Linked Life Data

11727894

Source:http://linkedlifedata.com/resource/pubmed/id/11727894

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-11-30
pubmed:abstractText
Several lines of evidence indicate that abnormalities in the functioning of the central serotonergic system are involved in the pathogenesis of depressive illness and suicidal behavior. Studies have shown that the number of brain and platelet serotonin transporter binding sites are reduced in patients with depression and in suicide victims, and that the density of 5-HT2A receptors is increased in brain regions of depressed in suicide victims and in platelets of depressed suicidal patients. Genes that code for proteins, such as tryptophan hydroxylase, 5-HT transporter, and 5-HT2A receptor, involved in regulating serotonergic neurotransmission, have thus been major candidate genes for association studies of suicide and suicidal behavior. Recent studies by our group and by others have shown that genetic variations in the serotonin-system-related genes might be associated with suicidal ideation and completed suicide. We have shown that the 102 C allele in 5-HT2A receptor gene was significantly associated with suicidal ideation (chi2 = 8.5. p < .005) in depressed patients. Patients with a 102 C/C genotype had a significantly higher mean HAMD item #3 score (indication of suicidal ideation) than T/C or T/7 genotype patients. Our results suggest that the 102T/C polymorphism in 5-HT2A receptor gene is primarily associated with suicidal ideation in patients with major depression and not with depression itself. We also found that the 5-HT transporter gene S/L polymorphism was significantly associated with completed suicide. The frequency of the L/L genotype in depressed suicide victims was almost double of that found in control group (48.6% vs. 26.2%). The odds ratio for the L allele was 2.1 (95% CI 1.2-3.7). The association between polymorphism in serotonergic genes and suicidality supports the hypothesis that genetic factors can modulate suicide risk by influencing serotonergic activity.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0227-5910
pubmed:author
pubmed:issnType
Print
pubmed:volume
22
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
54-60
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11727894-Alleles, pubmed-meshheading:11727894-Carrier Proteins, pubmed-meshheading:11727894-Genetic Predisposition to Disease, pubmed-meshheading:11727894-Genotype, pubmed-meshheading:11727894-Humans, pubmed-meshheading:11727894-Membrane Glycoproteins, pubmed-meshheading:11727894-Membrane Transport Proteins, pubmed-meshheading:11727894-Nerve Tissue Proteins, pubmed-meshheading:11727894-Polymorphism, Genetic, pubmed-meshheading:11727894-Receptor, Serotonin, 5-HT2A, pubmed-meshheading:11727894-Receptors, Serotonin, pubmed-meshheading:11727894-Risk Factors, pubmed-meshheading:11727894-Serotonin, pubmed-meshheading:11727894-Serotonin Plasma Membrane Transport Proteins, pubmed-meshheading:11727894-Suicide, pubmed-meshheading:11727894-Thinking, pubmed-meshheading:11727894-Tryptophan Hydroxylase
pubmed:year
2001
pubmed:articleTitle
Serotonergic genes and suicidality.
pubmed:affiliation
Institute of Mental Health Research at Royal Ottawa Hospital and University of Ottawa, Ontario, Canada,. ldu@rohcg.on.ca
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't