Titre
Redox dysregulation, neuroinflammation, and NMDA receptor hypofunction: A "central hub" in schizophrenia pathophysiology?
Type
synthèse (review)
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Périodique
Auteur(s)
Steullet, P.
Auteure/Auteur
Cabungcal, J.H.
Auteure/Auteur
Monin, A.
Auteure/Auteur
Dwir, D.
Auteure/Auteur
O'Donnell, P.
Auteure/Auteur
Cuenod, M.
Auteure/Auteur
Do, K.Q.
Auteure/Auteur
Liens vers les personnes
Liens vers les unités
ISSN
1573-2509
Statut éditorial
Publié
Date de publication
2016-09
Volume
176
Numéro
1
Première page
41
Dernière page/numéro d’article
51
Peer-reviewed
Oui
Langue
anglais
Notes
Publication types: Journal Article ; Review ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Publication Status: ppublish
Résumé
Accumulating evidence points to altered GABAergic parvalbumin-expressing interneurons and impaired myelin/axonal integrity in schizophrenia. Both findings could be due to abnormal neurodevelopmental trajectories, affecting local neuronal networks and long-range synchrony and leading to cognitive deficits. In this review, we present data from animal models demonstrating that redox dysregulation, neuroinflammation and/or NMDAR hypofunction (as observed in patients) impairs the normal development of both parvalbumin interneurons and oligodendrocytes. These observations suggest that a dysregulation of the redox, neuroimmune, and glutamatergic systems due to genetic and early-life environmental risk factors could contribute to the anomalies of parvalbumin interneurons and white matter in schizophrenia, ultimately impacting cognition, social competence, and affective behavior via abnormal function of micro- and macrocircuits. Moreover, we propose that the redox, neuroimmune, and glutamatergic systems form a "central hub" where an imbalance within any of these "hub" systems leads to similar anomalies of parvalbumin interneurons and oligodendrocytes due to the tight and reciprocal interactions that exist among these systems. A combination of vulnerabilities for a dysregulation within more than one of these systems may be particularly deleterious. For these reasons, molecules, such as N-acetylcysteine, that possess antioxidant and anti-inflammatory properties and can also regulate glutamatergic transmission are promising tools for prevention in ultra-high risk patients or for early intervention therapy during the first stages of the disease.
Sujets
PID Serval
serval:BIB_6A873971D7A6
PMID
Open Access
Oui
Date de création
2016-07-11T09:04:39.874Z
Date de création dans IRIS
2025-05-20T22:24:26Z
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Nom
BIB_6A873971D7A6.P001.pdf
Version du manuscrit
postprint
Taille
832.76 KB
Format
Adobe PDF
PID Serval
serval:BIB_6A873971D7A6.P001
URN
urn:nbn:ch:serval-BIB_6A873971D7A60
Somme de contrôle
(MD5):6651dcd6c86d37548b2c3f5e7662d5c3