Linked Life Data

14758783

Source:http://linkedlifedata.com/resource/pubmed/id/14758783

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2004-2-4
pubmed:abstractText
Schizophrenia is a relatively common but genetically complex disorder, making the identification of susceptibility genes formidable. However, progress in genetic studies on schizophrenia during the past ten years has revealed several replicated linkage loci, which span over multiple chromosomal regions. Since last year, several causal genes have been isolated from those linkage regions. All of these have proven to have some functional relevance to glutamatergic neurotransmission. These results are interesting because the "hypoglutamatergic hypothesis" for pathophysiology of schizophrenia has been articulated since the early eighties. This hypothesis has been supported both by pharmacological evidence that administration of NMDA-type glutamate receptor antagonists induces schizophrenia-like symptoms and by neurophysiological studies. Recent lines of evidence from a candidate gene approach have also endorsed the hypothesis. Here, we introduce the overview of recent progress in genetic studies that converge to depict the hypothesis of glutamatergic hypofunction in schizophrenia.
pubmed:language
jpn
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0033-2658
pubmed:author
pubmed:issnType
Print
pubmed:volume
105
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1349-62
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
[Hypoglutamatergic hypothesis of schizophrenia: evidence from genetic studies].
pubmed:affiliation
Department of Schizophrenia Research, Tokyo Institute of Psychiatry.
pubmed:publicationType
Journal Article, English Abstract, Review