Tuesday, December 14, 2004

More About Genetics and Depression A mutant gene that starves the brain of serotonin has been discovered. Preliminary studies describe it to be 10 times more prevalent in depressed patients than in control subjects. In a report from Duke University Department of Psychiatry sponsored by the National Institutes of Health's National Institute of Mental Health (NIMH) and National Heart Lung and Blood Institute (NHLBI), patients with this particular mutation failed to respond to antidepressant medication (SSRIs). It is theorized that this mutation may underlie a treatment-resistant subtype of depression that does not respond to the neurochemical manipulation of serotonin. According to an upcoming article in Neuron, this mutant gene codes for the brain enzyme, tryptophan hydroxylase-2, that makes serotonin, and results in an 80 percent reduction of the neurotransmitter. The Duke team of researchers describe that it was carried by nine of 87 depressed patients, three of 219 healthy controls and none of 60 bipolar disorder patients. More than 10 percent of the 87 patients with unipolar major depression carried the mutation, compared to only one percent of the 219 controls. Among the nine SSRI-resistant patient carriers, seven had a family history of mental illness or substance abuse, six had been suicidal and four had generalized anxiety. It is believed that major depression is approximately 40-70 percent heritable, but it most likely involves an interaction of several genes with environmental events. Previous studies have linked depression with the same region of chromosome 12, where the tryptophan hydroxylase-2 gene is located. Whether the absence of the mutation among 60 patients with bipolar disorder proves to be evidence of a different underlying biology remains to be investigated in future studies. The researchers believe that their finding provides a potential molecular mechanism for aberrant serotonin function in neuropsychiatric disorders. Recent research on chromosome 12 and depression 10:28:21 PM    comment []

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