Linking early-life NMDAR hypofunction and oxidative stress in schizophrenia pathogenesis.

Détails

Ressource 1Télécharger: BIB_0ECCF75A1F1F.P001.pdf (468.08 [Ko])
Etat: Public
Version: de l'auteur
ID Serval
serval:BIB_0ECCF75A1F1F
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Institution
Titre
Linking early-life NMDAR hypofunction and oxidative stress in schizophrenia pathogenesis.
Périodique
Nature Reviews. Neuroscience
Auteur(s)
Hardingham G.E., Do K.Q.
ISSN
1471-0048 (Electronic)
ISSN-L
1471-003X
Statut éditorial
Publié
Date de publication
2016
Peer-reviewed
Oui
Volume
17
Numéro
2
Pages
125-134
Langue
anglais
Notes
Publication types: Journal Article Publication Status: ppublish
Résumé
Molecular, genetic and pathological evidence suggests that deficits in GABAergic parvalbumin-positive interneurons contribute to schizophrenia pathophysiology through alterations in the brain's excitation-inhibition balance that result in impaired behaviour and cognition. Although the factors that trigger these deficits are diverse, there is increasing evidence that they converge on a common pathological hub that involves NMDA receptor hypofunction and oxidative stress. These factors have been separately linked to schizophrenia pathogenesis, but evidence now suggests that they are mechanistically interdependent and contribute to a common schizophrenia-associated pathology.
Pubmed
Web of science
Open Access
Oui
Création de la notice
19/01/2016 13:30
Dernière modification de la notice
20/08/2019 12:35
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