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<p>“How do we know that genes play a role in causing depression? Scientists look at patterns of illness in families to estimate their “heritability,” or roughly what percentage of their cause is due to genes. To do this we find people with the disease who have a twin, and then find out whether the twin is also ill. Identical (monozygotic) twins share 100% of their genes, while non-identical (“fraternal” or dizygotic) twins share 50% of their genes. If genes are part of the cause, we expect a patient’s identical twin to have a much higher risk of disease than a patient’s non-identical twin. That is the case for major depression. Heritability is probably 40-50%, and might be higher for severe depression.”</p>
<p>[GenRED</a> - Major Depression and Genetics - Genetics of Brain Function - Stanford University School of Medicine](<a href=“Genetics of Brain Function | Genetics of Brain Function | Stanford Medicine”>Genetics of Brain Function | Genetics of Brain Function | Stanford Medicine)</p>
<p>Also:</p>
<p>Flu in Pregnancy May Quadruple Child’s Risk for Bipolar Disorder</p>
<p>May 14, 2013 — Pregnant mothers’ exposure to the flu was associated with a nearly fourfold increased risk that their child would develop bipolar disorder in adulthood, in a study funded by the National Institutes of Health. The findings add to mounting evidence of possible shared underlying causes and illness processes with schizophrenia, which some studies have also linked to prenatal exposure to influenza.</p>
<p>[Flu</a> in pregnancy may quadruple child’s risk for bipolar disorder](<a href=“http://www.sciencedaily.com/releases/2013/05/130514101459.htm]Flu”>Flu in pregnancy may quadruple child's risk for bipolar disorder | ScienceDaily)</p>
<p>“Epidemiological studies indicate that maternal influenza viral infection increases the risk for schizophrenia in the adult offspring. The serotonin and glutamate systems are suspected in the etiology of schizophrenia, as well as in the mechanism of action of antipsychotic drugs. The effects of hallucinogens, such as psilocybin and mescaline, require the serotonin 5-HT2A receptor, and induce schizophrenia-like psychosis in humans. In addition, metabotropic glutamate receptor mGlu2/3 agonists show promise as a new treatment for schizophrenia. Here, we investigated the level of expression and behavioral function of 5-HT2A and mGlu2 receptors in a mouse model of maternal influenza viral infection. We show that spontaneous locomotor activity is diminished by maternal infection with the mouse-adapted influenza A/WSN/33 (H1N1) virus. The behavioral responses to hallucinogens and glutamate antipsychotics are both affected by maternal exposure to influenza virus, with increased head-twitch response to hallucinogens and diminished antipsychotic-like effect of the glutamate agonist. In frontal cortex of mice born to influenza virus-infected mothers, the 5-HT2A receptor is upregulated and the mGlu2 receptor is downregulated, an alteration that may be involved in the behavioral changes observed. Additionally, we find that the cortical 5-HT2A receptor-dependent signaling pathways are significantly altered in the offspring of infected mothers, showing higher c-fos, egr-1, and egr-2 expression in response to the hallucinogenic drug DOI. Identifying a biochemical alteration that parallels the behavioral changes observed in a mouse model of prenatal viral infection may facilitate targeting therapies for treatment and prevention of schizophrenia.”</p>
<p>[Maternal</a> Influenza Viral Infection Causes Schizophrenia-Like Alterations of 5-HT2A and mGlu2 Receptors in the Adult Offspring](<a href=“http://www.jneurosci.org/content/31/5/1863.full]Maternal”>http://www.jneurosci.org/content/31/5/1863.full)</p>