia @5 12
C03 07  X  FRE  @0 Stress oxydatif @5 13
C03 07  X  ENG  @0 Oxidative stress @5 13
C03 07  X  SPA  @0 Estrés oxidativo @5 13
C07 01  X  FRE  @0 Pathologie de l'encéphale @5 37
C07 01  X  ENG  @0 Cerebral disorder @5 37
C07 01  X  SPA  @0 Encéfalo patología @5 37
C07 02  X  FRE  @0 Syndrome extrapyramidal @5 38
C07 02  X  ENG  @0 Extrapyramidal syndrome @5 38
C07 02  X  SPA  @0 Extrapiramidal síndrome @5 38
C07 03  X  FRE  @0 Maladie dégénérative @5 39
C07 03  X  ENG  @0 Degenerative disease @5 39
C07 03  X  SPA  @0 Enfermedad degenerativa @5 39
C07 04  X  FRE  @0 Pathologie du système nerveux central @5 40
C07 04  X  ENG  @0 Central nervous system disease @5 40
C07 04  X  SPA  @0 Sistema nervosio central patología @5 40
C07 05  X  FRE  @0 Névroglie @5 42
C07 05  X  ENG  @0 Neuroglia @5 42
C07 05  X  SPA  @0 Neuroglia @5 42
N21       @1 126
N44 01      @1 OTO
N82       @1 OTO

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Pascal:08-0199299

Le document en format XML

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