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Genes may interact with obstetric complications to boost schizophrenia risk
January 15, 2008The cause of schizophrenia is thought to include both epistasis and gene-environment interactions. We sought to test whether a set of schizophrenia candidate genes regulated by hypoxia or involved in vascular function in the brain (AKT1, BDNF, CAPON, CHRNA7, COMT, DTNBP1, GAD1, GRM3, NOTCH4, NRG1, PRODH, RGS4, TNF-á) interacted with serious obstetric complications to influence risk for schizophrenia. A family-based study of transmission disequilibrium was conducted in 116 trios. Twenty-nine probands had at least one serious obstetric complication (OC) using the McNeil-Sjostrom Scale, and many of the OCs reported were associated with the potential for fetal hypoxia. Analyses were conducted using conditional logistic regression and a likelihood ratio test (LRT) between nested models was performed to assess significance. Of the 13 genes examined, 4 (AKT1 (3 SNPs), BDNF (2 SNPs), DTNBP1 (1 SNP) and GRM3 (1 SNP)) showed significant evidence for gene-by-environment interaction (LRT p-values ranged from 0.011-0.037). Although our sample size was modest and therefore the power to detect interactions was limited, we report significant evidence for genes involved in neurovascular function or regulated by hypoxia interacting with the presence of serious obstetric complications to increase risk for schizophrenia.
Molecular Psychiatry
Schizophrenia Current Events and Schizophrenia News RSSSchizophrenia gene's role may be broader, more potent, than thought
UCSF scientists studying nerve cells in fruit flies have uncovered a new function for a gene whose human equivalent may play a critical role in schizophrenia.
Full recovery now possible for an 'untreatable' mental illness
Patients coping with the chaos and misery of Borderline Personality Disorder now have reason for strong confidence in making major life changes through a new treatment, Schema Therapy.
Immune system activated in schizophrenia
Researchers at the Swedish medical university Karolinska Institutet have discovered that patients with recent-onset schizophrenia have higher levels of inflammatory substances in their brains. Their findings offer hope of being able to treat schizophrenia with drugs that affect the immune system.
Why can't chimps speak?
If humans are genetically related to chimps, why did our brains develop the innate ability for language and speech while theirs did not?
Developmental delay could stem from nicotinic receptor deletion
The loss of a gene through deletion of genetic material on chromosome 15 is associated with significant abnormalities in learning and behavior, said a consortium of researchers led by Baylor College of Medicine (www.bcm.edu) in a report that appears online today in the journal Nature Genetics.
Fighting Sleep, Penn Researchers Reverse the Cognitive Impairment Caused By Sleep Deprivation
A research collaboration led by biologists and neuroscientists at the University of Pennsylvania has found a molecular pathway in the brain that is the cause of cognitive impairment due to sleep deprivation.
Testicular tumors may explain why some diseases are more common in children of older fathers
A rare form of testicular tumour has provided scientists with new insights into how genetic changes (mutations) arise in our children.
CSHL-led team discovers rare mutation dramatically increasing schizophrenia risk
An international team of researchers led by geneticist Jonathan Sebat, Ph.D., of Cold Spring Harbor Laboratory (CSHL), has identified a mutation on human chromosome 16 that substantially increases risk for schizophrenia.
Faulty 'wiring' in the brain triggers onset of schizophrenia
A new study by researchers at the Institute of Psychiatry (IoP), King's College London has discovered abnormalities in the white matter of the brain that seem to be critical for the timing of schizophrenia.
General anesthetics lead to learning disabilities in animal models
Studies by researchers at Wake Forest University School of Medicine have shown that blocking the NMDA receptor in immature rats leads to profound, rapid brain injury and disruption of auditory function as the animals mature.
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