Linked Life Data

19481443

Source:http://linkedlifedata.com/resource/pubmed/id/19481443

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2009-7-27
pubmed:abstractText
In schizophrenia, a developmental redox dysregulation constitutes one 'hub' on which converge genetic impairments of glutathione synthesis and environmental vulnerability factors generating oxidative stress. Their timing at critical periods of neurodevelopment could play a decisive role in inducing impairment of neural connectivity and synchronization as observed in schizophrenia. In experimental models, such redox dysregulation induces anomalies strikingly similar to those observed in patients. This is mediated by hypoactive NMDA receptors, impairment of fast-spiking parvalbumin GABA interneurons and deficit in myelination. A treatment restoring the redox balance without side effects yields improvements of negative symptoms in chronic patients. Novel interventions based on these mechanisms if applied in early phases of the disease hold great therapeutic promise.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1873-6882
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
220-30
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Redox dysregulation, neurodevelopment, and schizophrenia.
pubmed:affiliation
Center for Psychiatric Neuroscience, Department of Psychiatry, Lausanne University Hospital, Site de Cery, CH-1008 Prilly-Lausanne, Switzerland. kim.do@chuv.ch
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't